Affiliation:
1. Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA 23501, USA
2. Department of Molecular and Cell Biology, and Cancer Research Laboratory, University of California, Berkeley, CA 94720, USA
Abstract
Following acute infection, murine cytomegalovirus (MCMV) replicates persistently in the salivary glands, despite the vigorous response of activated CD8 T cells that infiltrate this gland. Virus-specific CD8 T lymphocytes isolated from this organ were found to express the inhibitory CD94/NKG2A receptor that, in some virus models, confers an inhibitory response to cytotoxic T lymphocytes (CTLs). In response to MCMV infection, expression of the CD94/NKG2A ligand, Qa-1b, increased dramatically in the submandibular gland (SMG) prior to upregulation of H-2Dd. However, there was no net negative impact on virus-specific T-cell function, as virus titres were similar in CD94− and CD94+ mice. CD94/NKG2A expression, also known to inhibit apoptosis, did not influence the numbers of accumulated T, NK and NK T cells. These data indicate that expression of inhibitory CD94/NKG2A receptors does not account for the failure of MCMV-specific CTLs to clear the SMG of infection.
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14 articles.
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