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BAFF Expression is Modulated by Female Hormones in Human Immune Cells. | LitMetric

AI Article Synopsis

  • The study investigates the role of female hormones, particularly estrogen and progesterone, in regulating B-cell activating factor (BAFF) expression in immune cells, which is significant in autoimmune diseases.
  • It finds that estrogen substantially increases BAFF expression in both male and female immune cells, while progesterone elevates BAFF in females but decreases it in males.
  • These findings indicate that female hormones may influence the development of autoimmune disorders, thereby contributing to the observed gender differences in these diseases.

Article Abstract

Among several autoimmune diseases, one of the main risk factors is the female gender, and much consideration has been given to the involvement of female hormones in their etiology. B-cell activating factor (BAFF) is a key factor in survival and maturation of B cells and is overexpressed in several autoimmune patients although the mechanism behind this feature is unclear. In murine models, BAFF expression could be upregulated by exogenous estrogen treatment in splenocytes; however, no evidence of this relationship was available in humans. Here, leukocytes from healthy male and female individuals were collected and cultivated in the presence or absence of estrogen or progesterone. BAFF gene expression was accessed by quantitative PCR and compared between treated and untreated group of cells. In the presence of estrogen, BAFF expression was upregulated by more than 5 times in both genders. When exposed to progesterone, the female-originated cells showed increased expression, while the cells of male origin a significant downregulation of BAFF. Our results suggest that female hormones can modulate the expression of BAFF, a key cytokine in autoimmune pathways, in human immune cells. These data might contribute to the understanding of the etiology as well as the gender bias featured by several autoimmune disorders.

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Source
http://dx.doi.org/10.1007/s10528-016-9752-yDOI Listing

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