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10.4049/jimmunol.1502355 http://scihub22266oqcxt.onion/10.4049/jimmunol.1502355 C4799727!4799727 !26921309     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26921309 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye |pdf=|usr=}}{{26921309 }} gab.com Text Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26921309 #FOAvip Uveitis, which occurs in association with systemic immunological diseases, presents a considerable medical challenge because of incomplete understanding of its pathogenesis. The signals that initiate T cells to target the eye, which may be of infectious or noninfectious origin, are poorly understood. Experimental autoimmune uveoretinitis (EAU) develops in mice immunized with the endogenous retinal protein interphotoreceptor retinoid binding protein in the presence of the adjuvant CFA. EAU manifests as posterior ocular inflammation consisting of vasculitis, granulomas, retinal damage, and invasion of self-reactive T cells, which are key clinical features of human uveitis. Our studies uncover Card9 as a critical genetic determinant for EAU. Card9 was responsible for Th17 polarization and Th17-associated Ag-specific responses, but not Th1-associated responses. Nonetheless, Card9 expression was essential for accumulation of both lineages within the eye. Consistent with its recently identified role as an intracellular signaling mediator for C-type lectin receptors (CLRs), a Card9-dependent transcriptional response in the neuroretina was observed involving genes encoding the CLRs Dectin-1, Dectin-2, and Mincle. Genetic deletion of these individual CLRs revealed an essential role for Mincle. Mincle activation was sufficient to generate the EAU phenotype, and this required activation of both Syk and Card9. In contrast, Dectin-1 contributed minimally and a possible repressive role was shown for Dectin-2. These findings extend our understanding of CLRs in autoimmune uveitis. The newly identified role of Mincle and Syk/Card9-coupled signaling axis in autoimmune uveitis could provide novel targets for treatment of patients with ocular inflammatory disease. Twit Text FOAVip Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26921309 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26921309 #FOAvip English Wikipedia <ref>{{Cite pmid|26921309 }}</ref> Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the Development of Autoimmune Disease of the Eye #MMPMID26921309 Lee EJ ; Brown BR ; Vance EE ; Snow PE ; Silver PB ; Heinrichs D ; Lin X ; Iwakura Y ; Wells CA ; Caspi RR ; Rosenzweig HL J Immunol 2016[Apr]; 196 (7 ): 3148-58 PMID26921309 show ga Uveitis, which occurs in association with systemic immunological diseases, presents a considerable medical challenge because of incomplete understanding of its pathogenesis. The signals that initiate T cells to target the eye, which may be of infectious or noninfectious origin, are poorly understood. Experimental autoimmune uveoretinitis (EAU) develops in mice immunized with the endogenous retinal protein interphotoreceptor retinoid binding protein in the presence of the adjuvant CFA. EAU manifests as posterior ocular inflammation consisting of vasculitis, granulomas, retinal damage, and invasion of self-reactive T cells, which are key clinical features of human uveitis. Our studies uncover Card9 as a critical genetic determinant for EAU. Card9 was responsible for Th17 polarization and Th17-associated Ag-specific responses, but not Th1-associated responses. Nonetheless, Card9 expression was essential for accumulation of both lineages within the eye. Consistent with its recently identified role as an intracellular signaling mediator for C-type lectin receptors (CLRs), a Card9-dependent transcriptional response in the neuroretina was observed involving genes encoding the CLRs Dectin-1, Dectin-2, and Mincle. Genetic deletion of these individual CLRs revealed an essential role for Mincle. Mincle activation was sufficient to generate the EAU phenotype, and this required activation of both Syk and Card9. In contrast, Dectin-1 contributed minimally and a possible repressive role was shown for Dectin-2. These findings extend our understanding of CLRs in autoimmune uveitis. The newly identified role of Mincle and Syk/Card9-coupled signaling axis in autoimmune uveitis could provide novel targets for treatment of patients with ocular inflammatory disease. |*Signal Transduction [MESH] |Animals [MESH] |Autoimmune Diseases/diagnosis/genetics/*immunology/*metabolism [MESH] |CARD Signaling Adaptor Proteins/genetics/*metabolism [MESH] |Calcitonin Receptor-Like Protein/genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Eye Proteins/metabolism [MESH] |Gene Expression [MESH] |Gene Expression Profiling [MESH] |Intracellular Signaling Peptides and Proteins/*metabolism [MESH] |Lectins, C-Type/genetics/*metabolism [MESH] |Membrane Proteins/genetics/*metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Protein-Tyrosine Kinases/*metabolism [MESH] |Retina/immunology/metabolism/pathology [MESH] |Retinol-Binding Proteins/metabolism [MESH] |Syk Kinase [MESH] |T-Lymphocyte Subsets/immunology/metabolism [MESH] |Th17 Cells/immunology/metabolism [MESH] |Transcriptome [MESH]Mincle Activation and the Syk/Card9 Signaling Axis Are Central to the (epmc).pdf DeepDyve Pubget Overpricing