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10.4049/jimmunol.1203452 http://scihub22266oqcxt.onion/10.4049/jimmunol.1203452 C3660433!3660433 !23636056     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23636056 &cmd=llinks): Failed to open stream: HTTP request failed! 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T cell-specific notch inhibition blocks graft-versus-host disease by inducing a hyporesponsive program in alloreactive CD4+ and CD8+ T cells |pdf=|usr=}}{{23636056 }} gab.com Text T cell-specific notch inhibition blocks graft-versus-host disease by inducing a hyporesponsive program in alloreactive CD4+ and CD8+ T cells JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23636056 #FOAvip Graft-versus-host disease (GVHD) induced by donor-derived T cells remains the major limitation of allogeneic bone marrow transplantation (allo-BMT). We previously reported that the pan-Notch inhibitor dominant-negative form of Mastermind-like 1 (DNMAML) markedly decreased the severity and mortality of acute GVHD mediated by CD4(+) T cells in mice. To elucidate the mechanisms of Notch action in GVHD and its role in CD8(+) T cells, we studied the effects of Notch inhibition in alloreactive CD4(+) and CD8(+) T cells using mouse models of allo-BMT. DNMAML blocked GVHD induced by either CD4(+) or CD8(+) T cells. Both CD4(+) and CD8(+) Notch-deprived T cells had preserved expansion in lymphoid organs of recipients, but profoundly decreased IFN-? production despite normal T-bet and enhanced Eomesodermin expression. Alloreactive DNMAML T cells exhibited decreased Ras/MAPK and NF-?B activity upon ex vivo restimulation through the TCR. In addition, alloreactive T cells primed in the absence of Notch signaling had increased expression of several negative regulators of T cell activation, including Dgka, Cblb, and Pdcd1. DNMAML expression had modest effects on in vivo proliferation but preserved overall alloreactive T cell expansion while enhancing accumulation of pre-existing natural regulatory T cells. Overall, DNMAML T cells acquired a hyporesponsive phenotype that blocked cytokine production but maintained their expansion in irradiated allo-BMT recipients, as well as their in vivo and ex vivo cytotoxic potential. Our results reveal parallel roles for Notch signaling in alloreactive CD4(+) and CD8(+) T cells that differ from past reports of Notch action and highlight the therapeutic potential of Notch inhibition in GVHD. Twit Text FOAVip T cell-specific notch inhibition blocks graft-versus-host disease by inducing a hyporesponsive program in alloreactive CD4+ and CD8+ T cells ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23636056 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23636056 #FOAvip English Wikipedia <ref>{{Cite pmid|23636056 }}</ref> T cell-specific notch inhibition blocks graft-versus-host disease by inducing a hyporesponsive program in alloreactive CD4+ and CD8+ T cells #MMPMID23636056 Sandy AR ; Chung J ; Toubai T ; Shan GT ; Tran IT ; Friedman A ; Blackwell TS ; Reddy P ; King PD ; Maillard I J Immunol 2013[Jun]; 190 (11 ): 5818-28 PMID23636056 show ga Graft-versus-host disease (GVHD) induced by donor-derived T cells remains the major limitation of allogeneic bone marrow transplantation (allo-BMT). We previously reported that the pan-Notch inhibitor dominant-negative form of Mastermind-like 1 (DNMAML) markedly decreased the severity and mortality of acute GVHD mediated by CD4(+) T cells in mice. To elucidate the mechanisms of Notch action in GVHD and its role in CD8(+) T cells, we studied the effects of Notch inhibition in alloreactive CD4(+) and CD8(+) T cells using mouse models of allo-BMT. DNMAML blocked GVHD induced by either CD4(+) or CD8(+) T cells. Both CD4(+) and CD8(+) Notch-deprived T cells had preserved expansion in lymphoid organs of recipients, but profoundly decreased IFN-? production despite normal T-bet and enhanced Eomesodermin expression. Alloreactive DNMAML T cells exhibited decreased Ras/MAPK and NF-?B activity upon ex vivo restimulation through the TCR. In addition, alloreactive T cells primed in the absence of Notch signaling had increased expression of several negative regulators of T cell activation, including Dgka, Cblb, and Pdcd1. DNMAML expression had modest effects on in vivo proliferation but preserved overall alloreactive T cell expansion while enhancing accumulation of pre-existing natural regulatory T cells. Overall, DNMAML T cells acquired a hyporesponsive phenotype that blocked cytokine production but maintained their expansion in irradiated allo-BMT recipients, as well as their in vivo and ex vivo cytotoxic potential. Our results reveal parallel roles for Notch signaling in alloreactive CD4(+) and CD8(+) T cells that differ from past reports of Notch action and highlight the therapeutic potential of Notch inhibition in GVHD. |Animals [MESH] |CD4-Positive T-Lymphocytes/*immunology/metabolism [MESH] |CD8-Positive T-Lymphocytes/*immunology/metabolism [MESH] |Cytotoxicity, Immunologic [MESH] |Enzyme Activation [MESH] |Gene Expression Regulation [MESH] |Graft vs Host Disease/genetics/*immunology/metabolism [MESH] |Interferon-gamma/biosynthesis [MESH] |Lymphocyte Activation [MESH] |Mice [MESH] |Mitogen-Activated Protein Kinases/metabolism [MESH] |NF-kappa B/metabolism [MESH] |Proto-Oncogene Proteins p21(ras)/metabolism [MESH] |Receptors, Notch/*antagonists & inhibitors/metabolism [MESH] |T-Box Domain Proteins/genetics/metabolism [MESH] |T-Lymphocytes, Regulatory/immunology/metabolism [MESH]T cell-specific notch inhibition blocks graft-versus-host disease by i(epmc).pdf DeepDyve Pubget Overpricing