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10.4049/jimmunol.1403023 http://scihub22266oqcxt.onion/10.4049/jimmunol.1403023 C4402266!4402266!25801429     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2015 ; 194 (9): 4130-43 Nephropedia Template TP {{tp|p=25801429|t=2015. B cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolerance |pdf=|usr=}}{{25801429}} gab.com Text B cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolerance JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25801429 #FOAvip Signaling lymphocyte activation molecules (SLAMs) play an integral role in immune regulation. Polymorphisms in the SLAM family receptors are implicated in human and mouse model of lupus disease. The lupus-associated, somatically mutated and class-switched pathogenic autoantibodies are generated in spontaneously developed germinal centers (Spt-GCs) in secondary lymphoid organs. The role and mechanism of B cell-intrinsic expression of polymorphic SLAM receptors that affect B cell tolerance at the GC checkpoint is not clear. Here, we generated several bacterial artificial chromosome (BAC) transgenic mice that overexpress B6 alleles of different SLAM family genes in autoimmune-prone B6.Sle1b mice. B6.Sle1b mice overexpressing B6-derived Ly108 and CD84 exhibit a significant reduction in the Spt-GC response and autoantibody production compared to B6.Sle1b mice. These data suggest a prominent role of Sle1b-derived Ly108 and CD84 in altering the GC checkpoint. We further confirm that expression of lupus-associated CD84 and Ly108 specifically on GC B cells in B6.Sle1b mice is sufficient to break B cell tolerance leading to an increase in autoantibody production. In addition, we observe that B6.Sle1b B cells have reduced BCR signaling, and a lower frequency of B cell-T cell conjugates, which are reversed in B6.Sle1b mice overexpressing B6 alleles of CD84 and Ly108. Finally, we find a significant decrease in apoptotic GC B cells in B6.Sle1b mice compared to B6 controls. Our study establishes the central role of GC B cell-specific CD84 and Ly108 expression in maintaining B cell tolerance in GCs and in preventing autoimmunity. Twit Text FOAVip B cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolerance ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25801429 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25801429 #FOAvip English Wikipedia <ref>{{Cite pmid|25801429}}</ref> B cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolerance #MMPMID25801429 Wong EB; Soni C; Chan AY; Domeier PP; Shwetank; Abraham T; Limaye N; Khan TN; Elias MJ; Chodisetti SB; Wakeland EK; Rahman ZS J Immunol 2015[May]; 194 (9): 4130-43 PMID25801429show ga Signaling lymphocyte activation molecules (SLAMs) play an integral role in immune regulation. Polymorphisms in the SLAM family receptors are implicated in human and mouse model of lupus disease. The lupus-associated, somatically mutated and class-switched pathogenic autoantibodies are generated in spontaneously developed germinal centers (Spt-GCs) in secondary lymphoid organs. The role and mechanism of B cell-intrinsic expression of polymorphic SLAM receptors that affect B cell tolerance at the GC checkpoint is not clear. Here, we generated several bacterial artificial chromosome (BAC) transgenic mice that overexpress B6 alleles of different SLAM family genes in autoimmune-prone B6.Sle1b mice. B6.Sle1b mice overexpressing B6-derived Ly108 and CD84 exhibit a significant reduction in the Spt-GC response and autoantibody production compared to B6.Sle1b mice. These data suggest a prominent role of Sle1b-derived Ly108 and CD84 in altering the GC checkpoint. We further confirm that expression of lupus-associated CD84 and Ly108 specifically on GC B cells in B6.Sle1b mice is sufficient to break B cell tolerance leading to an increase in autoantibody production. In addition, we observe that B6.Sle1b B cells have reduced BCR signaling, and a lower frequency of B cell-T cell conjugates, which are reversed in B6.Sle1b mice overexpressing B6 alleles of CD84 and Ly108. Finally, we find a significant decrease in apoptotic GC B cells in B6.Sle1b mice compared to B6 controls. Our study establishes the central role of GC B cell-specific CD84 and Ly108 expression in maintaining B cell tolerance in GCs and in preventing autoimmunity. äB cell-intrinsic CD84 and Ly108 maintain germinal center B cell tolera(epmc).pdf DeepDyve Pubget Overpricing