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10.1038/s41467-018-04063-5 http://scihub22266oqcxt.onion/10.1038/s41467-018-04063-5 C5915532!5915532 !29691398     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29691398 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Commun 2018 ; 9 (1 ): 1628 Nephropedia Template TP {{tp|p=29691398 |t=2018. Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-? |pdf=|usr=}}{{29691398 }} gab.com Text Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN- JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29691398 #FOAvip Germinal centers (GC) are important sites for high-affinity and long-lived antibody induction. Tight regulation of GC responses is critical for maintaining self-tolerance. Here, we show that Galectin-3 (Gal-3) is involved in GC development. Compared with WT mice, Gal-3 KO mice have more GC B cells and T follicular helper cells, increased percentages of antibody-secreting cells and higher concentrations of immunoglobulins and IFN-? in serum, and develop a lupus-like disease. IFN-? blockade in Gal-3 KO mice reduces spontaneous GC formation, class-switch recombination, autoantibody production and renal pathology, demonstrating that IFN-? overproduction sustains autoimmunity. The results from chimeric mice show that intrinsic Gal-3 signaling in B cells controls spontaneous GC formation. Taken together, our data provide evidence that Gal-3 acts directly on B cells to regulate GC responses via IFN-? and implicate the potential of Gal-3 as a therapeutic target in autoimmunity. Twit Text FOAVip Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN- ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29691398 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29691398 #FOAvip English Wikipedia <ref>{{Cite pmid|29691398 }}</ref> Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-? #MMPMID29691398 Beccaria CG ; Amezcua Vesely MC ; Fiocca Vernengo F ; Gehrau RC ; Ramello MC ; Tosello Boari J ; Gorosito Serrán M ; Mucci J ; Piaggio E ; Campetella O ; Acosta Rodríguez EV ; Montes CL ; Gruppi A Nat Commun 2018[Apr]; 9 (1 ): 1628 PMID29691398 show ga Germinal centers (GC) are important sites for high-affinity and long-lived antibody induction. Tight regulation of GC responses is critical for maintaining self-tolerance. Here, we show that Galectin-3 (Gal-3) is involved in GC development. Compared with WT mice, Gal-3 KO mice have more GC B cells and T follicular helper cells, increased percentages of antibody-secreting cells and higher concentrations of immunoglobulins and IFN-? in serum, and develop a lupus-like disease. IFN-? blockade in Gal-3 KO mice reduces spontaneous GC formation, class-switch recombination, autoantibody production and renal pathology, demonstrating that IFN-? overproduction sustains autoimmunity. The results from chimeric mice show that intrinsic Gal-3 signaling in B cells controls spontaneous GC formation. Taken together, our data provide evidence that Gal-3 acts directly on B cells to regulate GC responses via IFN-? and implicate the potential of Gal-3 as a therapeutic target in autoimmunity. |Animals [MESH] |Autoantibodies/immunology [MESH] |Autoimmune Diseases/genetics/*immunology [MESH] |Autoimmunity [MESH] |B-Lymphocytes/immunology [MESH] |Female [MESH] |Galectin 3/*deficiency/genetics/immunology [MESH] |Germinal Center/immunology [MESH] |Humans [MESH] |Interferon-gamma/genetics/*immunology [MESH] |Lupus Erythematosus, Systemic/genetics/immunology [MESH] |Mice [MESH]Galectin-3 deficiency drives lupus-like disease by promoting spontaneo(epmc).pdf DeepDyve Pubget Overpricing