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The hallmark of chronic viral infections is a progressive exhaustion of antigen-specific CD8(+) T cells that leads to persisting viral replication. It is generally believed that exhaustion is a consequence of the accumulation of multiple inhibitory receptors on CD8(+) T cells that makes them dysfunctional. Here, we show that during human chronic HIV-1 infection, a CD8(+) T-cell positive costimulatory pathway mediated by DNAX-activating molecule-1 is also disrupted. Thus, DNAX-activating molecule-1 downregulation on CD8(+) T cells aggravates the impairment of CTL effector function in chronic HIV-1 infection.

Original publication

DOI

10.1002/eji.200940234

Type

Journal article

Journal

Eur J Immunol

Publication Date

04/2010

Volume

40

Pages

949 - 954

Keywords

Animals, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, Antigens, Viral, Apoptosis Regulatory Proteins, CD8-Positive T-Lymphocytes, Down-Regulation, Glycoproteins, HIV Infections, HIV-1, Humans, Lymphocyte Activation, Lymphocyte Count, Lymphocytic Choriomeningitis, Mice, Peptide Fragments, Programmed Cell Death 1 Receptor, Receptors, Virus, T-Cell Antigen Receptor Specificity, Viral Load, Viral Proteins, Virus Replication