Synergy between Th1 and Th2 responses during endometriosis: A review of current understanding

Ling-Yu Chang; Jing Shan; Xinxin Hou; Xin-Xin Hou; Da-Jin Li; Da‐Jin Li; Xiaoqiu Wang; Xiao-Qiu Wang

doi:10.1016/j.jri.2023.103975

Synergy between Th1 and Th2 responses during endometriosis: A review of current understanding

Ling-Yu Chang, Jing Shan, Xinxin Hou, Xin-Xin Hou, Da-Jin Li, Da‐Jin Li, Xiaoqiu Wang, Xiao-Qiu Wang

Journal of reproductive immunology · 2023 · vol. 158 , pp. 103975 · doi:10.1016/j.jri.2023.103975 · PMID:37331087 · W4379619479

review OA: closed CC0 ⤵ 10 in-corpus citations

View on OpenAlex View on PubMed View at publisher

⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

This review synthesizes current knowledge on the synergistic interplay between Th1 and Th2 immune responses in the pathogenesis of endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Endometriosis is widely perceived as an estrogen-dependent chronic disorder with infertility and pelvic pain. Although the etiology of endometriosis has remained elusive, many studies have proclaimed the relevance of immune system disorders with endometriosis. With the discovery that the dysregulation of multiple biological functions in endometriosis is caused by the aberrant differentiation of T helper cells, a shift towards Th2 immune response may account for the disease progression. This review attempts to present mechanisms of cytokines, chemokines, signal pathways, transcription factors and some other factors related with the derivation of Th1/Th2 immune response involved in the development of endometriosis. The current understanding of treatment approaches and potential therapeutic targets will also be outlined with brief discussion.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (10)

Source provenance

europepmc: last seen: 2026-06-21T06:12:49.409960+00:00
openalex: last seen: 2026-06-10T17:14:06.276822+00:00
pubmed: last seen: 2026-06-21T06:11:43.528101+00:00

License: CC0 · commercial use OK

[1] Aberrant activation of signal transducer and activator of transcription-3 (STAT3) signaling in endometriosis via openalex

[2] Aberrant reactive aldehyde detoxification by aldehyde dehydrogenase-2 influences endometriosis development and pain-associated behaviors via openalex

[3] Activated Hippo/Yes-Associated Protein Pathway Promotes Cell Proliferation and Anti-apoptosis in Endometrial Stromal Cells of Endometriosis via openalex

[4] Activation of the CXCL16/CXCR6 Axis by TNF-α Contributes to Ectopic Endometrial Stromal Cells Migration and Invasion via openalex

[5] All-trans retinoic acid inhibits epithelial-to-mesenchymal transition (EMT) through the down-regulation of IL-6 in endometriosis via openalex

[6] Cell proliferation effect of GnRH agonist on pathological lesions of women with endometriosis, adenomyosis and uterine myoma via openalex

[7] Chemokine CCL2 enhances survival and invasiveness of endometrial stromal cells in an autocrine manner by activating Akt and MAPK/Erk1/2 signal pathway via openalex

[8] Clinical immunology<br>Pro-inflammatory cytokines for evaluation of inflammatory status in endometriosis via openalex

[9] Co-expression of activating and inhibitory receptors on peritoneal fluid NK cells in women with endometriosis via openalex

[10] Combination of estrogen and dioxin is involved in the pathogenesis of endometriosis by promoting chemokine secretion and invasion of endometrial stromal cells via openalex

[11] Co-operation between the AKT and ERK signaling pathways may support growth of deep endometriosis in a fibrotic microenvironment in vitro† via openalex

[12] Curcumin attenuates proangiogenic and proinflammatory factors in human eutopic endometrial stromal cells through the NF‐κB signaling pathway via openalex

[13] CXCL8 enhances proliferation and growth and reduces apoptosis in endometrial stromal cells in an autocrine manner via a CXCR1-triggered PTEN/AKT signal pathway via openalex

[14] Cytokines, Angiogenesis, and Extracellular Matrix Degradation are Augmented by Oxidative Stress in Endometriosis via openalex

[15] Decreased Innate Migration of Pro-Inflammatory M1 Macrophages through the Mesothelial Membrane Is Affected by Ceramide Kinase and Ceramide 1-P via openalex

[16] Deficiency of MST1 in endometriosis related peritoneal macrophages promoted the autophagy of ectopic endometrial stromal cells by IL-10 via openalex

[17] Dual inhibition of ERK1/2 and AKT pathways is required to suppress the growth and survival of endometriotic cells and lesions via openalex

