Abstract

ROLE OF IMMUNE DYSREGULATION IN THE PATHOGENESIS OF ENDOMETRIAL HYPERPLASIA

Danish Khan* and Dr. Rinkal Patel

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Abstract

EH is a non-physiological, non-invasive oestrogen-driven expansion of the endometrium that is marked by an increase in gland to stroma ratio and atypical hyperplastic tissue demonstrates structural dissimilarity. Strogen and progesterone are also closely involved in the regulation of the menstrual cycle and initiation of hyperplastic processes. Hyperestrogenemia plays a role in the onset of EH by increasing inflammatory actions of cytokines, IL-1β, IL-6, and TNF-α being the biomarkers for the same. Cytotoxic T cells (Tc) increase in an inflammatory condition, and regulatory T cells (Tregs) partake in inducing tolerance and sustaining immune homeostasis. Calculable changes in T lymphocytes and their subpopulations have been affiliated with atypical endometrial hyperplasia and detected fluctuations in T cell populations and reallocation of lymphocytes that possess activation antigens to demonstrate processes called immunocompensation and immunosuppression, respectively. The dysfunctional interaction of hormones oestrogen and progesterone and their association with mechanisms of inflammatory cytokines like Interleukin 6, Regulatory T cells and interleukin 1 β, tumor necrosis factor α and can be exploited for the treatment of a number of inflammatory maladies of the endometrium from an immunological perspective. Therefore, the current review sheds light on the dysfunctional interaction of hormones oestrogen and progesterone and their association with mechanisms of inflammatory cytokines as well as highlights the research gap and suggests possible applications and future prospects.

Keywords: Endometrial hyperplasia, immune infiltration, Tregs, NK cells, oestrogen, progesterone.