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Upregulation of CD94/NKG2A receptors and Qa-1^b ligand during murine cytomegalovirus infection of salivary glands

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

Correspondence
Ann E. Campbell
campbeae{at}evms.edu

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-1^b, increased dramatically in the submandibular gland (SMG) prior to upregulation of H-2D^d. 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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