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10.1002/art.38716 http://scihub22266oqcxt.onion/10.1002/art.38716 C4146640!4146640 !24891301     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24891301 &cmd=llinks): Failed to open stream: HTTP request failed! 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Interleukin-6 deficiency corrects nephritis, lymphocyte abnormalities, and secondary Sjögren s syndrome features in lupus-prone Sle1 Yaa mice |pdf=|usr=}}{{24891301 }} gab.com Text Interleukin-6 deficiency corrects nephritis, lymphocyte abnormalities, and secondary Sjögren s syndrome features in lupus-prone Sle1 Yaa mice JO: Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=24891301 #FOAvip OBJECTIVE: To assess disease features in Sle1.Yaa mice with genetic interleukin-6 (IL-6) deficiency. METHODS: Sera and tissues were collected from C57BL/6 (B6), Sle1.Yaa, and Sle1.Yaa.IL-6(-/-) mice and analyzed for various features of disease. Using serum samples, autoantibody specificities were determined by enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescence, cytokine production was analyzed by Luminex and ELISA, and levels of blood urea nitrogen were determined by ELISA. Renal, lung, and salivary gland tissue sections were evaluated for pathologic changes. Lymphocyte phenotypes, including CD4+ T cell cytokine production, and those of follicular and extrafollicular T helper subsets, germinal center B cells, and plasma cells, were determined using flow cytometry. RESULTS: IL-6 deficiency not only ameliorated autoantibody production and renal disease in this model, but also effectively reduced inflammation of lungs and salivary glands. Furthermore, IL-6 deficiency abrogated differentiation of Th1 and extrafollicular T helper cells, germinal center B cells, and plasma cells in the spleen and eliminated renal T cells with IL-17, interferon-?, and IL-21 production potential. CONCLUSION: Our findings highlight IL-6-mediated T cell aberrations in Yaa-driven autoimmunity and support the concept of therapeutic IL-6/IL-6 receptor blockade in systemic lupus erythematosus and Sjögren's syndrome by impairing the production of autoantibodies and lymphocytic infiltration of the kidneys, lungs, and salivary glands. Twit Text FOAVip Interleukin-6 deficiency corrects nephritis, lymphocyte abnormalities, and secondary Sjögren s syndrome features in lupus-prone Sle1 Yaa mice ????Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=24891301 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24891301 #FOAvip English Wikipedia <ref>{{Cite pmid|24891301 }}</ref> Interleukin-6 deficiency corrects nephritis, lymphocyte abnormalities, and secondary Sjögren s syndrome features in lupus-prone Sle1 Yaa mice #MMPMID24891301 Maier-Moore JS ; Horton CG ; Mathews SA ; Confer AW ; Lawrence C ; Pan Z ; Coggeshall KM ; Farris AD Arthritis Rheumatol 2014[Sep]; 66 (9 ): 2521-31 PMID24891301 show ga OBJECTIVE: To assess disease features in Sle1.Yaa mice with genetic interleukin-6 (IL-6) deficiency. METHODS: Sera and tissues were collected from C57BL/6 (B6), Sle1.Yaa, and Sle1.Yaa.IL-6(-/-) mice and analyzed for various features of disease. Using serum samples, autoantibody specificities were determined by enzyme-linked immunosorbent assay (ELISA) and indirect immunofluorescence, cytokine production was analyzed by Luminex and ELISA, and levels of blood urea nitrogen were determined by ELISA. Renal, lung, and salivary gland tissue sections were evaluated for pathologic changes. Lymphocyte phenotypes, including CD4+ T cell cytokine production, and those of follicular and extrafollicular T helper subsets, germinal center B cells, and plasma cells, were determined using flow cytometry. RESULTS: IL-6 deficiency not only ameliorated autoantibody production and renal disease in this model, but also effectively reduced inflammation of lungs and salivary glands. Furthermore, IL-6 deficiency abrogated differentiation of Th1 and extrafollicular T helper cells, germinal center B cells, and plasma cells in the spleen and eliminated renal T cells with IL-17, interferon-?, and IL-21 production potential. CONCLUSION: Our findings highlight IL-6-mediated T cell aberrations in Yaa-driven autoimmunity and support the concept of therapeutic IL-6/IL-6 receptor blockade in systemic lupus erythematosus and Sjögren's syndrome by impairing the production of autoantibodies and lymphocytic infiltration of the kidneys, lungs, and salivary glands. |Animals [MESH] |Flow Cytometry [MESH] |Interleukin-6/blood/*deficiency [MESH] |Lung/immunology/pathology [MESH] |Lupus Erythematosus, Systemic/*immunology/pathology [MESH] |Lymphocytes/*immunology/pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Nephritis/*immunology/pathology [MESH] |Plasma Cells/immunology/pathology [MESH] |Salivary Glands/immunology/pathology [MESH] |Sjogren's Syndrome/*immunology/pathology [MESH]Interleukin-6 deficiency corrects nephritis, lymphocyte abnormalities,(epmc).pdf DeepDyve Pubget Overpricing