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Virus-Induced Inhibition of CD1d1-Mediated Antigen Presentation: Reciprocal Regulation by p38 and ERK¹

Gourapura J. Renukaradhya^*,, Tonya J. Roberts Webb^*,, Masood A. Khan^*,, Yin Ling Lin^*,, Wenjun Du, Jacquelyn Gervay-Hague and Randy R. Brutkiewicz^2,*,

^* Department of Microbiology and Immunology, Indiana University School of Medicine, Walther Oncology Center, Indianapolis, IN 46202; Walther Cancer Institute, Indianapolis, IN 46208; and Department of Chemistry, University of California, Davis, CA 95616

A critical component of the host’s innate immune response involves lipid Ag presentation by CD1d molecules to NK T cells. In this study we used murine CD1d1-transfected L (L-CD1) cells to study the effect of viruses on CD1d-mediated Ag presentation to NKT cells and found that an infection with vesicular stomatitis and vaccinia (but not lymphocytic choriomeningitis) virus inhibited murine CD1d1-mediated Ag presentation. This was under the reciprocal control of the MAPKs, p38 and ERK, and was due to changes in the intracellular trafficking of CD1d1. The reciprocal regulation of CD1d1-mediated Ag presentation by MAPK suggests that the targeting of these pathways is a novel means of immune evasion by viruses.

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