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10.3892/ijmm.2018.3688 http://scihub22266oqcxt.onion/10.3892/ijmm.2018.3688 C6034931!6034931!29786112     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29786112&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Mol+Med 2018 ; 42 (2): 703-12 Nephropedia Template TP {{tp|p=29786112|t=2018. CTLA-4 interferes with the HBV-specific T cell immune response (Review) |pdf=|usr=}}{{29786112}} gab.com Text CTLA-4 interferes with the HBV-specific T cell immune response (Review) JO: Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29786112 #FOAvip Hepatitis B virus (HBV) infection is a major cause of hepatic inflammation. Successful HBV clearance in patients is associated with sustained viral control by effector T cells. Compared with acute hepatitis B, chronic HBV infection is associated with the depletion of T cells, resulting in weak or absent virus-specific T cells reactivity, which is described as 'exhaustion'. This exhaustion is characterized by impaired cytokine production and sustained expression of multiple coinhibitory molecules. Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is one of many coinhibitory molecules that can attenuate T cell activation by inhibiting costimulation and transmitting inhibitory signals to T cells. Persistent HBV infection results in the upregulation of CTLA-4 on hepatic CD8+ T cells. This prompts CD8+ T cell apoptosis, and the activation of cytotoxic T lymphocytes is blocked. Similar to CD8+ T cells, CD4+ T helper (Th) cell proliferation is hindered following CTLA-4 upregulation. In addition, the differentiation of CD4+ Th is polarized toward the Th2/peripherally-inducible T regulatory cell types, increasing the levels of anti-inflammatory cytokines. Conversely, the activation of proinflammatory cells (Th1 and follicular helper T) is blocked, and the levels of proinflammatory cytokines decline. This review summarizes the current literature relevant to T cell exhaustion in patients with HBV-related chronic hepatitis, and discusses the roles of CTLA-4 in T cell exhaustion. Twit Text FOAVip CTLA-4 interferes with the HBV-specific T cell immune response (Review) ????Int J Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29786112 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29786112 #FOAvip English Wikipedia <ref>{{Cite pmid|29786112}}</ref> CTLA-4 interferes with the HBV-specific T cell immune response (Review) #MMPMID29786112 Cao H; Zhang R; Zhang W Int J Mol Med 2018[Aug]; 42 (2): 703-12 PMID29786112show ga Hepatitis B virus (HBV) infection is a major cause of hepatic inflammation. Successful HBV clearance in patients is associated with sustained viral control by effector T cells. Compared with acute hepatitis B, chronic HBV infection is associated with the depletion of T cells, resulting in weak or absent virus-specific T cells reactivity, which is described as 'exhaustion'. This exhaustion is characterized by impaired cytokine production and sustained expression of multiple coinhibitory molecules. Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is one of many coinhibitory molecules that can attenuate T cell activation by inhibiting costimulation and transmitting inhibitory signals to T cells. Persistent HBV infection results in the upregulation of CTLA-4 on hepatic CD8+ T cells. This prompts CD8+ T cell apoptosis, and the activation of cytotoxic T lymphocytes is blocked. Similar to CD8+ T cells, CD4+ T helper (Th) cell proliferation is hindered following CTLA-4 upregulation. In addition, the differentiation of CD4+ Th is polarized toward the Th2/peripherally-inducible T regulatory cell types, increasing the levels of anti-inflammatory cytokines. Conversely, the activation of proinflammatory cells (Th1 and follicular helper T) is blocked, and the levels of proinflammatory cytokines decline. This review summarizes the current literature relevant to T cell exhaustion in patients with HBV-related chronic hepatitis, and discusses the roles of CTLA-4 in T cell exhaustion. äCTLA-4 interferes with the HBV-specific T cell immune response (Review(epmc).pdf DeepDyve Pubget Overpricing