Skin Tape Stripping: A Non-invasive Approach Linking Epidermal Changes and Systemic Inflammation in Atopic Dermatitis

Skin Tape Stripping: A Non-invasive Approach Linking Epidermal Changes and Systemic Inflammation in Atopic Dermatitis | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 'https://ssl' : 'http://www') + '.google-analytics.com/ga.js'; var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s); })(); Skip to main content Preprints Collections Wiley Open Research IET Open Research Ecological Society of Japan All Collections About About Authorea FAQs Contact Us Quick Search anywhere Search for preprint articles, keywords, etc. Search Search ADVANCED SEARCH SCROLL This is a preprint and has not been peer reviewed. Data may be preliminary. 17 October 2025 V1 Latest version Share on Skin Tape Stripping: A Non-invasive Approach Linking Epidermal Changes and Systemic Inflammation in Atopic Dermatitis Authors : Ziyuan Tian 0009-0004-5372-136X , Ke Xue [email protected] , and Yong Cui Authors Info & Affiliations https://doi.org/10.22541/au.176070638.81323239/v1 456 views 134 downloads Contents Abstract Introduction STS: Technology and Advantages Clinical Applications in Disease Management Integrating Tape Stripping and Skin Biopsies: From Epidermis to Dermis Integrating Tape Stripping and Blood Analysis: Linking Local and Systemic Inflammation Multimodal Integration and Microbiome Insights: Broadening the Research Landscape Conclusion Supplementary Material References Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Atopic dermatitis (AD) is a complex, chronic inflammatory skin disease driven by skin barrier dysfunction, immune dysregulation, and microbial imbalance. Traditional sampling methods, such as biopsies and blood collection, have provided valuable pathophysiological insights. However, their invasiveness, associated discomfort, and limitations for repeated sampling have constrained a dynamic understanding of disease progression and treatment responses. In recent years, skin tape stripping (STS) has emerged as a minimally invasive or even non-invasive technique that overcomes these limitations. STS enables the collection of corneocytes and upper granular layer cells from the epidermis, and when combined with high-throughput multi-omics technologies, such as RNA sequencing, proteomics, lipidomics, and metatranscriptomics, it provides a powerful platform to dissect the molecular mechanisms of AD, identify novel biomarkers, and inform personalized therapeutic strategies. Article type: review Title: Skin Tape Stripping: A Non-invasive Approach Linking Epidermal Changes and Systemic Inflammation in Atopic Dermatitis Ziyuan Tian 1,2 , Ke Xue 1 , Yong Cui 1,2 1 Department of Dermatology, China-Japan Friendship Hospital, Beijing, China; 2 Graduate School, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China. Corresponding author : Ke Xue; Yong Cui, Department of Dermatology, China-Japan Friendship Hospital, Beijing, China, 100029; [email protected] , [email protected] Author contributions: Tian. wrote the main manuscript text and prepared the figures. Cui. and Xue. provided guidance and review for the article. All authors reviewed the manuscript Conflicts of Interest : None declared. Ethics statement: Not applicable. Data availability statement : The data that support the findings of this study are available from the corresponding author upon reasonable request. Manuscript word count : 3833 words Abstract word count : 124 words References : 70 Figures: 2 Tables: 1 Skin Tape Stripping: A Non-invasive Approach Linking Epidermal Changes and Systemic Inflammation in Atopic Dermatitis Abstract Atopic dermatitis (AD) is a complex, chronic inflammatory skin disease driven by skin barrier dysfunction, immune dysregulation, and microbial imbalance. Traditional sampling methods, such as biopsies and blood collection, have provided valuable pathophysiological insights. However, their invasiveness, associated discomfort, and limitations for repeated sampling have constrained a dynamic understanding of disease progression and treatment responses. In recent years, skin tape stripping (STS) has emerged as a minimally invasive or even non-invasive technique that overcomes these limitations. STS enables the collection of corneocytes and upper granular layer cells from the epidermis, and when combined with high-throughput multi-omics technologies, such as RNA sequencing, proteomics, lipidomics, and metatranscriptomics, it provides a powerful platform to dissect the molecular mechanisms of AD, identify novel biomarkers, and inform personalized therapeutic strategies. Keywords: Atopic Dermatitis; Skin tape stripping; Immunity; Biomarkers; Skin Barrier Introduction Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder characterized by intense pruritus, eczematous lesions, and recurrent flare-ups [1]. The disease markedly impairs quality of life and is often accompanied by comorbidities such as sleep disturbances, anxiety, and depression [2]. The pathogenesis of AD is multifactorial and clinically heterogeneous, driven primarily by defects in skin barrier integrity and dysregulation of immune responses [2-4]. Although traditional methods, such as skin biopsies and blood analyses, have yielded valuable insights into these mechanisms, their invasive nature limits their broad clinical applicability. Recently, skin tape stripping (STS) has emerged as a non-invasive and practical alternative that overcomes these limitations, providing a powerful tool and fresh perspective for elucidating the molecular basis of AD. Pathogenesis of AD The pathogenesis of AD is highly complex, centering on the dynamic interplay between skin barrier dysfunction and immune dysregulation [5]. The prevailing paradigm posits that AD is co-driven by impaired barrier integrity and aberrant immune activation, forming a self-perpetuating cycle in which barrier disruption triggers immune activation, which in turn exacerbates barrier damage. Furthermore, genetic predisposition, environmental exposures, microbial imbalance, and the involvement of multiple immune axes, including Th1, Th17, and Th22 pathways, collectively shape the heterogeneous clinical manifestations of AD [3]. Skin Barrier Dysfunction: A Core Driver Skin barrier dysfunction is a central pathogenic process in AD, and some studies even suggest it precedes immune activation [6]. This impairment involves both structural and functional abnormalities of the stratum corneum, leading to increased transepidermal water loss (TEWL) and enhanced susceptibility to allergens, irritants, and microbial invasion [3]. At the molecular level, barrier breakdown arises from the synergistic effects of genetic, biochemical, and structural factors. Loss-of-function mutations in the filaggrin (FLG) gene form the major genetic basis of this defect [7]. These mutations weaken the mechanical integrity of the stratum corneum and lead to xerosis due to reduced production of natural moisturizing factors (NMFs) derived from FLG degradation [6, 8]. In parallel, disruption of intercellular lipid homeostasis further compromises barrier function. AD skin displays both a reduction in total ceramide content and alterations in ceramide composition, particularly shortened fatty acid chains, which disturb the lamellar lipid organization and impair the hydrophobic barrier [9, 