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10.1038/nri.2017.24 http://scihub22266oqcxt.onion/10.1038/nri.2017.24 C5523822!5523822 !28393923     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28393923 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Rev+Immunol 2017 ; 17 (7 ): 421-436 Nephropedia Template TP {{tp|p=28393923 |t=2017. Altered B cell signalling in autoimmunity |pdf=|usr=}}{{28393923 }} gab.com Text Altered B cell signalling in autoimmunity JO: Nat Rev Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28393923 #FOAvip Recent work has provided new insights into how altered B cell-intrinsic signals - through the B cell receptor (BCR) and key co-receptors - function together to promote the pathogenesis of autoimmunity. These combined signals affect B cells at two distinct stages: first, in the selection of the naive repertoire; and second, during extrafollicular or germinal centre activation responses. Thus, dysregulated signalling can lead to both an altered naive BCR repertoire and the generation of autoantibody-producing B cells. Strikingly, high-affinity autoantibodies predate and predict disease in several autoimmune disorders, including type 1 diabetes and systemic lupus erythematosus. This Review summarizes how, rather than being a downstream consequence of autoreactive T cell activation, dysregulated B cell signalling can function as a primary driver of many human autoimmune diseases. Twit Text FOAVip Altered B cell signalling in autoimmunity ????Nat Rev Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28393923 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28393923 #FOAvip English Wikipedia <ref>{{Cite pmid|28393923 }}</ref> Altered B cell signalling in autoimmunity #MMPMID28393923 Rawlings DJ ; Metzler G ; Wray-Dutra M ; Jackson SW Nat Rev Immunol 2017[Jul]; 17 (7 ): 421-436 PMID28393923 show ga Recent work has provided new insights into how altered B cell-intrinsic signals - through the B cell receptor (BCR) and key co-receptors - function together to promote the pathogenesis of autoimmunity. These combined signals affect B cells at two distinct stages: first, in the selection of the naive repertoire; and second, during extrafollicular or germinal centre activation responses. Thus, dysregulated signalling can lead to both an altered naive BCR repertoire and the generation of autoantibody-producing B cells. Strikingly, high-affinity autoantibodies predate and predict disease in several autoimmune disorders, including type 1 diabetes and systemic lupus erythematosus. This Review summarizes how, rather than being a downstream consequence of autoreactive T cell activation, dysregulated B cell signalling can function as a primary driver of many human autoimmune diseases. |*Autoimmunity [MESH] |Animals [MESH] |B-Lymphocytes/*immunology/metabolism [MESH] |Humans [MESH] |Receptors, Antigen, B-Cell/metabolism [MESH]Altered B cell signalling in autoimmunity (epmc).pdf DeepDyve Pubget Overpricing