[18] Effect of Wnt/β-catenin signal pathway on of matrix metalloproteinase-7 and vascular endothelial growth factor gene expressions in endometriosis via openalex

[19] Expression and localization of CXCL16 and CXCR6 in ovarian endometriotic tissues via openalex

[20] Expression of monocyte chemotactic protein 2 and tumor necrosis factor alpha in human normal endometrium and endometriotic tissues via openalex

[21] Expression of Th1 and Th2 cytokine-associated transcription factors, T-bet and GATA-3, in the eutopic endometrium of women with endometriosis via openalex

[22] Expression of the pluripotent transcription factor OCT4 promotes cell migration in endometriosis via openalex

[23] Fractalkine/CX3CR1 Contributes to Endometriosis-Induced Neuropathic Pain and Mechanical Hypersensitivity in Rats via openalex

[24] Fractalkine in the peritoneal fluid of women with endometriosis via openalex

[25] Fractalkine/<scp>CX</scp>3<scp>CR</scp>1 is involved in the pathogenesis of endometriosis by regulating endometrial stromal cell proliferation and invasion via openalex

[26] Functional changes of immune cells: signal of immune tolerance of the ectopic lesions in endometriosis? via openalex

[27] G-CSF and IL-6 may be involved in formation of endometriosis lesions by increasing the expression of angiogenic factors in neutrophils via openalex

[28] Genomic Function of Estrogen Receptor β in Endometriosis via openalex

[29] Hypoxia‑induced lactate dehydrogenase A protects cells from apoptosis in endometriosis via openalex

[30] IL-27 triggers IL-10 production in Th17 cells via a c-Maf/RORγt/Blimp-1 signal to promote the progression of endometriosis via openalex

[31] IL-2 and IL-27 synergistically promote growth and invasion of endometriotic stromal cells by maintaining the balance of IFN-γ and IL-10 in endometriosis via openalex

[32] Immune-inflammation gene signatures in endometriosis patients via openalex

[33] Immunology of endometriosis via openalex

[34] Increased Expression of YAP Inhibited the Autophagy Level by Upregulating mTOR Signal in the Eutopic ESCs of Endometriosis via openalex

[35] Increased IL-25 levels in the peritoneal fluid of patients with endometriosis via openalex

[36] Inflammation and endometriosis via openalex

[37] Interleukin-12 but not interleukin-18 is associated with severe endometriosis via openalex

[38] Interleukin-1β stimulates the secretion of thymic stromal lymphopoietin (TSLP) from endometrioma stromal cells: possible involvement of TSLP in endometriosis via openalex

[39] Interleukin‐9 produced by helper T cells stimulates interleukin‐8 expression in endometriosis via openalex

[40] Intracellular Wnt/Beta-Catenin Signaling Underlying 17beta-Estradiol-Induced Matrix Metalloproteinase 9 Expression in Human Endometriosis1 via openalex

[41] Involvement of the nuclear factor-κB pathway in the pathogenesis of endometriosis via openalex

[42] Involvement of the Wnt/β-Catenin Signaling Pathway in the Cellular and Molecular Mechanisms of Fibrosis in Endometriosis via openalex

[43] Letrozole promotes the expression of integrin αvβ3 and HOXA10 in endometrium of endometriosis via openalex

[44] Lipoxin A4 Suppresses IL-1β-Induced Cyclooxygenase-2 Expression Through Inhibition of p38 MAPk Activation in Endometriosis via openalex

[45] Metformin Alleviates Endometriosis and Potentiates Endometrial Receptivity via Decreasing VEGF and MMP9 and Increasing Leukemia Inhibitor Factor and HOXA10 via openalex

[46] Metformin as a Potential Treatment Option for Endometriosis via openalex

[47] MiR-182 inhibits proliferation, migration, invasion and inflammation of endometrial stromal cells through deactivation of NF-κB signaling pathway in endometriosis via openalex

[48] Niclosamide As a Potential Nonsteroidal Therapy for Endometriosis That Preserves Reproductive Function in an Experimental Mouse Model via openalex

[49] Notch activity mediates oestrogen-induced stromal cell invasion in endometriosis via openalex

[50] Overexpressed MPS-1 contributes to endometrioma development through the NF-κB signaling pathway via openalex

[51] P2X3 receptor involvement in endometriosis pain via ERK signaling pathway via openalex

[52] Pathogenesis and pathophysiology of endometriosis via openalex

[53] Pentoxifylline for the treatment of endometriosis-associated pain and infertility via openalex

[54] Peritoneal fluid concentrations of β-chemokines in endometriosis via openalex

[55] Peritoneal Fluid from Patients with Ovarian Endometriosis Displays Immunosuppressive Potential and Stimulates Th2 Response via openalex