10]. Additionally, defective tight junctions in the granular layer weaken the secondary barrier that regulates paracellular permeability [11]. These factors collectively lead to the comprehensive damage of the skin barrier in AD. Importantly, the molecular characteristics of barrier dysfunction vary among AD subtypes. For example, patients with food allergy–associated AD (AD FA⁺) exhibit distinct alterations in epidermal architecture compared with those without food allergy [8]. Therefore, elucidating the molecular composition and functional disruption of the skin barrier is crucial for understanding the onset and progression of AD. Autoimmune Dysregulation: The Cytokine Network Immune dysregulation constitutes a central driver of AD, characterized by a predominant Th2-type immune response integrated within a complex cytokine network that also involves the Th1, Th17, and Th22 pathways [12]. The activation of this network is dynamic, varying across age, ethnicity, and disease stage, thereby shaping the diverse immunological endotypes and clinical phenotypes of AD [13, 14]. Debate over the initiating event of AD has evolved from the traditional dichotomy of ”barrier-initiated” versus ”immune-initiated” hypotheses to a more unified concept recognizing their reciprocal causality [3]. In the barrier-initiated model, epidermal disruption triggers keratinocytes to release epithelial-derived cytokines, or alarmins, such as thymic stromal lymphopoietin and interleukin (IL)-33, which in turn initiate downstream immune activation [15]. Conversely, in the immune-initiated model, intrinsic immune dysregulation—driven by genetic or epigenetic predisposition—precedes barrier damage. In these cases, excessive IL-4 and IL-13 production directly impairs epidermal integrity, a mechanism particularly evident in intrinsic AD, where the barrier appears macroscopically intact [14]. Despite distinct initiation routes, both pathways converge on Th2 axis activation, the hallmark of AD pathophysiology. The Th2 cytokines IL-4 and IL-13 exert dual pathogenic effects: they suppress the expression of key barrier proteins such as FLG via STAT6-mediated signaling [15], and they promote inflammatory cell recruitment through induction of chemokines such as TARC/CCL17 [16-18]. Beyond Th2-driven inflammation, additional immune axes modulate disease course. Th1 activation predominates in chronic lesions, whereas Th17 and Th22 pathways confer distinct immunological signatures in specific patient populations (such as Asian and pediatric cohorts) and synergistically amplify barrier dysfunction [13, 19, 20]. Pruritus, Microbiome Dysbiosis, and Environmental Factors Dysbiosis of the skin microbiome is a hallmark and exacerbating factor in AD. Lesional skin is often dominated by Staphylococcus aureus ( S. aureus ), whose overgrowth represents a characteristic feature of microbial imbalance in AD patients [8]. Proteases secreted by S. aureus can directly degrade desmosomal proteins that connect keratinocytes, compromising the structural integrity of the epidermal barrier. Simultaneously, S. aureus stimulates keratinocytes and immune cells to release pro-inflammatory factors, thereby amplifying type 2 inflammatory responses [21-23]. Environmental exposures, including air pollutants, further compromise barrier function by increasing TEWL and serving as ligands for the aryl hydrocarbon receptor, which activates inflammatory signaling pathways in the skin [24]. Pruritus (itching) is a central clinical feature and active driver of AD, rather than a passive symptom. Scratching in response to itch mechanically damages the barrier and triggers the release of inflammatory mediators. Type 2 cytokines, such as IL-31, act on sensory neurons to induce itch, establishing a self-perpetuating itch–scratch cycle that exacerbates disease progression [4]. Analysis of traditional samples, such as skin biopsies and blood samples, has allowed us to understand the pathogenesis of AD. Skin biopsies are unique in providing simultaneous access to both the epidermis and dermis, enabling comprehensive evaluation of histological changes, cellular infiltration, and inflammatory responses within the deep dermis [25-28]. Biopsies are particularly advantageous for investigating specific immune pathways, such as Th1 and Th22, and for detecting dermal cytokines (e.g., IFN-γ) and epidermal proliferation markers (e.g., KRT16) [29][30], offering novel insight into deep skin pathology [31]. However, their invasive nature poses significant limitations: they cause patient discomfort, may leave scars, and are poorly tolerated in pediatric populations, rendering frequent or longitudinal sampling impractical[18, 32]. Moreover, the pronounced spatial heterogeneity of AD lesions means that a single biopsy may not fully represent the molecular landscape of the affected area or capture dynamic changes across disease stages [33]. Furthermore, the coexistence of epidermis and dermis in biopsy samples can “dilute” signals from molecules predominantly expressed in the epidermis (such as FLG and loricrin), reducing detection sensitivity and potentially biasing assessments of functional protein levels [26, 29, 34]. In contrast, blood sampling offers a minimally invasive and convenient method, ideal for large-scale or longitudinal studies. Blood reflects the systemic immune dysregulation characteristic of moderate-to-severe AD and provides a valuable window for assessing responses to systemic therapies [17, 35]. However, its systemic nature is also a limitation: blood cannot accurately capture local skin barrier defects or the intricate interactions between epidermal and immune cells. Key local inflammatory signals (such as innate immune activation and elevated IL-1α and IL-18) are often weak or undetectable in circulation [35, 36]. Therefore, blood biomarkers may respond too subtly or with delay to reflect the effects of topical treatments, and systemic drug effects in the skin and blood are not always temporally synchronized [37]. Given these limitations, STS has emerged as a non-invasive alternative that bridges the gap between local and systemic perspectives. STS directly links epidermal pathophysiological changes with systemic inflammation, offering a more integrated view of disease biology A truly comprehensive understanding of AD requires a multi-modal sampling framework. Similar to conventional multi-omics, which integrates different molecular layers (e.g., transcriptomics, proteomics), the strategic combination of sampling modalities represents a form of ’methodological multi-omics.’ This approach, uniting the epidermal perspective from tape stripping, the dermal-epidermal perspective from biopsies, and the systemic perspective from blood, is crucial for constructing a perspective, multi-dimensional understanding of AD’s pathophysiology. Figure 1. The Pathophysiological Landscape of AD and the Complementary Roles of Different Sampling Modalities. It presents the core mechanisms of AD, highlighting the interplay between barrier defects and immune pathways. Three key sampling methods are contrasted: skin tape stripping, a non-invasive tool focused on the epidermis, is ideal for monitoring barrier integrity and superficial inflammation. A skin biopsy provides a complete, yet invasive, cross-section of the skin, essential for studying deep dermal processes. Finally, blood sampling assesses the systemic dimension of AD by detecting circulating cytokines that reflect the overall inflammatory load. Together, these approaches enable a multi-dimensional understanding of AD, from surface-level changes to systemic immune status. AD, atopic dermatitis. STS: Technology and Advantages The STS Protocol: From Sample Collection to Extraction STS is a non-invasive technique that uses specialized tape to collect corneocytes and biomolecules from the epidermis, avoiding dermal contamination inherent to biopsies [38]. STS samples can be used for various downstream analyses, including RNA, protein, lipidomics, and microbiome studies [32]. Its simplicity, safety, pain-free application, and repeatability make STS particularly suitable for pediatric populations and for longitudinal monitoring of dynamic changes in inflammatory skin diseases [32, 33, 39]. Various professional tapes are commercially available for STS; while sampling efficiency may vary, most are effective for successful biomolecule collection [40]. The core STS procedure involves repeated application and removal of the tape at the same site under consistent pressure, removing the epidermis layer by layer. The sampling depth is primarily determined by the number of sequential strips. For example, 35 D-squame strips can fully remove the stratum corneum [40, 41]. The stable concentration of biomarkers across successive strips confirms the technique’s high reliability and support streamlined protocols [42]. Extraction protocols are tailored to the physicochemical properties of target analytes. For RNA, tape samples are initially treated with a strong lysis buffer, such as RNA lysis buffer, followed by purification using commercial kits. Due to the limited yield from a single strip [43], a pooling strategy—combining multiple strips—is commonly employed to enrich RNA content for downstream analysis [44]. The extracted RNA is remarkably stable, remaining suitable for sequencing for up to three days at room temperature, facilitating sample handling and logistics [45]. Protein extraction is well established: the tape is typically immersed in a buffer (e.g., PBS or RIPA) containing detergents (e.g., Tween-20) and protease inhibitors, with elution aided by physical disruption, including sonication [17, 18, 35]. For small, specialized proteins, such as antimicrobial peptides, chemical denaturation using 8 M urea can be used [46]. Lipid extraction is straightforward, often involving methanol as a solvent, followed by vortexing and storage at -20 °C [47]. Synergy with Modern Analytical Technologies Although STS yields relatively small amounts of biomolecules, the high sensitivity of modern analytical technologies fully compensates for this limitation. Next-generation sequencing enables comprehensive profiling of gene expression in AD skin from minute samples, revealing dysregulated pathways, barrier gene defects, and microbiome activity [29, 30, 45, 48]. Similarly, high-resolution mass spectrometry provides direct insight into barrier protein damage, inflammatory mediators, and lipid abnormalities, including ceramide deficiencies [8, 9, 49-51]. The combination of STS with advanced analytical techniques offers several prominent advantages. First, its non-invasive and convenient nature minimizes the physiological and psychological burden on patients, especially children and other sensitive populations [52]. This method has been successfully used for dynamic monitoring of lesional and non-lesional skin in pediatric AD patients, uncovering age-specific molecular phenotypes without the need for repeated biopsies or frequent blood draws [30, 53]. This capability opens new avenues for long-term clinical monitoring and longitudinal studies. Second, STS enables precise characterization of the molecular heterogeneity of AD. Its simplicity allows multi-site sampling to capture spatial and inter-individual differences [54, 55]. Furthermore, STS can be applied to non-lesional skin to detect early or subclinical molecular changes, providing critical insight into disease progression and potential recurrence [30]. Together, these features make STS a powerful platform for integrating molecular analysis with patient-centered, minimally invasive sampling. Figure 2. The Skin Tape Stripping Workflow for Multi-omics Analysis. It outlines the standardized procedure for utilizing skin tape stripping as a powerful tool for molecular research. The workflow begins with sampling, where an adhesive tape non-invasively collects corneocytes and biomolecules from the stratum corneum. Immediately following is preservation, where the tape is submerged in a solution to stabilize fragile molecules like RNA and proteins. In the extraction stage, target biomolecules arc eluted and isolated from the adhesive matrix. Finally, the purified extract is subjected to downstream analysis using high-throughput technologies, enabling comprehensive multi-omics profiling-including transcriptomics, proteomics, lipidomics, and microbiome analysis-to provide deep molecular insights into skin health and disease. Clinical Applications in Disease Management By integrating proteomics, lipidomics, and sensitive immunoassays such as Multiple Analyte Profiling (MSD), STS provides a unique window into the core pathogenesis of AD. Studies consistently demonstrate elevated innate immunity cytokines (IL-1β, IL-18, IL-8) and Th2-associated chemokines (TARC, CCL22) in tape strips from lesional AD skin [13, 36, 56]. Proteomic analyses of tape strip samples have revealed a cluster of 45 proteins (PC1) strongly correlated with TEWL and allergen polysensitization in pediatric patients with AD FA⁺, suggesting a distinct proteomic endotype [51]. Levels of NMF, a FLG breakdown product, are significantly reduced in tape strip samples from AD patients and correlate with both disease severity and treatment response [18, 27, 52]. Lipidomic studies have confirmed ceramide deficiencies in AD skin [57], and combined analyses of lipid profiles, family history, and type 2 cytokines have demonstrated strong predictive power for the risk of AD [56]. Interestingly, STS has also revealed AD-like ceramide deficiencies in the healthy skin of pediatric patients with eosinophilic esophagitis, suggesting potential utility for monitoring internal disease states [10]. These molecular insights have direct clinical applications. In healthy infants, elevated TARC/CCL17 at 2 months can predict future AD onset, serving as an early risk biomarker [58, 59]. In infants with established lesions, elevated IL-2, CCL26, and CCL20 levels indicate a higher risk of AD progression, with IL-2 acting as a key prognostic marker once inflammation is present [56, 60]. STS also enables sensitive monitoring of treatment responses. Proteomic studies have showed that dupilumab reduces 136 proteins, including immune and cardiovascular risk markers [50, 61]. Although both abrocitinib and dupilumab improve barrier function, they modulate distinct protein networks, with abrocitinib demonstrating superior restoration of key proteins such as FLG-2 [61, 62]. Post-JAK inhibitor treatment, some patients show clinical improvement while retaining elevated inflammatory proteins (e.g., TARC/CCL17), suggesting a risk of recurrence [49]. Furthermore, STS can distinguish the efficacy of different topical medications: betamethasone more