Association Between Impaired Dendritic Cell Maturation and Uterine Adenomyosis Pain

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This study found that impaired dendritic cell maturation correlates with pain in adenomyosis patients, suggesting neuro-immune interactions contribute to uterine adenomyosis symptoms.

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AI-generated deep summary by claude@2026-06, 2026-06-13 · read from full text

This cross-sectional observational study examined uterine tissue from 24 adenomyosis patients and 15 controls to assess neuro-immune markers related to pain at the endometrial-myometrial interface (EMI) and middle myometrium (MM). Using immunohistochemistry and qRT-PCR, the authors found higher PGP9.5 and NGF expression in adenomyosis tissues and a reduced CD83+/CD1a+ ratio, indicating impaired dendritic cell maturation. The CD83+/CD1a+ ratio was negatively correlated with PGP9.5 expression, and VAS pain scores were also negatively correlated with dendritic cell maturation, while NGF showed no direct association with pain. The paper explicitly concludes that dendritic cell maturation deficits are associated with adenomyosis pain, but NGF functions independently of dendritic cell maturation. This paper is centrally about adenomyosis — it links impaired dendritic cell maturation and specific neuro-immune markers to adenomyosis pain.

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Abstract

PURPOSE: To investigate the association between dendritic cell maturation deficits and pain in patients with adenomyosis and explore potential neuro-immune mechanisms. METHODS: Uterine tissues from 24 patients with adenomyosis (AM) and 15 controls were analyzed. Samples from the endometrial-myometrial interface (EMI) and middle myometrium (MM) were tested. To study the expression of nerve fiber marker (PGP9.5), nerve growth factor (NGF), mature DC (CD83+), and immature DC (CD1a+), the team used immunohistochemistry (IHC) and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The correlation between these findings and pain scores was also analyzed. RESULTS: PGP9.5 and NGF expression in both EMI and MM regions were significantly higher in the AM group (p < 0.05), whereas the CD83+/CD1a+ ratio was reduced (p < 0.01). A significant negative correlation was observed between PGP9.5 and the CD83+/CD1a+ ratio (MM: r = -0.650, p = 0.011; EMI: r = -0.812, p < 0.001). VAS scores (VAS) were negatively correlated with the CD83+/CD1a+ ratio (MM: r = -0.851, p < 0.001; EMI: r = -0.814, p = 0.001), but there was no direct association with NGF. Two-way analysis of variance (ANOVA) revealed that the disease state (AM) was the main factor affecting the proportion of NGF and DC maturation (p < 0.05), whereas anatomical location had no significant impact. CONCLUSIONS: Based on our cross-sectional observational study, DC maturation deficits are associated with AM pain, potentially through neuro-immune interactions. However, NGF functions independently of DC. Exploring neuro-immune interactions is a new approach for treating AM-related pain.
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Abstract

Purpose To investigate the association between dendritic cell maturation deficits and pain in patients with adenomyosis and explore potential neuro-immune mechanisms.

Methods

Uterine tissues from 24 patients with adenomyosis (AM) and 15 controls were analyzed. Samples from the endometrial-myometrial interface (EMI) and middle myometrium (MM) were tested. To study the expression of nerve fiber marker (PGP9.5), nerve growth factor (NGF), mature DC (CD83+), and immature DC (CD1a+), the team used immunohistochemistry (IHC) and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The correlation between these findings and pain scores was also analyzed.

Results

PGP9.5 and NGF expression in both EMI and MM regions were significantly higher in the AM group (p < 0.05), whereas the CD83+/CD1a+ ratio was reduced (p < 0.01). A significant negative correlation was observed between PGP9.5 and the CD83+/CD1a+ ratio (MM: r = −0.650, p = 0.011; EMI: r = −0.812, p < 0.001). VAS scores (VAS) were negatively correlated with the CD83+/CD1a+ ratio (MM: r = −0.851, p < 0.001; EMI: r = −0.814, p = 0.001), but there was no direct association with NGF. Two-way analysis of variance (ANOVA) revealed that the disease state (AM) was the main factor affecting the proportion of NGF and DC maturation (p < 0.05), whereas anatomical location had no significant impact.

Conclusions

Based on our cross-sectional observational study, DC maturation deficits are associated with AM pain, potentially through neuro-immune interactions. However, NGF functions independently of DC. Exploring neuro-immune interactions is a new approach for treating AM-related pain. Disclosure The authors confirm that this work has not been previously presented at any conference, nor has it been published in abstract form. Conflicts of Interest The authors declare no conflicts of interest. Data Availability Statement The datasets generated and/or analyzed during the current study, including the raw data, are available in the Supporting Information accompanying this article.

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Outcome instruments

VAS-pain

Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis

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europepmc
last seen: 2026-09-13T09:25:22.628771+00:00
pubmed
last seen: 2026-09-13T06:05:23.326767+00:00
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last seen: 2026-09-13T06:26:10.529621+00:00
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