期刊
JOURNAL OF IMMUNOLOGY
卷 175, 期 7, 页码 4301-4308出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.7.4301
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- NCI NIH HHS [CA89026] Funding Source: Medline
- NIAID NIH HHS [P01 AI056097, R01AI46455] Funding Source: Medline
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 stornatitis and v accinia (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 MO. 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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