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

Fengyi Xiao, Xishi Liu, Sun-Wei Guo, Sun‐Wei Guo
Frontiers in immunology · 2020 · vol. 11 , pp. 610963 · doi:10.3389/fimmu.2020.610963 · PMID:33381124 · PMC7767909 · W3113161383
article OA: gold CC0 ⤵ 36 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Platelets and regulatory T cells promote endometriosis progression and fibrogenesis by inducing a type 2 immune response, with depletion of either slowing lesion growth via suppression of specific signaling pathways and immune cell aggregation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated how platelet and regulatory T cell (Treg) depletion affects the lesional immune microenvironment and downstream endometriosis lesion progression and fibrogenesis in a mouse model induced by intraperitoneal uterine fragment transplantation. In two mouse experiments, platelet depletion or Treg depletion disrupted predominantly type 2 immunity in lesions, with associated suppression of TGF-β1/Smad3 and PDGFR-β/PI3K/Akt signaling pathways, reduced lesion progression and fibrogenesis, and shifts in immune aggregation (including reduced M2 macrophages, Th2 and Th17 cells, and Tregs alongside increased Th1 cells); platelet depletion specifically reduced lesional thymic stromal lymphopoietin (TSLP) expression and altered macrophage and T cell distributions, while Treg depletion also reduced platelet aggregation. A key limitation is that findings are based on mouse model intervention and immune-cell/lesion readouts rather than human lesion sampling. This paper is centrally about endometriosis — it tests how platelets and Tregs coordinate type 2 immunity to drive lesional progression and fibrogenesis.

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Abstract

Endometriosis is a hormonal disease, as well as a chronic inflammatory disease. While various immune cells are documented to be involved in endometriosis, there is a wanton lack of a bigger picture on how these cells are coordinated to work concertedly. Since endometriotic lesions experience cyclical bleeding, they are fundamentally wounds that undergo repeated tissue injury and repair (ReTIAR). In this study, we attempted to characterize the role of platelets and regulatory T cells (Tregs) in modulating the lesional immune microenvironment and its subsequent effects on lesional progression and fibrogenesis. Through two mouse experiments, we show that, by disrupting predominantly a type 2 immune response in lesional microenvironment, both platelets and Tregs depletion decelerated lesional progression and fibrogenesis, likely through the suppression of the TGF-β1/Smad3 and PDGFR-β/PI3K/Akt signaling pathways. In particular, platelet depletion resulted in significantly reduced lesional expression of thymic stromal lymphopoietin (TSLP), leading to reduced aggregation of macrophages and alternatively activated (M2) macrophages, and of Tregs, T helper 2 (Th2) and Th17 cells but increased aggregation of Th1 cells, in lesions, which, in turn, yields retarded fibrogenesis. Similarly, Tregs depletion resulted in suppression of platelet aggregation, and reduced aggregation of M2 macrophages, Th2 and Th17 cells but increased aggregation of Th1 cells, in lesions. Thus, both platelet and Tregs depletion decelerated lesional progression and fibrogenesis by disrupting predominantly a type 2 immunity in lesional microenvironment. Taken together, this suggests that both platelets and Tregs may induce a type 2 immunity in lesional microenvironment that is conducive to lesional progression and fibrogenesis.

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Condition tags

endometriosis

MeSH descriptors

Blood Platelets Endometriosis Endometrium T-Lymphocytes, Regulatory Animals Blood Platelets Blood Platelets Cellular Microenvironment Disease Models, Animal Disease Progression Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Fibrosis Macrophages

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