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10.2119/molmed.2014.00264 http://scihub22266oqcxt.onion/10.2119/molmed.2014.00264 C4503655!4503655 !25569805     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25569805 &cmd=llinks): Failed to open stream: HTTP request failed! 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Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion |pdf=|usr=}}{{25569805 }} gab.com Text Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion JO: Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25569805 #FOAvip Experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), is mediated by myelin-specific autoreactive T cells that cause inflammation and demyelination in the central nervous system (CNS), with significant contributions from activated microglia and macrophages. The molecular bases for expansion and activation of these cells, plus trafficking to the CNS for peripheral cells, are not fully understood. Allograft inflammatory factor-1 (Aif-1) (also known as ionized Ca(2+) binding adapter-1 [Iba-1]) is induced in leukocytes in MS and EAE; here we provide the first assessment of Aif-1 function in this setting. After myelin oligodendrocyte glycoprotein peptide (MOG35-55) immunization, Aif-1-deficient mice were less likely than controls to develop EAE and had less CNS leukocyte infiltration and demyelination; their spinal cords contained fewer CD4 T cells and microglia and more CD8 T cells. These mice also showed significantly less splenic CD4 T-cell expansion and activation, plus decreased proinflammatory cytokine expression. These findings identify Aif-1 as a potent molecule that promotes expansion and activation of CD4 T cells, plus elaboration of a proinflammatory cytokine milieu, in MOG35-55-induced EAE and as a potential therapeutic target in MS. Twit Text FOAVip Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion ????Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=25569805 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25569805 #FOAvip English Wikipedia <ref>{{Cite pmid|25569805 }}</ref> Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoimmune Encephalomyelitis by Limiting Encephalitogenic CD4 T-Cell Expansion #MMPMID25569805 Chinnasamy P ; Lutz SE ; Riascos-Bernal DF ; Jeganathan V ; Casimiro I ; Brosnan CF ; Sibinga NE Mol Med 2015[Jan]; 21 (1 ): 233-41 PMID25569805 show ga Experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), is mediated by myelin-specific autoreactive T cells that cause inflammation and demyelination in the central nervous system (CNS), with significant contributions from activated microglia and macrophages. The molecular bases for expansion and activation of these cells, plus trafficking to the CNS for peripheral cells, are not fully understood. Allograft inflammatory factor-1 (Aif-1) (also known as ionized Ca(2+) binding adapter-1 [Iba-1]) is induced in leukocytes in MS and EAE; here we provide the first assessment of Aif-1 function in this setting. After myelin oligodendrocyte glycoprotein peptide (MOG35-55) immunization, Aif-1-deficient mice were less likely than controls to develop EAE and had less CNS leukocyte infiltration and demyelination; their spinal cords contained fewer CD4 T cells and microglia and more CD8 T cells. These mice also showed significantly less splenic CD4 T-cell expansion and activation, plus decreased proinflammatory cytokine expression. These findings identify Aif-1 as a potent molecule that promotes expansion and activation of CD4 T cells, plus elaboration of a proinflammatory cytokine milieu, in MOG35-55-induced EAE and as a potential therapeutic target in MS. |Animals [MESH] |CD4-Positive T-Lymphocytes/*immunology/*metabolism [MESH] |Calcium-Binding Proteins/*deficiency [MESH] |Demyelinating Diseases/genetics/immunology/metabolism [MESH] |Disease Models, Animal [MESH] |Encephalomyelitis, Autoimmune, Experimental/diagnosis/*genetics/*immunology/metabolism [MESH] |Leukocytes/immunology/metabolism/pathology [MESH] |Lymphocyte Activation [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Microfilament Proteins/*deficiency [MESH] |Severity of Illness Index [MESH] |Spleen/immunology/metabolism/pathology [MESH]Loss of Allograft Inflammatory Factor-1 Ameliorates Experimental Autoi(epmc).pdf DeepDyve Pubget Overpricing