The Role of T Lymphocyte-Mediated Immune Imbalance in the Pathogenesis of Endometriosis
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Abstract
Endometriosis is a chronic inflammatory disease characterized by the growth of endometrial-like tissue outside the uterine cavity, affecting approximately 10% of women of reproductive age worldwide. Its pathogenesis is complex and involves multiple factors, including immune, endocrine, and inflammatory processes. Recent research has increasingly highlighted the critical role of the immune system, particularly T lymphocytes—the core effector cells of adaptive immunity—in the adhesion, invasion, proliferation, vascularization, and pain development associated with ectopic endometrial lesions. This article systematically reviews the phenotypic and functional alterations of T cells within the microenvironment of endometriosis. It focuses on various immune dysregulations, including Th1/Th2 imbalance, Th17 cells, Treg cells, and the functional exhaustion of cytotoxic T cells. By providing an in-depth understanding of the imbalance between T cell-mediated immune tolerance and inflammatory responses, this review not only offers new perspectives on the pathogenesis of endometriosis but also points the way for developing novel diagnostic biomarkers and targeted immunomodulatory therapies.
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