Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many individuals infected with HBV become chronic carriers and they liver disease may progress to cirrhosis and HCC. The newest data suggests that the interaction between positive and negative costimulatory molecules expressed on T cells are performing the role in the regulation ofT cells immune response. In the last years they were described programmed death-1 (PD-1) [CD279] and programmed death-ligand 1 (PD-L1) [CD274] in immunopathology of HBV infections. In acute exacerbation of hepatitis B, high level of PD-1 expression significantly mediated CD8+T cells apoptosis and protecting before damaging the liver. In the period of recovering, activation of the PD-1/PD-L 1 pathway should dynamically decrease, and if it isn't taking place, increased expression of the PD-1 plays a crucial role in inhibiting the function of virus-specific CD4+ and CD8+ T cells in chronic viral infections. The aim of this article was to explore the potential role of (PD-1/PD-L) pathway in antiviral immunity during HBV infection. Blockade of PD-1/PD-L1 pathway may open a novel therapeutic strategy for restoring the function of the exhausted CD8+ T cells, and enhancing viral control during chronic viral infections.
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PMID:[Role of the PD-1/PD-L1 pathway in immunopathology of HBV infection as the chance on the new therapeutic strategy]. 2147 62

Cancer immunoprevention is achieved through promoting antitumor immune surveillance to block tumor formation and progression. Following the success of prophylactic vaccines against human papillomavirus (HPV) in preventing HPV-associated cancer, immunopreventive cancer vaccines targeting tumor antigens have been increasingly evaluated against cancers of noninfectious origin. While advances in cancer immunotherapy with immune checkpoint inhibitors (ICI) have clearly shown that the host immune system can mount effective antitumor immunity against tumor antigens when immune checkpoints are optimally blocked, the use of ICIs in the prevention setting has not been widely explored because of concerns of ICI-associated adverse events. In this issue of Cancer Prevention Research, Chung and colleagues demonstrate that the human cirrhotic liver harbors neoantigens, which accumulate further as the disease progresses to hepatocellular carcinoma (HCC), suggesting that cirrhotic liver may be susceptible to ICI therapy. Utilizing an established mouse model of carcinogen-induced liver fibrosis and HCC, they show that intermittent intervention by ICI, anti-mouse PD-1 (CD279) antibody, can prevent the progression of the precancerous stage of cirrhosis to HCC accompanied by increased T-cell infiltrates in the liver parenchyma. Importantly, there were no overt ICI-associated toxicities in the treated mice, indicating that safe dosing regimens could be established. This work is both significant and timely, opening the door to future studies, where the utility of ICI therapy can be further investigated not only in cirrhosis but other high-risk precancerous conditions. In this perspective, we discuss the implications of their findings, and the challenges and potential opportunities for use of ICIs for cancer immunoprevention.See related article by Chung et al., p. 911.
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PMID:Cancer Immunoprevention: Challenges and Potential Opportunities for Use of Immune Checkpoint Inhibitors. 3283 4