effectively reduces skin cytokines, whereas tacrolimus primarily enhances skin hydration [52]. STS also elucidates site-specific therapeutic challenges. Cytokine expression varies between lesion locations; for example, forehead lesions show higher levels of Th1/Th17-related factors, which may explain their slower resolution when treated with IL-4 receptor inhibitors [55]. Biomarker levels in tape strips correlate with disease severity: cytokines such as TARC, CTACK, IL-8, and IL-18 correlate with SCORAD and TEWL [13, 16]. Moreover, NMF and cytokine profiles differ in patients with FLG mutations and food allergies, suggesting STS may surpass biopsies in detecting these specific biomarkers [63]. STS also supports differential diagnosis. RNA sequencing of tape strip samples can distinguish AD from psoriasis through unique immune signatures and NOS2/iNOS expression [48]. It can differentiate types of hand eczema (allergic versus irritant contact dermatitis) and characterize chronic hand eczema subtypes with or without AD [64, 65]. Collectively, these findings confirm STS is a powerful tool, with significant potential in disease prediction, prognosis, treatment monitoring, severity assessment, and differential diagnosis in AD. Integrating Tape Stripping and Skin Biopsies: From Epidermis to Dermis A comprehensive understanding of AD requires the integration of the complementary strengths of different sampling methods. Skin biopsies provide detailed information on deep tissue structures and molecular changes within the dermis, whereas STS focuses on the epidermis, offering non-invasive, repeatable access to its dynamic alterations. Therefore, discrepancies between biopsy and STS results should be interpreted not as methodological conflicts but as insights into layered pathological mechanisms. Several RNA sequencing studies have directly compared tape strips and biopsies in AD patients, highlighting their complementary value [26, 29]. Tape strips are particularly sensitive to epidermal features, including pruritus-associated genes (e.g., IL-31), innate immune activation, and defects in terminal keratinocyte differentiation. In contrast, biopsies more accurately capture dermal cytokine dynamics, the Th22 inflammatory response, and tissue-level abnormalities such as epidermal hyperplasia [34]. This differential sensitivity provides a strategic entry point for in-depth mechanistic investigation. For example, high Th1 immune signaling is predominantly observed in adult AD and is largely undetectable in tape strip samples. Further analysis revealed that Th1 signals originate primarily from the deep dermis, explaining STS detection limitations. This raises a critical question: does elevated Th1 expression in adult AD reflect an age-related change, or is it a chronic disease phenotype emerging from systemic immune dysregulation in adulthood [13]? The difference between deep tissue and superficial epidermis also highlights a more fundamental issue: does a molecule’s potential correspond to its actual function? This discrepancy is particularly evident at the transcript and protein levels. A comparison study within the same individuals have demonstrated a lack of correlation between cytokine mRNA levels (potential) in biopsies and corresponding protein levels (function) in tape strips. These findings likely reflect complex post-transcriptional and translational regulation, accounting for differences between full-thickness gene transcripts and epidermal protein profiles [34]. These seemingly contradictory findings precisely highlight the unique insights offered by STS and emphasize the value of integrating multiple technologies. Combining STS with biopsies allows construction of a complete molecular map from the epidermis to the dermis, enabling a deeper analysis of the complex pathophysiological mechanisms underlying AD. Integrating Tape Stripping and Blood Analysis: Linking Local and Systemic Inflammation Combining STS with blood analysis is essential for an integrated assessment of local and systemic inflammation in AD. While blood samples capture systemic immune status, they often fail to reflect specific pathological changes occurring within the skin. STS, in contrast, is particularly sensitive to innate pro-inflammatory cytokines, T-cell–recruiting chemokines, and tissue repair proteins, whereas serum better represents systemic immune activity, including key T-cell-derived cytokines such as IL-4 and IL-13 [35]. This complementary approach has significant clinical value. In patients in remission, blood tests may reveal residual minimal persistent inflammation, whereas NMF levels measured by STS indicate whether the local epidermal barrier has been fully restored. Together, these measurements provide a more comprehensive assessment of recurrence risk [37]. Studies in infants further demonstrate that local corticosteroid treatment not only ameliorates epidermal inflammation, as detected by STS, but also normalizes systemic Th2 biomarkers in blood, supporting the concept that the skin is a major source of systemic inflammatory cytokines [17, 27]. Multimodal Integration and Microbiome Insights: Broadening the Research Landscape Beyond integration with blood analysis, STS serves as a central hub for molecular data, which can be combined with other non-invasive skin assessment techniques to achieve multi-modal data fusion. Combining molecular data from tape strips with physiological indicators, like TEWL and skin conductance, as well as imaging modalities like reflectance confocal microscopy, enables cross-validation and enrichment of findings across multiple perspectives [6, 16, 41]. For example, combining tape strip proteomic data with TEWL measurements has identified protein clusters strongly correlated with barrier function, providing a precise foundation for the diagnosis, monitoring, and treatment of AD [51]. In microbiome research, STS has similarly advanced our understanding. Integrated RNA sequencing and lipidomics enable simultaneous characterization of microbial communities and lipid composition in AD skin [57], revealing the critical role of commensal microbiota in regulating ceramide metabolism and opening new avenues for investigating microbe-lipid interactions [8, 9, 54]. Studies have also demonstrated that the natural variation in microbial diversity across different skin habitats—dry, moist, and sebaceous—is diminished in AD, indicating that the disease state overrides intrinsic environmental influences [66]. Importantly, metagenomic analyses reveal microbial functional potential (DNA), but metatranscriptomics is required to capture actual activity (RNA). Significant discrepancies are observed: abundant bacteria such as Propionibacterium acnes can exhibit low transcriptional activity, whereas larger eukaryotes like Malassezia may exert disproportionate functional effects. RNA-based analysis is therefore crucial to distinguish microbial presence from activity and to identify key pathogenic contributors in a compromised skin barrier [67]. Variability in STS data should be interpreted not as a limitation but as a source of mechanistic insight. The spatial heterogeneity between STS and biopsies, for example, reflects the stratified pathology of AD rather than methodological conflict: STS sensitively captures superficial epidermal processes, while biopsies reveal deeper dermal