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

J Gen Virol. 2007 May;88(Pt 5):1440-1445. doi: 10.1099/vir.0.82444-0.

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cytomegalovirus / immunology
  • Cytomegalovirus / pathogenicity*
  • Cytomegalovirus Infections / immunology
  • Gene Expression Regulation
  • HLA-B Antigens / immunology*
  • Humans
  • Mice
  • Mice, Inbred DBA
  • NK Cell Lectin-Like Receptor Subfamily C
  • NK Cell Lectin-Like Receptor Subfamily D / genetics*
  • Receptors, Immunologic / immunology
  • Receptors, Natural Killer Cell
  • Salivary Glands / physiopathology
  • Salivary Glands / virology*

Substances

  • HLA-B Antigens
  • KLRC1 protein, human
  • Klrc1 protein, mouse
  • NK Cell Lectin-Like Receptor Subfamily C
  • NK Cell Lectin-Like Receptor Subfamily D
  • Receptors, Immunologic
  • Receptors, Natural Killer Cell