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Dietary vitamin E is critical for T cell trafficking to the brain during infection
Author(s) -
Sheridan Patricia Ann,
Beck Melinda A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.298.7
Subject(s) - t cell , immunology , biology , cd8 , cytokine , immune system , priming (agriculture) , chemokine , central nervous system , endocrinology , botany , germination
Previous studies from our laboratory have shown that dietary a‐tocopherol (VE) is critical to regulating the cytokine and chemokine response in the brain to herpes simplex virus (HSV) infection. In addition to the cytokine response, the timing of T cell infiltration is critical to the resolution of central nervous system HSV‐1 infections. Specifically, the appearance of “neuroprotective” IFN‐g‐producing CD8+ T cells is crucial. During CNS infection CD8+ T cell priming and expansion occurs in the draining lymph node, followed by recruitment and expansion occurs in the spleen with subsequent accumulation in the brain. In order to determine how VE deficiency and VE supplementation would alter T cell trafficking during HSV‐1 infection of the brain, we placed weanling male BALB/cByJ mice on VE deficient (Def), adequate (Adq) or 10X supplemented (Sup) diets for 4 weeks and then infected the mice intranasally with HSV‐1. VE Def mice had suppressed antigen‐specific T cell trafficking to the brain. In contrast, VE supplementation had no effect on T cell trafficking. In contrast to both VE Def and VE Adq mice, VE Sup mice did not increase splenic regulatory T cells in response to infection. Our results demonstrate that adequate levels of VE are important for trafficking antigen‐specific T cells to the brain and dietary VE levels modulate T regulatory and dendritic cells in the periphery. Support:P30ES10126 and DK56350.