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10.1002/art.39535 http://scihub22266oqcxt.onion/10.1002/art.39535 26636548!4848130!26636548     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26636548&cmd=llinks): Failed to open stream: HTTP request failed! 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Development of Th17-Associated Interstitial Kidney Inflammation in Lupus-Prone Mice Lacking the Gene Encoding STAT-1 |pdf=|usr=}}{{26636548}} gab.com Text Development of Th17-Associated Interstitial Kidney Inflammation in Lupus-Prone Mice Lacking the Gene Encoding STAT-1 JO: Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=26636548 #FOAvip OBJECTIVE: Type I interferon (IFN) signaling is a central pathogenic pathway in systemic lupus erythematosus (SLE), and therapeutics targeting type I IFN signaling are in development. Multiple proteins with overlapping functions play a role in IFN signaling, but the signaling events downstream of receptor engagement are unclear. This study was undertaken to investigate the roles of the type I and type II IFN signaling components IFN-alpha/beta/omega receptor 2 (IFNAR-2), IFN regulatory factor 9 (IRF-9), and STAT-1 in a mouse model of SLE. METHODS: We used immunohistochemical staining and highly multiplexed assays to characterize pathologic changes in histology, autoantibody production, cytokine/chemokine profiles, and STAT phosphorylation in order to investigate the individual roles of IFNAR-2, IRF-9, and STAT-1 in MRL/lpr mice. RESULTS: We found that STAT-1(-/-) mice, but not IRF-9(-/-) or IFNAR-2(-/-) mice, developed interstitial nephritis characterized by infiltration with retinoic acid receptor-related orphan nuclear receptor gammat-positive lymphocytes, macrophages, and eosinophils. Despite pronounced interstitial kidney disease and abnormal kidney function, STAT-1(-/-) mice had decreased proteinuria, glomerulonephritis, and autoantibody production. Phosphospecific flow cytometry revealed shunting of STAT phosphorylation from STAT-1 to STAT-3/4. CONCLUSION: We describe unique contributions of STAT-1 to pathology in different kidney compartments in a mouse model, and provide potentially novel insight into tubulointerstitial nephritis, a poorly understood complication that predicts end-stage kidney disease in SLE patients. Twit Text FOAVip Development of Th17-Associated Interstitial Kidney Inflammation in Lupus-Prone Mice Lacking the Gene Encoding STAT-1 ????Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=26636548 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26636548 #FOAvip English Wikipedia <ref>{{Cite pmid|26636548}}</ref> Development of Th17-Associated Interstitial Kidney Inflammation in Lupus-Prone Mice Lacking the Gene Encoding STAT-1 #MMPMID26636548 Yiu G; Rasmussen TK; Ajami B; Haddon DJ; Chu AD; Tangsombatvisit S; Haynes WA; Diep V; Steinman L; Faix J; Utz PJ Arthritis Rheumatol 2016[May]; 68 (5): 1233-44 PMID26636548show ga OBJECTIVE: Type I interferon (IFN) signaling is a central pathogenic pathway in systemic lupus erythematosus (SLE), and therapeutics targeting type I IFN signaling are in development. Multiple proteins with overlapping functions play a role in IFN signaling, but the signaling events downstream of receptor engagement are unclear. This study was undertaken to investigate the roles of the type I and type II IFN signaling components IFN-alpha/beta/omega receptor 2 (IFNAR-2), IFN regulatory factor 9 (IRF-9), and STAT-1 in a mouse model of SLE. METHODS: We used immunohistochemical staining and highly multiplexed assays to characterize pathologic changes in histology, autoantibody production, cytokine/chemokine profiles, and STAT phosphorylation in order to investigate the individual roles of IFNAR-2, IRF-9, and STAT-1 in MRL/lpr mice. RESULTS: We found that STAT-1(-/-) mice, but not IRF-9(-/-) or IFNAR-2(-/-) mice, developed interstitial nephritis characterized by infiltration with retinoic acid receptor-related orphan nuclear receptor gammat-positive lymphocytes, macrophages, and eosinophils. Despite pronounced interstitial kidney disease and abnormal kidney function, STAT-1(-/-) mice had decreased proteinuria, glomerulonephritis, and autoantibody production. Phosphospecific flow cytometry revealed shunting of STAT phosphorylation from STAT-1 to STAT-3/4. CONCLUSION: We describe unique contributions of STAT-1 to pathology in different kidney compartments in a mouse model, and provide potentially novel insight into tubulointerstitial nephritis, a poorly understood complication that predicts end-stage kidney disease in SLE patients. |Animals[MESH] |Antibody Formation[MESH] |Autoantibodies/immunology[MESH] |Fluorescent Antibody Technique[MESH] |Glomerulonephritis/genetics/immunology[MESH] |Interferon Type I[MESH] |Interferon-Stimulated Gene Factor 3, gamma Subunit/*genetics/immunology[MESH] |Interferon-gamma[MESH] |Kidney/pathology[MESH] |Lupus Erythematosus, Systemic/*genetics/immunology[MESH] |Mice[MESH] |Mice, Inbred MRL lpr[MESH] |Mice, Knockout[MESH] |Nephritis, Interstitial/*genetics/immunology/pathology[MESH] |Proteinuria/genetics/immunology[MESH] |Receptor, Interferon alpha-beta/*genetics/immunology[MESH] |STAT1 Transcription Factor/*genetics/immunology[MESH]Development of Th17-Associated Interstitial Kidney Inflammation in Lup(epmc).pdf DeepDyve Pubget Overpricing