signals, highlighting their complementarity in constructing a complete molecular map of the skin. Discrepancies within tape strip analyses at different molecular levels are similarly informative. For instance, the core Th2 cytokine IL-13 shows consistent transcript upregulation in RNA sequencing, yet the corresponding protein is often difficult to detect. This paradox underscores complex post-transcriptional and post-translational regulation, providing insight into the dynamic relationship between transcriptional potential and functional protein expression in epidermal cells. Furthermore, the heterogeneity between local STS findings and systemic blood biomarkers further emphasizes STS’s role as a bridge. STS can detect subclinical inflammation in the skin even when systemic markers are normal, supporting the concept of the skin as a primary source of systemic cytokines and capturing the local-to-systemic cascade. This approach also reveals temporal heterogeneity, showing that different biomarkers are predictive for disease risk versus prognosis. Investigating multi-dimensional heterogeneity across spatial, molecular, systemic, and temporal domains therefore provides a more complete, dynamic, and nuanced understanding of AD pathophysiology . Despite the considerable promise of integrating STS with multi-omics technologies, several key challenges must be addressed to translate this approach from a research tool into routine clinical practice. Standardization of the STS method is critical to ensure reproducibility and comparability across studies. Currently, research protocols vary in tape type, number of applications, applied pressure, sampling site, and sample processing procedures. Different tapes require different numbers of applications to remove the stratum corneum, and individual variation in stratum corneum thickness further complicates sampling [41]. Establishing rigorous, unified standard operating procedures—including optimized sampling parameters, standardized sample handling, and coordinated multi-center protocols—will enhance the external validity and reliability of STS studies. The integration of STS samples with multi-omics platforms generates large, complex datasets, posing significant bioinformatics challenges. Advanced analytical tools tailored to STS multi-omics data are needed for effective data integration, dimensionality reduction, and pattern recognition. Open-access STS multi-omics databases would facilitate data sharing and re-analysis, accelerating the discovery of universal biomarkers and core pathological mechanisms. Moreover, network biology methods that map host gene-protein-lipid-microbe interactions can identify key regulatory nodes and pathways in AD pathogenesis, providing new avenues for targeted therapies. Beyond RNA, proteins, and lipids, STS also provides access to novel biomolecules. For example, adhesive sebum collection tapes have been used to sample skin hormones, opening new opportunities to explore the role of local endocrine factors in inflammatory skin diseases [47]. A key future goal is the clinical translation of STS findings, developing low-cost, rapid, point-of-care tools for early diagnosis, efficacy prediction, and personalized treatment strategies in AD. The utility of STS extends beyond AD. It has been successfully applied to psoriasis [39, 68], juvenile dermatomyositis [43], hidradenitis suppurativa [69], and seborrheic dermatitis [70], revealing unique molecular signatures across these conditions. Future studies could leverage STS to compare molecular profiles across different skin diseases, identifying shared pathological mechanisms or disease-specific biomarkers, thereby promoting a holistic understanding of inflammatory skin diseases. Conclusion As a chronic, relapsing inflammatory skin disease, the management of AD and the assessment of treatment response rely on longitudinal molecular data. However, traditional sampling methods are invasive, often painful, and may leave scars, limiting patient compliance, particularly in infants and young children, and creating a bottleneck for clinical research. In this context, STS represents a major advancement. As a minimally invasive epidermal sampling technique, STS enables high-quality longitudinal studies, capturing the full molecular trajectory of individual patients. In the era of multi-omics, STS systematically illuminates the molecular complexity of AD, facilitating the discovery of novel biomarkers for early prediction, precise phenotyping, and personalized treatment strategies. More importantly, STS exemplifies a conceptual shift towards “methodological multi-omics”, serving as a critical epidermal bridge. A holistic understanding of AD emerges not from relying on a single technique, but from integrating complementary methods: STS captures epidermal dynamics, biopsies reveal deep tissue pathology, and blood analysis reflects systemic inflammation. This multi-dimensional framework provides insights unattainable by any single approach and positions STS as a cornerstone of integrated research strategies, essential for advancing precision medicine in AD. In summary, STS is more than a novel sampling method; it is a conceptual bridge linking basic research and clinical practice, facilitating the implementation of precision medicine. While challenges remain in standardization, data integration, and bioinformatics, the prospects are promising. Future efforts should focus on establishing robust standard operating procedures, developing advanced tools for multi-omics data integration, and accelerating the clinical translation of findings. By complementing biopsies and blood-based analyses, STS will continue to strengthen this bridge, ultimately advancing precision medicine for AD and improving the health and quality of life of millions of patients worldwide. Table 1 Applications and Discoveries of Skin Tape Stripping Combined with Multi-omics Technologies in AD Research Skin Barrier Function Proteomics - Identified PC1 specific to AD FA + , associated with TEWL and allergen sensitization - NMF levels correlate with AD severity and treatment response - Revealed differences in barrier protein repair mechanisms between abrocitinib and dupilumab Lipidomics - Revealed disease-specific lipid-microbe correlations in AD skin (e.g., S. hominis and ceramides) - Identified unique lipid deficiencies in AD FA+ patients Immune Pathways & Cytokines Proteomics / Cytokine Profiling - Detected elevated inflammatory markers in AD skin (e.g., IL-1β, IL-18, CCL17, etc.) - Revealed immune signatures of AD patients across different age groups - Monitored immunological changes following treatments (e.g., dupilumab, JAK inhibitors) Microbiome Metagenomics / 16S rRNA - Identified increased Staphylococcus aureus abundance in non-lesional skin of AD FA + - Revealed complex interactions between S. hominis and host lipid metabolism Metatranscriptomics - Identified active microbial species and their functions - Provided more dynamic functional information than genomics Novel Biomakers Proteomics / Cytokine Profiling - Elevated skin TARC/CCL17 levels in infancy can predict AD onset - Identified a unique proteomic endotype for AD FA + - Identified immune markers for monitoring treatment response RNA Sequencing - Differentiated unique immune and barrier features of AD from psoriasis and hand eczema - Assessed biomarkers related to disease severity, FLG mutations, and food allergies AD, Atopic Dermatitis; AD FA+, Food-Allergy-Associated AD; TEWL, Transepidermal Water Loss; NMF, Natural Moisturizing Factor; IL, Interleukin; CCL17, Chemokine (C-C motif) Ligand 17; TARC, Thymus and Activation-Regulated Chemokine; FLG, Filaggrin; JAK, Janus Kinase; RNA, Ribonucleic Acid; 16S rRNA, 16S Ribosomal RNA; S. hominis, Staphylococcus hominis; S. aureus, Staphylococcus aureus; PC1, Protein Cluster 1 Supplementary Material File (table 1 applications and discoveries of skin tape stripping combined with multi-omics technologies in ad research.docx) Download 11.26 KB References 1. 