Nature Immunology 7, 835 - 842 (2006)
Published online: 16 July 2006; | doi:10.1038/ni1364
Herpes simplex virus evades natural killer T cell recognition by suppressing CD1d recyclingWeiming Yuan1, Anindya Dasgupta1, 2
& Peter Cresswell11
Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011, USA. 2
Present address: Vaccine and Gene Therapy Institute, Oregon Health and Sciences University, Beaverton, Oregon 97006, USA.
Correspondence should be addressed to Peter Cresswell peter.cresswell@yale.edu Natural killer T cells, which are stimulated by lipids presented by CD1d molecules, are crucial in antiviral host defense. How viruses evade natural killer T cell recognition remains unclear. Here we show that infection with herpes simplex virus type 1 (HSV-1) reduced CD1d surface expression on antigen-presenting cells. HSV-1 did not inhibit CD1d protein synthesis or enhance constitutive CD1d endocytosis. Instead, HSV-1 prevented the reappearance of endocytosed CD1d on the cell surface by redistributing endocytosed CD1d to the lysosome limiting membrane. HSV-1 might also inhibit the transport of newly synthesized CD1d to the cell surface. Such inhibition of CD1d surface expression impaired antigen-presenting cell–mediated stimulation of natural killer T cells, supporting the idea that this mechanism may be an important HSV-1 immune evasion strategy.
MORE ARTICLES LIKE THIS These links to content published by NPG are automatically generated.
|
