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10.1126/sciadv.aas9944 http://scihub22266oqcxt.onion/10.1126/sciadv.aas9944 C6040844!6040844 !30009261     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30009261 &cmd=llinks): Failed to open stream: HTTP request failed! 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BAFF inhibition attenuates fibrosis in scleroderma by modulating the regulatory and effector B cell balance |pdf=|usr=}}{{30009261 }} gab.com Text BAFF inhibition attenuates fibrosis in scleroderma by modulating the regulatory and effector B cell balance JO: Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=30009261 #FOAvip Systemic sclerosis (SSc) is an autoimmune disease characterized by skin and lung fibrosis. More than 90% of patients with SSc are positive for autoantibodies. In addition, serum B cell activating factor (BAFF) level is correlated with SSc severity and activity. Thus, B cells are considered to play a pathogenic role in SSc. However, there are two opposing subsets: regulatory B cells (Bregs) and effector B cells (Beffs). Interleukin-10 (IL-10)-producing Bregs negatively regulate the immune response, while IL-6-producing Beffs positively regulate it. Therefore, a protocol that selectively depletes Beffs would represent a potent therapy for SSc. The aims of this study were to investigate the roles of Bregs and Beffs in SSc and to provide a scientific basis for developing a new treatment strategy targeting B cells. A bleomycin-induced scleroderma model was induced in mice with a B cell-specific deficiency in IL-6 or IL-10. We also examined whether BAFF regulates cytokine-producing B cells and its effects on the scleroderma model. IL-6-producing Beffs increased in number and infiltrated the inflamed skin in the scleroderma model. The skin and lung fibrosis was attenuated in B cell-specific IL-6-deficient mice, whereas B cell-specific IL-10-deficient mice showed more severe fibrosis. In addition, BAFF increased Beffs but suppressed Bregs. Furthermore, BAFF antagonist attenuated skin and lung fibrosis in the scleroderma model with reduction of Beffs but not of Bregs. The current study indicates that Beffs play a pathogenic role in the scleroderma model, while Bregs play a protective role. BAFF inhibition is a potential therapeutic strategy for SSc via alteration of B cell balance. Twit Text FOAVip BAFF inhibition attenuates fibrosis in scleroderma by modulating the regulatory and effector B cell balance ????Sci Adv http://www.kidney.de/pget.php?&tw=1&pmid=30009261 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30009261 #FOAvip English Wikipedia <ref>{{Cite pmid|30009261 }}</ref> BAFF inhibition attenuates fibrosis in scleroderma by modulating the regulatory and effector B cell balance #MMPMID30009261 Matsushita T ; Kobayashi T ; Mizumaki K ; Kano M ; Sawada T ; Tennichi M ; Okamura A ; Hamaguchi Y ; Iwakura Y ; Hasegawa M ; Fujimoto M ; Takehara K Sci Adv 2018[Jul]; 4 (7 ): eaas9944 PMID30009261 show ga Systemic sclerosis (SSc) is an autoimmune disease characterized by skin and lung fibrosis. More than 90% of patients with SSc are positive for autoantibodies. In addition, serum B cell activating factor (BAFF) level is correlated with SSc severity and activity. Thus, B cells are considered to play a pathogenic role in SSc. However, there are two opposing subsets: regulatory B cells (Bregs) and effector B cells (Beffs). Interleukin-10 (IL-10)-producing Bregs negatively regulate the immune response, while IL-6-producing Beffs positively regulate it. Therefore, a protocol that selectively depletes Beffs would represent a potent therapy for SSc. The aims of this study were to investigate the roles of Bregs and Beffs in SSc and to provide a scientific basis for developing a new treatment strategy targeting B cells. A bleomycin-induced scleroderma model was induced in mice with a B cell-specific deficiency in IL-6 or IL-10. We also examined whether BAFF regulates cytokine-producing B cells and its effects on the scleroderma model. IL-6-producing Beffs increased in number and infiltrated the inflamed skin in the scleroderma model. The skin and lung fibrosis was attenuated in B cell-specific IL-6-deficient mice, whereas B cell-specific IL-10-deficient mice showed more severe fibrosis. In addition, BAFF increased Beffs but suppressed Bregs. Furthermore, BAFF antagonist attenuated skin and lung fibrosis in the scleroderma model with reduction of Beffs but not of Bregs. The current study indicates that Beffs play a pathogenic role in the scleroderma model, while Bregs play a protective role. BAFF inhibition is a potential therapeutic strategy for SSc via alteration of B cell balance. |Animals [MESH] |B-Cell Activating Factor/antagonists & inhibitors/*metabolism [MESH] |B-Lymphocyte Subsets/cytology/drug effects/*immunology/metabolism [MESH] |B-Lymphocytes, Regulatory/cytology/drug effects/*immunology/metabolism [MESH] |Bleomycin/toxicity [MESH] |Collagen/metabolism [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Fibrosis [MESH] |Interleukin-10/blood/deficiency/genetics [MESH] |Interleukin-6/blood/deficiency/genetics [MESH] |Lipopolysaccharides/pharmacology [MESH] |Lung Diseases/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Scleroderma, Systemic/chemically induced/metabolism/pathology [MESH]BAFF inhibition attenuates fibrosis in scleroderma by modulating the r(epmc).pdf DeepDyve Pubget Overpricing