Pivotal Advance: CTLA-4+ T cells exhibit normal antiviral functions during acute viral infection

Hans Peter Raué, Mark Slifka

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    Abstract

    Previous studies have shown that T cells, which are genetically deficient in CTLA-4/CD152 expression, will proliferate uncontrollably, resulting in lethal autoimmune disease. This and other evidence indicate that CTLA-4 plays a critical role in the negative regulation of effector T cell function. In contrast to expectations, BrdU incorporation experiments demonstrated that CTLA-4 expression was associated with normal or even enhanced in vivo proliferation of virus-specific CD4+ and CD8+ T cells following acute lymphocytic choriomeningitis virus or vaccinia virus infection. When compared with CTLA-4- T cells directly ex vivo, CTLA-4 + T cells also exhibited normal antiviral effector functions following stimulation with peptide-coated cells, virus-infected cells, plate-bound anti-CD3/anti-CTLA-4, or the cytokines IL-12 and IL-18. Together, this indicates that CTLA-4 does not directly inhibit antiviral T cell expansion or T cell effector functions, at least not under the normal physiological conditions associated with either of these two acute viral infections.

    Original languageEnglish (US)
    Pages (from-to)1165-1175
    Number of pages11
    JournalJournal of Leukocyte Biology
    Volume81
    Issue number5
    DOIs
    StatePublished - May 2007

    Fingerprint

    Virus Diseases
    Antiviral Agents
    T-Lymphocytes
    Viruses
    Lymphocytic choriomeningitis virus
    Interleukin-18
    Vaccinia virus
    Bromodeoxyuridine
    Interleukin-12
    Autoimmune Diseases
    Cytokines
    Peptides

    Keywords

    • CD4
    • CD8
    • LCMV
    • Vaccinia

    ASJC Scopus subject areas

    • Cell Biology

    Cite this

    Pivotal Advance : CTLA-4+ T cells exhibit normal antiviral functions during acute viral infection. / Raué, Hans Peter; Slifka, Mark.

    In: Journal of Leukocyte Biology, Vol. 81, No. 5, 05.2007, p. 1165-1175.

    Research output: Contribution to journalArticle

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