CD4+Foxp3+ regulatory T cell differentiation mediated by endometrial stromal cell-derived TECK promotes the growth and invasion of endometriotic lesions

M-Q Li, Ming‐Qing Li, Y Wang, K.-K. Chang, K-K Chang, Y.-H. Meng, Y-H Meng, Liu Lb, L-B Liu, J Mei, Jie Mei, X-Q Wang, Xiuquan Wang, L-P Jin, D-J Li, Li Dj
Cell death & disease · 2014 · vol. 5(10) , pp. e1436 · doi:10.1038/cddis.2014.414 · PMID:25275597 · PMC4649519 · W2066872697
article OA: gold CC0 ⤵ 82 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Endometrial stromal cell-derived TECK promotes CD4+Foxp3+ regulatory T cell differentiation and function, enhancing the proliferation and invasion of endometriotic lesions.

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

Abstract

Endometriosis is associated with an abnormal immune response to endometrial cells, which can facilitate the implantation and proliferation of ectopic endometrial tissue. The proportion of CD4(+)Foxp3(+) regulatory T cells (Tregs) is significantly increased in the peritoneal fluid of women with endometriosis. The thymus-expressed chemokine TECK/CCL25 directly promotes the invasiveness of endometrial stromal cells (ESCs). The aim of this study was to investigate the effects of ESC-derived TECK on the crosstalk between Tregs and ESCs in the progress of endometriosis. We determined that the percentage of Tregs and the concentration of TECK increased in the peritoneal fluid with the progression of endometriosis. The supernatant from co-cultured human ESCs and macrophages not only induced Treg differentiation and increased Treg expression of interleukin-10 (IL-10), transforming growth factor-β (TGF-β) and CD73 by activating the AKT/STAT3 signaling pathway but also repressed Treg apoptosis by downregulating Fas and FasL expression and enhanced the Treg-mediated suppression of CD4(+)CD25(-) T cells. In addition, in vitro and in vivo trials confirmed that these effects could be inhibited by anti-TECK neutralizing Abs. The secretion of IL-10 and TGF-β by Tregs increased MMP2 expression and decreased TIMP1 expression and further stimulated the proliferation and invasion of ESCs and the growth of ectopic lesions. These results indicate that TECK derived from ESCs and macrophages upregulates the number and function of Tregs in the ectopic milieu, which contributes to endometriotic immunotolerance and high levels of ESC proliferation and invasion, thereby facilitating the progression of endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cell Differentiation Cell Proliferation Chemokines, CC Endometriosis Stromal Cells T-Lymphocytes, Regulatory Adult CD4 Antigens CD4 Antigens Chemokines, CC Chemokines, CC Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Forkhead Transcription Factors Forkhead Transcription Factors

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 (37)

Cited by (50)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:18:15.805398+00:00
License: CC0 · commercial use OK