1. Laughter MR, Maymone MBC, Mashayekhi S, Arents BWM, Karimkhani C, Langan SM, Dellavalle RP, Flohr C: The global burden of atopic dermatitis: lessons from the Global Burden of Disease Study 1990-2017 . The British journal of dermatology 2021, 184 (2):304-309.2. Afshari M, Kolackova M, Rosecka M, Čelakovská J, Krejsek J: Unraveling the skin; a comprehensive review of atopic dermatitis, current understanding, and approaches . Frontiers in immunology 2024, 15 :1361005.3. Facheris P, Jeffery J, Del Duca E, Guttman-Yassky E: The translational revolution in atopic dermatitis: the paradigm shift from pathogenesis to treatment . Cellular & molecular immunology 2023, 20 (5):448-474.4. Nakajima S, Nakamizo S, Nomura T, Ishida Y, Sawada Y, Kabashima K: Integrating multi-omics approaches in deciphering atopic dermatitis pathogenesis and future therapeutic directions . Allergy 2024, 79 (9):2366-2379.5. Leung DY, Guttman-Yassky E: Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches . The Journal of allergy and clinical immunology 2014, 134 (4):769-779.6. Yoshida T, Beck LA, De Benedetto A: Skin barrier defects in atopic dermatitis: From old idea to new opportunity . Allergology international : official journal of the Japanese Society of Allergology 2022, 71 (1):3-13.7. Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP, Curtin JA, Bønnelykke K, Tian C, Takahashi A et al : Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis . Nature genetics 2015, 47 (12):1449-1456.8. Leung DYM, Calatroni A, Zaramela LS, LeBeau PK, Dyjack N, Brar K, David G, Johnson K, Leung S, Ramirez-Gama M et al : The nonlesional skin surface distinguishes atopic dermatitis with food allergy as a unique endotype . Science translational medicine 2019, 11 (480).9. Bhattacharyya M, Lauffer F, Jargosch M, Frey K, Dadras MS, Raunegger T, Wasserer S, Schmidt-Weber CB, Biedermann T, Eyerich K et al : Skin Lipid-Microbe Interplay Links Staphylococcus hominis to Barrier Control in Adult Atopic Dermatitis . Allergy 2025.10. Goleva E, Leung DY, Chaiboonma K, Tom W, Dohil R, Lyubchenko K, Bronova I, Bronoff AS, Berdyshev E, Aceves SS: Cutaneous ceramide synthesis is dysregulated in pediatric eosinophilic esophagitis . The Journal of allergy and clinical immunology 2025, 155 (6):2075-2079.e2071.11. De Benedetto A, Rafaels NM, McGirt LY, Ivanov AI, Georas SN, Cheadle C, Berger AE, Zhang K, Vidyasagar S, Yoshida T et al : Tight junction defects in patients with atopic dermatitis . The Journal of allergy and clinical immunology 2011, 127 (3):773-786.e771-777.12. Gittler JK, Shemer A, Suárez-Fariñas M, Fuentes-Duculan J, Gulewicz KJ, Wang CQ, Mitsui H, Cardinale I, de Guzman Strong C, Krueger JG et al : Progressive activation of T(H)2/T(H)22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis . The Journal of allergy and clinical immunology 2012, 130 (6):1344-1354.13. Renert-Yuval Y, Del Duca E, Pavel AB, Fang M, Lefferdink R, Wu J, Diaz A, Estrada YD, Canter T, Zhang N et al : The molecular features of normal and atopic dermatitis skin in infants, children, adolescents, and adults . The Journal of allergy and clinical immunology 2021, 148 (1):148-163.14. Tokura Y, Hayano S: Subtypes of atopic dermatitis: From phenotype to endotype . Allergology international : official journal of the Japanese Society of Allergology 2022, 71 (1):14-24.15. Furue M: Regulation of Filaggrin, Loricrin, and Involucrin by IL-4, IL-13, IL-17A, IL-22, AHR, and NRF2: Pathogenic Implications in Atopic Dermatitis . International journal of molecular sciences 2020, 21 (15).16. Lyubchenko T, Collins HK, Goleva E, Leung DYM: Skin tape sampling technique identifies proinflammatory cytokines in atopic dermatitis skin . Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology 2021, 126 (1):46-53.e42.17. McAleer MA, Jakasa I, Stefanovic N, McLean WHI, Kezic S, Irvine AD: Topical corticosteroids normalize both skin and systemic inflammatory markers in infant atopic dermatitis . The British journal of dermatology 2021, 185 (1):153-163.18. Hulshof L, Hack DP, Hasnoe QCJ, Dontje B, Jakasa I, Riethmüller C, McLean WHI, van Aalderen WMC, Van’t Land B, Kezic S et al : A minimally invasive tool to study immune response and skin barrier in children with atopic dermatitis . The British journal of dermatology 2019, 180 (3):621-630.19. Gutowska-Owsiak D, Schaupp AL, Salimi M, Selvakumar TA, McPherson T, Taylor S, Ogg GS: IL-17 downregulates filaggrin and affects keratinocyte expression of genes associated with cellular adhesion . Experimental dermatology 2012, 21 (2):104-110.20. Czarnowicki T, He H, Krueger JG, Guttman-Yassky E: Atopic dermatitis endotypes and implications for targeted therapeutics . The Journal of allergy and clinical immunology 2019, 143 (1):1-11.21. Kudryavtseva A, Fluer F, Khachatryan L, Makarova S, Osipenko O, Ryzhii E, Titarev S, Zaslavsky D, Gelezhe K: Staphylococcus Strains in Atopic Dermatitis in Children: Toxins Production and Resistance Properties . Life (Basel, Switzerland) 2025, 15 (7).22. Clowry J, Dempsey DJ, Claxton TJ, Towell AM, Turley MB, Sutton M, Geoghegan JA, Kezic S, Jakasa I, White A et al : Distinct T cell signatures are associated with Staphylococcus aureus skin infection in pediatric atopic dermatitis . JCI insight 2024, 9 (9).23. Nakatsuji T, Chen TH, Two AM, Chun KA, Narala S, Geha RS, Hata TR, Gallo RL: Staphylococcus aureus Exploits Epidermal Barrier Defects in Atopic Dermatitis to Trigger Cytokine Expression . The Journal of investigative dermatology 2016, 136 (11):2192-2200.24. Dijkhoff IM, Drasler B, Karakocak BB, Petri-Fink A, Valacchi G, Eeman M, Rothen-Rutishauser B: Impact of airborne particulate matter on skin: a systematic review from epidemiology to in vitro studies . Particle and fibre toxicology 2020, 17 (1):35.25. Grieco T, Paolino G, Moliterni E, Chello C, Sernicola A, Egan CG, Morelli M, Nannipieri F, Battaglia S, Accoto M et al : Transcriptomic Profiling of Lesional and Perilesional Skin in Atopic Dermatitis Suggests Barrier Dysfunction, Inflammatory Activation, and Alterations to Vitamin D Metabolism . International journal of molecular sciences 2025, 26 (13).26. Del Duca E, He H, Liu Y, Pagan AD, David E, Cheng J, Carroll B, Renert-Yuval Y, Bar J, Estrada YD et al : Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape-strips and biopsies . Allergy 2024, 79 (1):80-92.27. McAleer MA, Jakasa I, Hurault G, Sarvari P, McLean WHI, Tanaka RJ, Kezic S, Irvine AD: Systemic and stratum corneum biomarkers of severity in infant atopic dermatitis include markers of innate and T helper cell-related immunity and angiogenesis . The British journal of dermatology 2019, 180 (3):586-596.28. Dyjack N, Goleva E, Rios C, Kim BE, Bin L, Taylor P, Bronchick