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    Apoptotic regulation of T cells and absence of immune deficiency in virus-infected gamma interferon receptor knockout mice

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    Authors
    Lohman, Barbara L.
    Welsh, Raymond M.
    UMass Chan Affiliations
    Department of Pathology
    Document Type
    Journal Article
    Publication Date
    1998-09-12
    Keywords
    Animals
    Antigens, CD95
    Apoptosis
    CD8-Positive T-Lymphocytes
    Cell Division
    Interferon Type II
    Lymphocytic Choriomeningitis
    Mice
    Mice, Knockout
    Receptors, Interferon
    Spleen
    Life Sciences
    Medicine and Health Sciences
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    Abstract
    Acute viral infections often induce a transient period of immune deficiency in which the host's T cells fail to proliferate in response to T-cell mitogens and fail to make an antigen-specific memory recall response. This has been associated with the enhanced sensitivity of these highly activated T cells to undergo apoptosis, or activation-induced cell death (AICD), upon T-cell receptor ligation. Here we show that gamma interferon receptor-deficient (IFN-gamma R-/-) mice mount a T-cell response to lymphocytic choriomeningitis virus (LCMV) infection but fail to undergo the transient immune deficiency. Instead, their T cells were hyperproliferative and relatively, but not completely, resistant to AICD. The immune response returned to homeostasis, but with delayed kinetics, in parallel with delayed clearance of the virus. Wild-type mice receiving high doses of disseminating LCMV Clone 13 are known to undergo clonal exhaustion of their virus-specific cytotoxic T lymphocytes (CTL). To determine whether this process was mediated by AICD associated with IFN-gamma or with Fas-Fas ligand interactions, LCMV-specific precursor CTL frequencies were examined in LCMV Clone 13-infected IFN-gamma R-/- or lpr (Fas-deficient) mice. In both instances, viral persistence was established and CTL precursors were greatly eliminated. This finding indicates that clonal exhaustion of CTL does not require IFN-gamma or Fas, even though both molecules influence AICD and the transient immune deficiency seen in the LCMV infection.
    Source
    J Virol. 1998 Oct;72(10):7815-21.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/38686
    PubMed ID
    9733817
    Related Resources
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    UMass Chan Faculty and Researcher Publications

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