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10.1002/eji.201141696 http://scihub22266oqcxt.onion/10.1002/eji.201141696 21728175!ä!21728175 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Eur+J+Immunol 2011 ; 41 (10): 2871-82 Nephropedia Template TP {{tp|p=21728175|t=2011. Delayed type hypersensitivity-induced myeloid-derived suppressor cells regulate autoreactive T cells |pdf=|usr=}}{{21728175}} gab.com Text Delayed type hypersensitivity-induced myeloid-derived suppressor cells regulate autoreactive T cells JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=21728175 #FOAvip Mild but efficient treatments of autoimmune diseases are urgently required. One such therapy, long-term maintenance of chronic delayed type hypersensitivity, has been described for alopecia areata (AA), a hair follicle-affecting autoimmune disease. The molecular mechanisms underlying the therapeutic efficacy are unknown, but may involve myeloid-derived suppressor cells (MDSCs). AA-affected mice were treated with squaric acid dibutyl ester (SADBE). The immunoreactivity of SADBE-treated AA lymphocytes and of AA lymphocytes co-cultured with SADBE-induced MDSCs was analyzed. The curative effect of SADBE was abolished by all-transretinoic acid, which drives MDSCs into differentiation, confirming a central role for MDSCs in therapeutic SADBE treatment. SADBE and SADBE-induced MDSCs strongly interfered with sustained autoreactive T-cell proliferation in response to AA skin lysate (autoantigen), which was accompanied by weak zeta-chain down-regulation and strongly impaired Lck activation. In contrast, activation of the mitochondrial apoptosis pathway and blockade of the anti-apoptotic PI3K/Akt pathway by SADBE-induced MDSCs did not require T-cell receptor engagement. Apoptosis induction correlated with high TNF-alpha expression in SADBE-induced MDSCs and elevated TNFRI levels in AA lymphocytes. SADBE-induced MDSCs interfere with persisting autoreactive T-cell proliferation and promote apoptosis of these T cells, which qualifies MDSCs induced and maintained by chronic delayed type hypersensitivity reactions as promising therapeutics in organ-related autoimmune diseases. Twit Text FOAVip Delayed type hypersensitivity-induced myeloid-derived suppressor cells regulate autoreactive T cells ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=21728175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21728175 #FOAvip English Wikipedia <ref>{{Cite pmid|21728175}}</ref> Delayed type hypersensitivity-induced myeloid-derived suppressor cells regulate autoreactive T cells #MMPMID21728175 Singh V; Mueller U; Freyschmidt-Paul P; Zoller M Eur J Immunol 2011[Oct]; 41 (10): 2871-82 PMID21728175show ga Mild but efficient treatments of autoimmune diseases are urgently required. One such therapy, long-term maintenance of chronic delayed type hypersensitivity, has been described for alopecia areata (AA), a hair follicle-affecting autoimmune disease. The molecular mechanisms underlying the therapeutic efficacy are unknown, but may involve myeloid-derived suppressor cells (MDSCs). AA-affected mice were treated with squaric acid dibutyl ester (SADBE). The immunoreactivity of SADBE-treated AA lymphocytes and of AA lymphocytes co-cultured with SADBE-induced MDSCs was analyzed. The curative effect of SADBE was abolished by all-transretinoic acid, which drives MDSCs into differentiation, confirming a central role for MDSCs in therapeutic SADBE treatment. SADBE and SADBE-induced MDSCs strongly interfered with sustained autoreactive T-cell proliferation in response to AA skin lysate (autoantigen), which was accompanied by weak zeta-chain down-regulation and strongly impaired Lck activation. In contrast, activation of the mitochondrial apoptosis pathway and blockade of the anti-apoptotic PI3K/Akt pathway by SADBE-induced MDSCs did not require T-cell receptor engagement. Apoptosis induction correlated with high TNF-alpha expression in SADBE-induced MDSCs and elevated TNFRI levels in AA lymphocytes. SADBE-induced MDSCs interfere with persisting autoreactive T-cell proliferation and promote apoptosis of these T cells, which qualifies MDSCs induced and maintained by chronic delayed type hypersensitivity reactions as promising therapeutics in organ-related autoimmune diseases. |*Myeloid Cells/drug effects/immunology/metabolism[MESH] |Adaptor Proteins, Signal Transducing/metabolism[MESH] |Alopecia Areata/*drug therapy/*immunology[MESH] |Animals[MESH] |Apoptosis/drug effects[MESH] |Autoimmune Diseases/drug therapy/immunology[MESH] |Autoimmunity/drug effects/immunology[MESH] |CD4-CD8 Ratio[MESH] |Cell Differentiation[MESH] |Cell Proliferation[MESH] |Cells, Cultured[MESH] |Cyclobutanes/administration & dosage/antagonists & inhibitors/*pharmacology/therapeutic use[MESH] |Hypersensitivity, Delayed/*immunology/metabolism[MESH] |Lymphocyte Activation/immunology[MESH] |Mice[MESH] |Mice, Inbred C3H[MESH] |Mitochondria/metabolism[MESH] |Phosphoinositide-3 Kinase Inhibitors[MESH] |Proto-Oncogene Proteins c-akt/antagonists & inhibitors[MESH] |Receptors, Antigen, T-Cell[MESH] |Receptors, Tumor Necrosis Factor/biosynthesis[MESH] |Signal Transduction/drug effects[MESH] |T-Lymphocytes/drug effects/immunology/metabolism[MESH] |Tretinoin/pharmacology[MESH]Delayed type hypersensitivity-induced myeloid-derived suppressor cells(epmc).pdf DeepDyve Pubget Overpricing