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10.3389/fimmu.2017.00195 http://scihub22266oqcxt.onion/10.3389/fimmu.2017.00195 C5332470!5332470 !28303136     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28303136 &cmd=llinks): Failed to open stream: HTTP request failed! 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Expansions of Cytotoxic CD4(+)CD28(-) T Cells Drive Excess Cardiovascular Mortality in Rheumatoid Arthritis and Other Chronic Inflammatory Conditions and Are Triggered by CMV Infection |pdf=|usr=}}{{28303136 }} gab.com Text Expansions of Cytotoxic CD4(+)CD28(-) T Cells Drive Excess Cardiovascular Mortality in Rheumatoid Arthritis and Other Chronic Inflammatory Conditions and Are Triggered by CMV Infection JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28303136 #FOAvip A large proportion of cardiovascular (CV) pathology results from immune-mediated damage, including systemic inflammation and cellular proliferation, which cause a narrowing of the blood vessels. Expansions of cytotoxic CD4(+) T cells characterized by loss of CD28 ("CD4(+)CD28(-) T cells" or "CD4(+)CD28(null) cells") are closely associated with cardiovascular disease (CVD), in particular coronary artery damage. Direct involvement of these cells in damaging the vasculature has been demonstrated repeatedly. Moreover, CD4(+)CD28(-) T cells are significantly increased in rheumatoid arthritis (RA) and other autoimmune conditions. It is striking that expansions of this subset beyond 1-2% occur exclusively in CMV-infected people. CMV infection itself is known to increase the severity of autoimmune diseases, in particular RA and has also been linked to increased vascular pathology. A review of the recent literature on immunological changes in CVD, RA, and CMV infection provides strong evidence that expansions of cytotoxic CD4(+)CD28(-) T cells in RA and other chronic inflammatory conditions are limited to CMV-infected patients and driven by CMV infection. They are likely to be responsible for the excess CV mortality observed in these situations. The CD4(+)CD28(-) phenotype convincingly links CMV infection to CV mortality based on a direct cellular-pathological mechanism rather than epidemiological association. Twit Text FOAVip Expansions of Cytotoxic CD4(+)CD28(-) T Cells Drive Excess Cardiovascular Mortality in Rheumatoid Arthritis and Other Chronic Inflammatory Conditions and Are Triggered by CMV Infection ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28303136 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28303136 #FOAvip English Wikipedia <ref>{{Cite pmid|28303136 }}</ref> Expansions of Cytotoxic CD4(+)CD28(-) T Cells Drive Excess Cardiovascular Mortality in Rheumatoid Arthritis and Other Chronic Inflammatory Conditions and Are Triggered by CMV Infection #MMPMID28303136 Broadley I ; Pera A ; Morrow G ; Davies KA ; Kern F Front Immunol 2017[]; 8 (ä): 195 PMID28303136 show ga A large proportion of cardiovascular (CV) pathology results from immune-mediated damage, including systemic inflammation and cellular proliferation, which cause a narrowing of the blood vessels. Expansions of cytotoxic CD4(+) T cells characterized by loss of CD28 ("CD4(+)CD28(-) T cells" or "CD4(+)CD28(null) cells") are closely associated with cardiovascular disease (CVD), in particular coronary artery damage. Direct involvement of these cells in damaging the vasculature has been demonstrated repeatedly. Moreover, CD4(+)CD28(-) T cells are significantly increased in rheumatoid arthritis (RA) and other autoimmune conditions. It is striking that expansions of this subset beyond 1-2% occur exclusively in CMV-infected people. CMV infection itself is known to increase the severity of autoimmune diseases, in particular RA and has also been linked to increased vascular pathology. A review of the recent literature on immunological changes in CVD, RA, and CMV infection provides strong evidence that expansions of cytotoxic CD4(+)CD28(-) T cells in RA and other chronic inflammatory conditions are limited to CMV-infected patients and driven by CMV infection. They are likely to be responsible for the excess CV mortality observed in these situations. The CD4(+)CD28(-) phenotype convincingly links CMV infection to CV mortality based on a direct cellular-pathological mechanism rather than epidemiological association. äExpansions of Cytotoxic CD4(+)CD28(-) T Cells Drive Excess Cardiovascu(epmc).pdf DeepDyve Pubget Overpricing