RESUMEN
Systemic Lupus Erythematosus (SLE) is a chronic autoimmune polymorphous disease that primarily affects women of reproductive age. This gender disparity has suggested the importance of investigating the role of reproductive hormones in the pathogenesis of the disease. Estradiol, the most potent form of estrogen, plays a key role in shaping the immune system including the production of lymphocytes, the peripheral differentiation of regulatory T cells (T-regs), antibody production, and the complement and interferon systems, and has been studied in the pathogenesis of systemic lupus erythematosus (SLE). It operates by binding to estrogen receptors (ERs) α and ß, initiating cellular responses including alterations in gene expression. Regulatory T cells are instrumental in preserving immunological self-tolerance and moderating immune responses. Estradiol's serum levels correlate with the expansion of CD4+CD25+ and FoxP3+ in healthy females. However, this response is reduced in lupus patients. Estradiol also interacts with microRNAs (miRNAs) in gene regulation. Hsa-miR-10b-5p, a miRNA targeting SRSF1, is overexpressed in SLE patients and its levels increase with exposure to estrogens. Other miRNAs also show correlation with plasma Estradiol levels. The precise role of Estradiol in the pathogenesis of SLE remains complex and multifaceted and is a topic for further research.