Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.4049/jimmunol.0903275 http://scihub22266oqcxt.onion/10.4049/jimmunol.0903275 C2925247!2925247!20574007     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 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 2010 ; 185 (3): 1383-92 Nephropedia Template TP {{tp|p=20574007|t=2010. Tim-3/galectin-9 pathway: regulation of Th1 immunity through promotion of CD11b+Ly-6G+ myeloid cells |pdf=|usr=}}{{20574007}} gab.com Text Tim-3/galectin-9 pathway: regulation of Th1 immunity through promotion of CD11b+Ly-6G+ myeloid cells JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=20574007 #FOAvip IFN-? plays a central role in anti-tumor immunity. Tim-3 is expressed on IFN-?-producing Th1 cells; upon interaction with its ligand, galectin-9, it terminates Th1 immunity. Here, we show that transgenic over-expression of Tim-3 on T cells results in an increase in CD11b+Ly-6G+ cells and inhibition of immune responses. Molecular characterization of CD11b+Ly-6G+ cells reveals a phenotype consistent with granulocytic myeloid-derived suppressor cells (MDSC). Accordingly, we find that modulation of the Tim-3/galectin-9 pathway impacts on tumor growth. Similarly, overexpression of Tim-3 ligand, galectin-9, results in an increase in CD11b+Ly-6G+ cells and inhibition of immune responses. Loss of Tim-3 restores normal levels of CD11b+Ly-6G+ cells and normal immune responses in galectin-9 transgenic mice. Our data uncover a novel mechanism by which the Tim-3/galectin-9 pathway regulates immune responses and identifies this pathway as a therapeutic target in diseases where MDSC are disadvantageous.This is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence it may differ from the final version published in The JI (online and in print). AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the United States National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org. Twit Text FOAVip Tim-3/galectin-9 pathway: regulation of Th1 immunity through promotion of CD11b+Ly-6G+ myeloid cells ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=20574007 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20574007 #FOAvip English Wikipedia <ref>{{Cite pmid|20574007}}</ref> Tim-3/galectin-9 pathway: regulation of Th1 immunity through promotion of CD11b+Ly-6G+ myeloid cells #MMPMID20574007 Dardalhon V; Anderson AC; Karman J; Apetoh L; Chandwaskar R; Lee DH; Cornejo M; Nishi N; Yamauchi A; Quintana FJ; Sobel RA; Hirashima M; Kuchroo VK J Immunol 2010[Aug]; 185 (3): 1383-92 PMID20574007show ga IFN-? plays a central role in anti-tumor immunity. Tim-3 is expressed on IFN-?-producing Th1 cells; upon interaction with its ligand, galectin-9, it terminates Th1 immunity. Here, we show that transgenic over-expression of Tim-3 on T cells results in an increase in CD11b+Ly-6G+ cells and inhibition of immune responses. Molecular characterization of CD11b+Ly-6G+ cells reveals a phenotype consistent with granulocytic myeloid-derived suppressor cells (MDSC). Accordingly, we find that modulation of the Tim-3/galectin-9 pathway impacts on tumor growth. Similarly, overexpression of Tim-3 ligand, galectin-9, results in an increase in CD11b+Ly-6G+ cells and inhibition of immune responses. Loss of Tim-3 restores normal levels of CD11b+Ly-6G+ cells and normal immune responses in galectin-9 transgenic mice. Our data uncover a novel mechanism by which the Tim-3/galectin-9 pathway regulates immune responses and identifies this pathway as a therapeutic target in diseases where MDSC are disadvantageous.This is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence it may differ from the final version published in The JI (online and in print). AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the United States National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org. äTim-3/galectin-9 pathway: regulation of Th1 immunity through promotion(epmc).pdf DeepDyve Pubget Overpricing