T Cell Immunity in Pathogenesis, Progression, and Malignant Transformation of Endometriosis

Abstract

Endometriosis is a common gynecological condition characterized by special features such as invasive growth, recurrence, and potential distant metastasis. Recent studies indicate an increasing incidence of malignant transformation of endometriosis. The mechanisms underlying the occurrence, progression, and malignancy of endometriosis are multifactorial, involving genetic alterations, environmental factors, hormonal imbalances, and immuno-inflammatory responses. Various T cell subsets play crucial roles in regulating immune responses and influencing disease progression and malignant risk. CD4+ T cells, including T helper (Th) cells (Th1, Th2, and Th17), regulatory T (Treg) cells, follicular helper T (Tfh) cells, and Th9 cells, alongside CD8+ T cells are essential for maintaining the immune microenvironment in endometriosis. Disruption of the balance among these T cell subtypes can promote chronic inflammation, immune evasion, and tissue remodeling that may facilitate malignant transformation. Therapeutic strategies targeting T cell function or restoring immune homeostasis hold promise for managing endometriosis through immunomodulation or checkpoint blockade therapy to prevent its malignant progression. This article reviews the role of T cells in the malignant transformation of endometriosis and proposes potential immunoregulatory treatment approaches.