Programmed death-1/programmed death-L1 signaling pathway and its blockade in hepatitis C virus immunotherapy
نویسندگان
چکیده
منابع مشابه
Immunotherapy of chronic hepatitis C virus infection with antibodies against programmed cell death-1 (PD-1).
Hepatitis C virus (HCV) persistence is facilitated by exhaustion of CD8+ T cells that express the inhibitory receptor programmed cell death 1 (PD-1). Blockade of PD-1 signaling improves in vitro proliferation of HCV-specific T lymphocytes, but whether antiviral function can be restored in infected individuals is unknown. To address this question, chimpanzees with persistent HCV infection were t...
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The aim of T-cell-based immune therapy for cancer has been to generate durable clinical benefit for patients. Following a generation of therapies that largely showed minimal activity, substantial toxicity, and no biomarkers to identify which patients benefit from treatment, early studies are showing signs that programmed death-ligand 1 (PD-L1) and programmed death-1 (PD-1) inhibitors are highly...
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In this issue of Neuro-Oncology, Berghoff et al present the results of their investigations into the expression of programmed death-ligand 1 (PD-L1) in human glioblastoma specimens and their relationship to other tissue-based and clinical parameters. In specimens from adults with newly diagnosed or recurrent glioblastoma, the investigators reported that diffuse/fibrillary PD-L1 expression of va...
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متن کاملEnhancement of Programmed Death Ligand 2 on Hepatitis C Virus Infected Hepatocytes by Calcineurin Inhibitors
BACKGROUND Post orthotopic liver transplantation (OLT) viral hepatitis is an immunological condition where immune cells induce hepatitis during conditions of immune-suppression. The immune-regulatory programmed death-1 (PD-1)/PD-ligand 1 system is acknowledged to play important roles in immune-mediated diseases. However, the PD-1/PD-L2 interaction is not well characterized, with PD-L2 also exhi...
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ژورنال
عنوان ژورنال: World Journal of Hepatology
سال: 2015
ISSN: 1948-5182
DOI: 10.4254/wjh.v7.i23.2449