dc.creatorMackern Oberti, Juan Pablo
dc.creatorJara, Evelyn
dc.creatorRiedel, Claudia
dc.creatorKalergis, Alexis
dc.date.accessioned2018-06-22T19:35:22Z
dc.date.accessioned2018-11-06T14:02:43Z
dc.date.available2018-06-22T19:35:22Z
dc.date.available2018-11-06T14:02:43Z
dc.date.created2018-06-22T19:35:22Z
dc.date.issued2017-04
dc.identifierMackern Oberti, Juan Pablo; Jara, Evelyn; Riedel, Claudia; Kalergis, Alexis; Hormonal Modulation of Dendritic Cells Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity; Birkhauser Verlag Ag; Archivum Immunologiae Et Therapiae Experimentalis; 65; 2; 4-2017; 123-136
dc.identifier0004-069X
dc.identifierhttp://hdl.handle.net/11336/49730
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1882181
dc.description.abstractHormonal homeostasis is crucial for keeping a competent and healthy immune function. Several hormones can modulate the function of various immune cells such as dendritic cells (DCs) by influencing the initiation of the immune response and the maintenance of peripheral tolerance to self-antigens. Hormones, such as estrogens, prolactin, progesterone and glucocorticoids may profoundly affect DCs differentiation, maturation and function leading to either a pro-inflammatory or an anti-inflammatory (or tolerogenic) phenotype. If not properly regulated, these processes can contribute to the pathogenesis of autoimmune disease. An unbalanced hormonal status may affect the production of pro-inflammatory cytokines, the expression of activating/inhibitory receptors and co-stimulatory molecules on conventional and plasmacytoid DCs (pDCs), conferring susceptibility to develop autoimmunity. Estrogen receptor (ER)-α signaling in conventional DCs can promote IFN-α and IL-6 production and induce the expression of CD40, CD86 and MHCII molecules. Furthermore, estrogen modulates the pDCs response to Toll-like receptor ligands enhancing T cell priming. During lupus pathogenesis, ER-α deficiency decreased the expression of MHC II on pDCs from the spleen. In contrast, estradiol administration to lupus-prone female mice increased the expression of co-stimulatory molecules, enhanced the immunogenicity and produced large amounts of IL-6, IL-12 and TNF-α by bone marrow-derived DCs. These data suggest that estradiol/ER signaling may play an active role during lupus pathology. Similarly, understanding hormonal modulation of DCs may favor the design of new therapeutic strategies based on autologous tolerogenic DCs transfer, especially in sex-biased systemic autoimmune diseases. In this review, we discuss recent data relative to the role of different hormones (estrogen, prolactin, progesterone and glucocorticoids) in DC function during systemic autoimmune pathogenesis.
dc.languageeng
dc.publisherBirkhauser Verlag Ag
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s00005-016-0418-6
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs00005-016-0418-6
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectAUTOIMMUNITY
dc.subjectDENDRITIC CELLS
dc.subjectESTROGEN
dc.subjectGLUCOCORTICOIDS
dc.subjectPROGESTERONE
dc.subjectPROLACTIN
dc.subjectSYSTEMIC LUPUS ERYTHEMATOSUS
dc.titleHormonal Modulation of Dendritic Cells Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity
dc.typeArtículos de revistas
dc.typeArtículos de revistas
dc.typeArtículos de revistas


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