C, Hall CF, Richers BN, Seibold MA et al : Minimally invasive skin tape strip RNA sequencing identifies novel characteristics of the type 2-high atopic dermatitis disease endotype . The Journal of allergy and clinical immunology 2018, 141 (4):1298-1309.29. Fritz B, Halling AS, Cort ID, Christensen MO, Rønnstad ATM, Olesen CM, Knudgaard MH, Zachariae C, Heegaard S, Thyssen JP et al : RNA-sequencing of paired tape-strips and skin biopsies in atopic dermatitis reveals key differences . Allergy 2024, 79 (6):1548-1559.30. Pavel AB, Renert-Yuval Y, Wu J, Del Duca E, Diaz A, Lefferdink R, Fang MM, Canter T, Rangel SM, Zhang N et al : Tape strips from early-onset pediatric atopic dermatitis highlight disease abnormalities in nonlesional skin . Allergy 2021, 76 (1):314-325.31. Liu TJ, Lin LL, McMeniman E, Wu J, Kao YC, Kumari S, Boyle GM, Wells JW, Soyer HP, Gonzalez-Cruz JL: Cytokine/Chemokine assessment as a complementary diagnostic tool for inflammatory skin diseases . Frontiers in immunology 2022, 13 :1028435.32. Liu D, Hu BD, Mishra A, Patel D, Lau M, Navrazhina K, He H, Guttman-Yassky E: Tape Strips in Inflammatory Skin Disease: A Noninvasive Method for Molecular Insights and Personalized Care . The British journal of dermatology 2025.33. Frew JW, Navrazhina K, Byrd AS, Garg A, Ingram JR, Kirby JS, Lowes MA, Naik H, Piguet V, Prens EP: Defining lesional, perilesional and unaffected skin in hidradenitis suppurativa: proposed recommendations for clinical trials and translational research studies . The British journal of dermatology 2019, 181 (6):1339-1341.34. Simonsen S, Brøgger P, Kezic S, Thyssen JP, Skov L: Comparison of Cytokines in Skin Biopsies and Tape Strips from Adults with Atopic Dermatitis . Dermatology (Basel, Switzerland) 2021, 237 (6):940-945.35. van der Rijst LP, Knol EF, Zuithoff NPA, den Hartog Jager CF, van Wijk F, de Bruin-Weller MS, de Graaf M: Complementary Analysis of Local and Systemic Effects of Dupilumab in Paediatric AD Using Tape Strips and Serum . Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 2025, 55 (7):552-563.36. He H, Del Duca E, Diaz A, Kim HJ, Gay-Mimbrera J, Zhang N, Wu J, Beaziz J, Estrada Y, Krueger JG et al : Mild atopic dermatitis lacks systemic inflammation and shows reduced nonlesional skin abnormalities . The Journal of allergy and clinical immunology 2021, 147 (4):1369-1380.37. Sánchez A, Caraballo A, Alvarez L, Valencia O, Restrepo MN, Gaviria R, Velasquez-Lopera M, Urrego JR, Sánchez J: Molecular characteristics of atopic dermatitis patients with clinical remission . The World Allergy Organization journal 2024, 17 (11):100983.38. Li W, Turner A, Aggarwal P, Matter A, Storvick E, Arnett DK, Broeckel U: Comprehensive evaluation of AmpliSeq transcriptome, a novel targeted whole transcriptome RNA sequencing methodology for global gene expression analysis . BMC genomics 2015, 16 :1069.39. Berekmeri A, Macleod T, Hyde I, Ojak GJ, Mann C, Kramer D, Stacey M, Wittmann M: Epidermal proteomics demonstrates Elafin as a psoriasis-specific biomarker and highlights increased anti-inflammatory activity around psoriatic plaques . Journal of the European Academy of Dermatology and Venereology : JEADV 2025, 39 (7):1324-1335.40. Olesen CM, Fuchs CSK, Philipsen PA, Hædersdal M, Agner T, Clausen ML: Advancement through epidermis using tape stripping technique and Reflectance Confocal Microscopy . Scientific reports 2019, 9 (1):12217.41. Sølberg J, Ulrich NH, Krustrup D, Ahlström MG, Thyssen JP, Menné T, Bonefeld CM, Gadsbøll A, Balslev E, Johansen JD: Skin tape stripping: Which layers of the epidermis are removed? Contact dermatitis 2019, 80 (5):319-321.42. Clausen ML, Kezic S, Olesen CM, Agner T: Cytokine concentration across the stratum corneum in atopic dermatitis and healthy controls . Scientific reports 2020, 10 (1):21895.43. Turnier JL, Vandenbergen SM, McClune ME, Goudsmit C, Matossian S, Riebschleger M, Saad N, Madison JA, Mohan S, Gudjonsson JE et al : Tape strip expression profiling of juvenile dermatomyositis skin reveals mitochondrial dysfunction contributing to disease endotype . JCI insight 2025, 10 (8).44. Hu T, Todberg T, Andersen D, Danneskiold-Samsøe NB, Hansen SBN, Kristiansen K, Ewald DA, Brix S, Rosa JCD, Hoof I et al : Profiling the Atopic Dermatitis Epidermal Transcriptome by Tape Stripping and BRB-seq . International journal of molecular sciences 2022, 23 (11).45. Sølberg J, Jacobsen SB, Andersen JD, Litman T, Ulrich NH, Ahlström MG, Kampmann ML, Morling N, Thyssen JP, Johansen JD: The stratum corneum transcriptome in atopic dermatitis can be assessed by tape stripping . Journal of dermatological science 2021, 101 (1):14-21.46. Jenei A, Kalló G, Dajnoki Z, Gáspár K, Szegedi A, Kapitány A, Csősz É: Detection of Antimicrobial Peptides in Stratum Corneum by Mass Spectrometry . International journal of molecular sciences 2021, 22 (8).47. Sturges CI, Jain S, Velasquez M, Gedamu H, Komarovsky J, McDonald J, Harris-Tryon T: Cutaneous Hormone Sampling and Analysis for Dermatologic Research . The Journal of investigative dermatology 2025, 145 (8):1850-1857.48. Tape strips in dermatology researchHe H, Bissonnette R, Wu J, Diaz A, Saint-Cyr Proulx E, Maari C, Jack C, Louis M, Estrada Y, Krueger JG et al : Tape strips detect distinct immune and barrier profiles in atopic dermatitis and psoriasis . The Journal of allergy and clinical immunology 2021, 147 (1):199-212.49. Boesjes CM, van der Gang LF, Bakker DS, den Hartog Jager CF, de Graaf M, de Bruin-Weller MS, van Wijk F, Knol EF: Increased Levels of Inflammatory Proteins, Including TARC/CCL17, in Skin of AD Patients During JAK Inhibitor Treatment . Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology 2025, 55 (3):260-263.50. He H, Olesen CM, Pavel AB, Clausen ML, Wu J, Estrada Y, Zhang N, Agner T, Guttman-Yassky E: Tape-Strip Proteomic Profiling of Atopic Dermatitis on Dupilumab Identifies Minimally Invasive Biomarkers . Frontiers in immunology 2020, 11 :1768.51. 、Goleva E, Calatroni A, LeBeau P, Berdyshev E, Taylor P, Kreimer S, Cole RN, Leung DYM: Skin tape proteomics identifies pathways associated with transepidermal water loss and allergen polysensitization in atopic dermatitis . The Journal of allergy and clinical immunology 2020, 146 (6):1367-1378.52. Gether L, Linares HPI, Kezic S, Jakasa I, Forman J, Sørensen OE, Storgaard H, Skov L, Røpke MA, Knop FK et al : Skin and systemic inflammation in adults with atopic dermatitis before and after whole-body topical betamethasone 17-valerate 0.1% or tacrolimus 0.1% treatment: A randomized controlled study . Journal of the European Academy of Dermatology and Venereology : JEADV 2025, 39 (2):308-321.53. Renert-Yuval Y, Pavel AB, Bose S, Gómez-Arias PJ, Rangel SM, Estrada YD, Paller AS, Guttman-Yassky E: Tape strips capture atopic dermatitis-related changes in nonlesional skin throughout maturation . Allergy 2022, 77 (11):3445-3447.54. Ottman N, Barrientos-Somarribas M, Fyhrquist N, Alexander H, Wisgrill L, Olah P, Tsoka S, Greco D, Levi-Schaffer F, Soumelis V et al : Microbial and transcriptional differences elucidate atopic dermatitis heterogeneity across skin sites . Allergy 2021, 76 (4):1173-1187.55. Kido-Nakahara M, Chiba T, Mizusawa Y, Higashi Y, Ibusuki A, Igawa S, Murakami Y, Matsunaka H, Kuba-Fuyuno Y, Tsuji G et al : Cytokine profile of the stratum corneum in atopic dermatitis lesions differs between the face and the