Vesicular stomatitis virus matrix protein impairs CD1d-mediated antigen presentation through activation of the p38 MAPK pathway
UMass Chan Affiliations
Department of Microbiology and ImmunologyDepartment of Pathology
Graduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
2008-09-26
Metadata
Show full item recordAbstract
Natural killer T (NKT) cells are unique T lymphocytes that recognize CD1d-bound lipid antigens and play an important role in both innate and acquired immune responses against infectious diseases and tumors. We have already shown that a vesicular stomatitis virus (VSV) infection results in the rapid inhibition of murine CD1d-mediated antigen presentation to NKT cells. In the present study, it was found that the VSV matrix (VSV-M) protein is an important element in this decrease in antigen presentation postinfection. The VSV-M protein altered the intracellular distribution of murine CD1d molecules, resulting in qualitative (but not quantitative) changes in cell surface CD1d expression. The M protein was distributed throughout the infected cell, and it was found to activate the mitogen-activated protein kinase (MAPK) p38 very early postinfection. Infection of CD1d(+) cells with a temperature-sensitive VSV-M mutant at the nonpermissive temperature both substantially reversed the inhibition of antigen presentation by CD1d and delayed the activation of p38. Thus, the VSV-M protein plays an important role in permitting the virus to evade important components of the innate immune response by regulating specific MAPK pathways.Source
J Virol. 2008 Dec;82(24):12535-42. Epub 2008 Sep 24. Link to article on publisher's siteDOI
10.1128/JVI.00881-08Permanent Link to this Item
http://hdl.handle.net/20.500.14038/33012PubMed ID
18815300; 18815300Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1128/JVI.00881-08