Hormonal Modulation of Dendritic Cells Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity

摘要: Hormonal homeostasis is crucial for keeping a competent and healthy immune function. Several hormones can modulate the function of various cells such as dendritic (DCs) by influencing initiation response maintenance peripheral tolerance to self-antigens. Hormones, estrogens, prolactin, progesterone glucocorticoids may profoundly affect DCs differentiation, maturation leading either pro-inflammatory or an anti-inflammatory (or tolerogenic) phenotype. If not properly regulated, these processes contribute pathogenesis autoimmune disease. An unbalanced hormonal status production cytokines, expression activating/inhibitory receptors co-stimulatory molecules on conventional plasmacytoid (pDCs), conferring susceptibility develop autoimmunity. Estrogen receptor (ER)-α signaling in promote IFN-α IL-6 induce CD40, CD86 MHCII molecules. Furthermore, estrogen modulates pDCs Toll-like ligands enhancing T cell priming. During lupus pathogenesis, ER-α deficiency decreased MHC II from spleen. In contrast, estradiol administration lupus-prone female mice increased molecules, enhanced immunogenicity produced large amounts IL-6, IL-12 TNF-α bone marrow-derived DCs. These data suggest that estradiol/ER play active role during pathology. Similarly, understanding modulation favor design new therapeutic strategies based autologous tolerogenic transfer, especially sex-biased systemic diseases. this review, we discuss recent relative different (estrogen, glucocorticoids) DC pathogenesis.