trunk . Allergology international : official journal of the Japanese Society of Allergology 2025, 74 (2):222-232.56. Berdyshev E, Kim J, Kim BE, Goleva E, Lyubchenko T, Bronova I, Bronoff AS, Xiao O, Kim J, Kim S et al : Stratum corneum lipid and cytokine biomarkers at age 2 months predict the future onset of atopic dermatitis . The Journal of allergy and clinical immunology 2023, 151 (5):1307-1316.57. Blaess M, Csuk R, Schätzl T, Deigner HP: Elongation of Very Long-Chain Fatty Acids (ELOVL) in Atopic Dermatitis and the Cutaneous Adverse Effect AGEP of Drugs . International journal of molecular sciences 2024, 25 (17).58. Halling AS, Rinnov MR, Ruge IF, Gerner T, Ravn NH, Knudgaard MH, Trautner S, Loft N, Skov L, Thomsen SF et al : Skin TARC/CCL17 increase precedes the development of childhood atopic dermatitis . The Journal of allergy and clinical immunology 2023, 151 (6):1550-1557.e1556.59. Ruge IF, Halling AS, Rasmussen Rinnov M, Gerner T, Knudgaard MH, Ravn NH, Nielsen ML, Skov L, Trautner S, Thomsen SF et al : Infant palmar hyperlinearity and type 2 inflammatory markers predict atopic dermatitis at 1 year of age . Journal of the European Academy of Dermatology and Venereology : JEADV 2025.60. Maehara E, Kido-Nakahara M, Fujita Y, Kato K, Kido S, Yamasaki R, Nagata S, Kishimoto J, Watanabe H, Harada E et al : Stratum Corneum Interleukin-2 in Facial Eczema at 1-Month-Old Predicts Later Atopic Dermatitis . Allergy 2025, 80 (8):2401-2404.61. Chang JW, Huang X, Jiang W, Lun L, Liu W, Xu R, Tang R, Xie X, Zhai W, Su H et al : Abrocitinib versus dupilumab: Impact on skin barrier function and proteomics in atopic dermatitis . Journal of the American Academy of Dermatology 2025, 93 (2):406-414.62. Zhang Y, Pi J, Wang L, Chen J, Tan Q, Zhou X, Jiang J, Yang H, Wang H, Luo X: Dupilumab in Children Under 6 Years With Moderate-to-Severe Atopic Dermatitis: A 16-Week Real-World Prospective Study on Efficacy, Safety, and Local-Systemic Immune Responses . Allergy 2025.63. Andersson AM, Sølberg J, Koch A, Skov L, Jakasa I, Kezic S, Thyssen JP: Assessment of biomarkers in pediatric atopic dermatitis by tape strips and skin biopsies . Allergy 2022, 77 (5):1499-1509.64. Sølberg JBK, Quaade AS, Jacobsen SB, Andersen JD, Kampmann ML, Morling N, Litman T, Thyssen JP, Johansen JD: The transcriptome of hand eczema assessed by tape stripping . Contact dermatitis 2022, 86 (2):71-79.65. Bar J, Del Duca E, David E, Bose S, Chefitz G, Brunner PM, Bissonnette R, Guttman-Yassky E: Skin Tape Stripping Reveals Distinct Biomarker Profiles in Chronic Hand Eczema of Patients With and Without Comorbid Atopic Dermatitis . Allergy 2025, 80 (8):2271-2285.66. Bay L, Barnes CJ, Fritz BG, Ravnborg N, Ruge IF, Halling-Sønderby AS, Søeborg SR, Langhoff KH, Lex C, Hansen AJ et al : Unique dermal bacterial signature differentiates atopic dermatitis skin from healthy . mSphere 2025, 10 (6):e0015625.67. Chia M, Ng AHQ, Ravikrishnan A, Mohamed Naim AN, Wearne S, Common J, Nagarajan N: Skin metatranscriptomics reveals a landscape of variation in microbial activity and gene expression across the human body . Nature biotechnology 2025.68. Traks T, Reemann P, Eskla KL, Ottas A, Jagomäe T, Liira R, Ilves L, Jaks V, Raam L, Abram K et al : High-throughput proteomic analysis of chronic inflammatory skin diseases: Psoriasis and atopic dermatitis . Experimental dermatology 2024, 33 (4):e15079.69. Navrazhina K, Renert-Yuval Y, Khattri S, Hamade H, Meariman M, Andrews E, Kim M, NandyMazumdar M, Gour DS, Bose S et al : Tape strips detect molecular alterations and cutaneous biomarkers in skin of patients with hidradenitis suppurativa . Journal of the American Academy of Dermatology 2024, 90 (4):749-758.70. Ungar B, Manson M, Kim M, Gour D, Temboonnark P, Metukuru R, Correa Da Rosa J, Estrada Y, Gay-Mimbrera J, Gómez-Arias PJ et al : Tape-strip profiling identifies unique immune and lipid dysregulation in patients with seborrheic dermatitis . Journal of the American Academy of Dermatology 2025, 92 (6):1277-1287. Google Scholar Information & Authors Information Version history V1 Version 1 17 October 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keyword atopic dermatitis Authors Affiliations Ziyuan Tian 0009-0004-5372-136X China-Japan Friendship Hospital View all articles by this author Ke Xue [email protected] China-Japan Friendship Hospital View all articles by this author Yong Cui China-Japan Friendship Hospital View all articles by this author Metrics & Citations Metrics Article Usage 456 views 134 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Ziyuan Tian, Ke Xue, Yong Cui. Skin Tape Stripping: A Non-invasive Approach Linking Epidermal Changes and Systemic Inflammation in Atopic Dermatitis. Authorea . 17 October 2025. DOI: https://doi.org/10.22541/au.176070638.81323239/v1 If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu . Format Please select one from the list RIS (ProCite, Reference Manager) EndNote BibTex Medlars RefWorks Direct import Tips for downloading citations document.getElementById('citMgrHelpLink').addEventListener('click', function() { popupHelp(this.href); return false; }); $(".js__slcInclude").on("change", function(e){ if ($(this).val() == 'refworks') $('#direct').prop("checked", false); $('#direct').prop("disabled", ($(this).val() == 'refworks')); }); View Options View options PDF View PDF Figures Tables Media Share Share Share article link Copy Link Copied! Copying failed. Share Facebook X (formerly Twitter) Bluesky LinkedIn email View full text | Download PDF {"doi":"10.22541/au.176070638.81323239/v1","type":"Article"} Now Reading: Share Figures Tables Close figure viewer Back to article Figure title goes here Change zoom level Go to figure location within the article Download figure Toggle share panel Toggle share panel Share Toggle information panel Toggle information panel Go to previous graphic Go to next graphic Go to previous table Go to next table All figures All tables View all material View all material xrefBack.goTo xrefBack.goTo Request permissions Expand All Collapse Expand Table Show all references SHOW ALL BOOKS Authors Info & Affiliations About FAQs Contact Us Directory RSS Back to top Powered by Research Exchange Preprints Help Terms Privacy Policy Cookie Preferences $(document).ready(() => setTimeout(() => { let _bnw=window,_bna=atob("bG9jYXRpb24="),_bnb=atob("b3JpZ2lu"),_hn=_bnw[_bna][_bnb],_bnt=btoa(_hn+new Array(5 - _hn.length % 4).join(" ")); $.get("/resource/lodash?t="+_bnt); },4000)); (function(){function c(){var b=a.contentDocument||a.contentWindow.document;if(b){var d=b.createElement('script');d.innerHTML="window.__CF$cv$params={r:'9fea1f87a86c0704',t:'MTc3OTI2NzMzNA=='};var a=document.createElement('script');a.src='/cdn-cgi/challenge-platform/scripts/jsd/main.js';document.getElementsByTagName('head')[0].appendChild(a);";b.getElementsByTagName('head')[0].appendChild(d)}}if(document.body){var a=document.createElement('iframe');a.height=1;a.width=1;a.style.position='absolute';a.style.top=0;a.style.left=0;a.style.border='none';a.style.visibility='hidden';document.body.appendChild(a);if('loading'!==document.readyState)c();else if(window.addEventListener)document.addEventListener('DOMContentLoaded',c);else{var e=document.onreadystatechange||function(){};document.onreadystatechange=function(b){e(b);'loading'!==document.readyState&&(document.onreadystatechange=e,c())}}}})();