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• W1736243164 abstract "Abstract IL-17 plays critical roles in host defenses, combating bacterial and fungal infections, as well as the pathogenesis of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). The signaling adaptor SAP is essential for normal immune homeostasis and mutations within SH2D1A, the locus encoding this protein, result in serious and sometimes fatal syndromes, including X-linked lymphoproliferative disease and severe cases of common variable immunodeficiency. However, the precise cellular basis of how SAP deficiency contributes to immune dysfunction remains incompletely understood. In this study, we found that CD4 and CD8 T cells lacking SAP had a diminished capacity to differentiate into IL-17–producing Th17 and T cytotoxic (Tc17) cells relative to wild-type lymphocytes. The use of costimulating SLAM Abs was found to augment the differentiation of IL-17–secreting effectors in wild-type but not Sh2d1a−/− splenic T cells under IL-17–polarizing conditions. In addition, SAP’s regulation of IL-17–secreting T cells was shown to be a T cell–intrinsic role, as purified naive Sh2d1a−/− CD4 and CD8 T cells were inherently defective at converting into Th17 and Tc17 cells in vitro and in vivo. Furthermore, Sh2d1a−/− mice were protected from EAE and exhibited greatly decreased numbers of CNS-infiltrating Th17 and Tc17 effector T cells and reduced disease severity. Collectively, these results suggest that SLAM–SAP signaling drives the differentiation and function of Th17 and Tc17 cells in vitro and in vivo and contributes to the pathogenesis of autoimmunity in EAE." @default.
• W1736243164 created "2016-06-24" @default.
• W1736243164 creator A5001637205 @default.
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• W1736243164 creator A5049987477 @default.
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• W1736243164 date "2014-12-15" @default.
• W1736243164 modified "2023-10-16" @default.
• W1736243164 title "SLAM–SAP Signaling Promotes Differentiation of IL-17–Producing T Cells and Progression of Experimental Autoimmune Encephalomyelitis" @default.
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• W1736243164 doi "https://doi.org/10.4049/jimmunol.1301435" @default.
• W1736243164 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25362182" @default.
• W1736243164 hasPublicationYear "2014" @default.
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