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Innate Immune Response to Encephalomyocarditis Virus Infection Mediated by CD1d
  • Mark A. Exley
  • Nancy J. Bigley, Wright State University - Main Campus
  • Olivia Cheng
  • Angela Shaulov
  • Syed Muhammad Ali Tahir
  • Quincy L. Carter
  • Jorge Garcia
  • Carren Wang
  • Kurt Patten
  • Harold F. Stills, Jr.
  • Frederick W. Alt
  • Scott B. Snapper
  • Steven P. Balk
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CD1d-reactive natural killer T (NKT) cells can rapidly produce T helper type 1 (Th1) and/or Th2 cytokines, can activate antigen-presenting cell (APC) interleukin-12 (IL-12) production, and are implicated in the regulation of adaptive immune responses. The role of the CD1d system was assessed during infection with encephalomyocarditis virus (EMCV-D), a picornavirus that causes acute diabetes, paralysis and myocarditis. EMCV-D resistance depends on IL-12-mediated interferon-γ (IFN-γ) production. CD1d-deficient mice, which also lack CD1d-reactive NKT cells, were substantially more sensitive to infection with EMCV-D. Infected CD1d knockout mice had decreased IL-12 levels in vitro and in vivo, and indeed were protected by treatment with exogenous IL-12. IFN-γ production in CD1d knockout mice was decreased compared with that in wild-type (WT) mice in response to EMCV-D in vitro, although differences were not detected in vivo. Treatment with anti-asialo-GM1 antibody, to deplete NK cells, caused a marked increase in susceptibility of WT mice to EMCV-D infection, whereas CD1d knockout mice were little affected, suggesting that NK-cell-mediated protection is CD1d-dependent. Therefore, these data indicate that CD1d is essential for optimal responses to acute picornaviral infection. We propose that CD1d-reactive T cells respond to early immune signals and function in the innate immune response to a physiological viral infection by rapidly augmenting APC IL-12 production and activating NK cells.
Citation Information
Mark A. Exley, Nancy J. Bigley, Olivia Cheng, Angela Shaulov, et al.. "Innate Immune Response to Encephalomyocarditis Virus Infection Mediated by CD1d" Immunology Vol. 110 Iss. 4 (2003) p. 519 - 526 ISSN: 0741-5400
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