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10.4049/jimmunol.1402854 http://scihub22266oqcxt.onion/10.4049/jimmunol.1402854 C4546929!4546929!26216892     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2015 ; 195 (5): 2374-82 Nephropedia Template TP {{tp|p=26216892|t=2015. B cell-intrinsic Indoleamine 2,3-dioxygenase1 regulates humoral immunity to T cell independent antigens |pdf=|usr=}}{{26216892}} gab.com Text B cell-intrinsic Indoleamine 2,3-dioxygenase1 regulates humoral immunity to T cell independent antigens JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26216892 #FOAvip Humoral responses to non-proteinaceous antigens (i.e. T cell independent, TI) are a key component of the early response to bacterial and viral infection and a critical driver of systemic autoimmunity. However, mechanisms that regulate TI humoral immunity are poorly defined. Herein we report that B cell-intrinsic induction of the tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase1 (IDO1), is a key mechanism limiting TI antibody responses. When Ido1?/? mice were immunized with TI antigens, there was a significant increase in antibody titers and formation of extrafollicular antibody secreting cells (ASCs) compared to controls. This effect was specific to TI antigens, as Ido1 disruption did not affect immunoglobulin production after immunization with protein antigens. The effect of IDO1 abrogation was confined to the B cell compartment, as adoptive transfer of Ido1?/? B cells to B cell deficient mice was sufficient to replicate increased TI responses observed in Ido1?/? mice. Moreover, in vitro activation with toll-like receptor ligands or B cell receptor crosslinking rapidly induced Ido1 expression and activity in purified B cells, and Ido1?/? B cells displayed enhanced proliferation and cell survival associated with increased immunoglobulin and cytokine production compared to wild type B cells. Thus, our results demonstrate a novel, B cell intrinsic, role for IDO1 as a regulator of humoral immunity that has implications for both vaccine design and prevention of autoimmunity. Twit Text FOAVip B cell-intrinsic Indoleamine 2,3-dioxygenase1 regulates humoral immunity to T cell independent antigens ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26216892 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26216892 #FOAvip English Wikipedia <ref>{{Cite pmid|26216892}}</ref> B cell-intrinsic Indoleamine 2,3-dioxygenase1 regulates humoral immunity to T cell independent antigens #MMPMID26216892 Shinde R; Shimoda M; Chaudhary K; Liu H; Mohamed E; Bradley J; Kandala S; Li X; Liu K; McGaha TL J Immunol 2015[Sep]; 195 (5): 2374-82 PMID26216892show ga Humoral responses to non-proteinaceous antigens (i.e. T cell independent, TI) are a key component of the early response to bacterial and viral infection and a critical driver of systemic autoimmunity. However, mechanisms that regulate TI humoral immunity are poorly defined. Herein we report that B cell-intrinsic induction of the tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase1 (IDO1), is a key mechanism limiting TI antibody responses. When Ido1?/? mice were immunized with TI antigens, there was a significant increase in antibody titers and formation of extrafollicular antibody secreting cells (ASCs) compared to controls. This effect was specific to TI antigens, as Ido1 disruption did not affect immunoglobulin production after immunization with protein antigens. The effect of IDO1 abrogation was confined to the B cell compartment, as adoptive transfer of Ido1?/? B cells to B cell deficient mice was sufficient to replicate increased TI responses observed in Ido1?/? mice. Moreover, in vitro activation with toll-like receptor ligands or B cell receptor crosslinking rapidly induced Ido1 expression and activity in purified B cells, and Ido1?/? B cells displayed enhanced proliferation and cell survival associated with increased immunoglobulin and cytokine production compared to wild type B cells. Thus, our results demonstrate a novel, B cell intrinsic, role for IDO1 as a regulator of humoral immunity that has implications for both vaccine design and prevention of autoimmunity. äB cell-intrinsic Indoleamine 2,3-dioxygenase1 regulates humoral immuni(epmc).pdf DeepDyve Pubget Overpricing