[56] Platelets and Regulatory T Cells May Induce a Type 2 Immunity That Is Conducive to the Progression and Fibrogenesis of Endometriosis via openalex

[57] Pro-inflammatory Cytokines (IL6, IL8 and TNF-a) in the Evaluation of Ovarian Endometriosis Cyst via openalex

[58] Protein Inhibitor of Activated STAT3 (PIAS3) Is Down-Regulated in Eutopic Endometrium of Women with Endometriosis via openalex

[59] Protein kinase inhibitors can control the progression of endometriosis <i>in vitro</i> and <i>in vivo</i> via openalex

[60] Proteome-Wide Effect of 17-β-Estradiol and Lipoxin A4 in an Endometriotic Epithelial Cell Line via openalex

[61] Pyrvinium pamoate induces in-vitro suppression of IL-6 and IL-8 produced by human endometriotic stromal cells via openalex

[62] Regulation of Matrix Metalloproteinase-2 Activity by COX-2-PGE2-pAKT Axis Promotes Angiogenesis in Endometriosis via openalex

[63] Relugolix, an oral gonadotropin-releasing hormone receptor antagonist, reduces endometriosis-associated pain in a dose–response manner: a randomized, double-blind, placebo-controlled study via openalex

[64] Retinoic acid has the potential to suppress endometriosis development via openalex

[65] RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial‐mesenchymal transition and proliferation in endometriosis via openalex

[66] Serum anti-inflammatory cytokines for the evaluation of inflammatory status in endometriosis via openalex

[67] Simultaneous Detection and Evaluation of Four Subsets of CD4+ T Lymphocyte in Lesions and Peripheral Blood in Endometriosis via openalex

[68] TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis via openalex

[69] Th1 and Th2 immune responses related to pelvic endometriosis via openalex

[70] The Anti‐Inflammatory Impact of Omega‐3 Polyunsaturated Fatty Acids During the Establishment of Endometriosis‐Like Lesions via openalex

[71] The Content of Cytokines IL-6, IL-8, TNF-α, IL-4 and the Level of CD86 and CD163 Expression in Peritoneal Fluid Macrophages Has a Reverse Correlation with the Degree of Severity of External Genital Endometriosis via openalex

[72] The Delicate Balance between the Good and the Bad IL-1 Proinflammatory Effects in Endometriosis via openalex

[73] The high level of RANTES in the ectopic milieu recruits macrophages and induces their tolerance in progression of endometriosis via openalex

[74] The involvement of multifunctional TGF-β and related cytokines in pathogenesis of endometriosis via openalex

[75] T helper (Th)1, Th2, and Th17 interleukin pathways in infertile patients with minimal/mild endometriosis via openalex

[76] The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights via openalex

[77] The <scp>CCL</scp>17‐<scp>CCR</scp>4 axis between endometrial stromal cells and macrophages contributes to the high levels of <scp>IL</scp>‐6 in ectopic milieu via openalex

[78] The WNT/β-catenin signaling pathway and expression of survival promoting genes in luteinized granulosa cells: endometriosis as a paradigm for a dysregulated apoptosis pathway via openalex

[79] Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression via openalex

[80] Transcription factor 21 regulates expression of ERβ and SF-1 via upstream stimulatory factor-2 in endometriotic tissues via openalex

[81] Treatment of Endometriosis-Associated Pain with Elagolix, an Oral GnRH Antagonist via openalex

[82] Unus pro omnibus, omnes pro uno: A novel, evidence-based, unifying theory for the pathogenesis of endometriosis via openalex

[83] Upregulation of Interleukin 35 in Patients With Endometriosis Stimulates Cell Proliferation via openalex

[84] Use of dopamine agonists to target angiogenesis in women with endometriosis via openalex

[85] USP10 promotes proliferation and migration and inhibits apoptosis of endometrial stromal cells in endometriosis through activating the Raf-1/MEK/ERK pathway via openalex

[86] Valproic Acid and Progestin Inhibit Lesion Growth and Reduce Hyperalgesia in Experimentally Induced Endometriosis in Rats via openalex

[87] W2396023791 via openalex

[88] W2152014155 via openalex

[89] W2155227851 via openalex

[90] W2157710399 via openalex

[91] W2267931422 via openalex

[92] W2279338972 via openalex

[93] W2055897422 via openalex

[94] W2442851072 via openalex

[95] W2046439307 via openalex

[96] W2045142779 via openalex

[97] W2793528890 via openalex

[98] W2801967759 via openalex

[99] W2042923816 via openalex

[100] W2040159806 via openalex