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Publication : The GITRL-GITR system alters TLR-4 expression on DC during fungal infection.

First Author  Vecchiarelli A Year  2009
Journal  Cell Immunol Volume  257
Issue  1-2 Pages  13-22
PubMed ID  19272591 Mgi Jnum  J:148548
Mgi Id  MGI:3845696 Doi  10.1016/j.cellimm.2009.02.001
Citation  Vecchiarelli A, et al. (2009) The GITRL-GITR system alters TLR-4 expression on DC during fungal infection. Cell Immunol 257(1-2):13-22
abstractText  The glucocorticoid-induced TNFR-related (GITR) protein is a member of the tumor necrosis factor receptor superfamily influencing natural and acquired immune response. GITR is activated by its ligand, GITRL, mainly expressed on antigen presenting cells. Previously, we demonstrated that GITR plays a role in regulating immune response to Candida albicans. Here we analyzed whether GITRL-GITR interaction influences the recognition of C. albicans by regulating the expression of pattern recognition receptors on splenic dendritic cells. Our report demonstrates that under physiological conditions and during candidiasis the GITRL-GITR system affects TLR-2 and TLR-4 expression on DC. These changes correlate with decrease in: MyD88 activation; CD80 and CD40 expression on DC; T cell activation response, including CD28 expression, IL-2 and IFN-gamma production. Our results point out that, during fungal infection, GITRL-GITR interaction modulates TLR-4 and TLR-2 expression, thereby altering the antigen presentation process, and suggesting a role of GITRL-GITR interaction in resistance against infectious diseases.
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