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    Acute Erythemal Ultraviolet Radiation Causes Systemic Immunosuppression in the Absence of Increased 25-Hydroxyvitamin D-3 Levels in Male Mice

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    Author
    Gorman, S; Scott, NM; Tan, DHW; Weeden, CE; Tuckey, RC; Bisley, JL; Grimbaldeston, MA; Hart, PH
    Date
    2012-09-26
    Source Title
    PLoS One
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    Weeden, Claire
    Affiliation
    Surgery (St Vincent's)
    Metadata
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    Document Type
    Journal Article
    Citations
    Gorman, S., Scott, N. M., Tan, D. H. W., Weeden, C. E., Tuckey, R. C., Bisley, J. L., Grimbaldeston, M. A. & Hart, P. H. (2012). Acute Erythemal Ultraviolet Radiation Causes Systemic Immunosuppression in the Absence of Increased 25-Hydroxyvitamin D-3 Levels in Male Mice. PLOS ONE, 7 (9), https://doi.org/10.1371/journal.pone.0046006.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256882
    DOI
    10.1371/journal.pone.0046006
    Abstract
    Vitamin D is synthesised by ultraviolet (UV) irradiation of skin and is hypothesized to be a direct mediator of the immunosuppression that occurs following UV radiation (UVR) exposure. Both UVR and vitamin D drive immune responses towards tolerance by ultimately increasing the suppressive activities of regulatory T cells. To examine a role for UVR-induced vitamin D, vitamin D(3)-deficient mice were established by dietary vitamin D(3) restriction. In comparison to vitamin D(3)-replete mice, vitamin D(3)-deficient mice had significantly reduced serum levels of 25-hydroxyvitamin D(3) (25(OH)D(3), <20 nmol.L(-1)) and 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3), <20 pmol.L(-1)). Following either acute erythemal UVR, or chronic sub-erythemal UVR (8 exposures over 4 weeks) treatment, serum 25(OH)D(3) levels significantly increased in vitamin D(3)-deficient female but not male mice. To determine if UVR-induced vitamin D was a mediator of UVR-induced systemic immunosuppression, responses were measured in mice that were able (female) or unable (male) to increase systemic levels of 25(OH)D(3) after UVR. Erythemal UVR (≥ 4 kJ/m(2)) suppressed contact hypersensitivity responses (T helper type-1 or -17), aspects of allergic airway disease (T helper type-2) and also the in vivo priming capacity of bone marrow-derived dendritic cells to a similar degree in female and male vitamin D(3)-deficient mice. Thus, in male mice, UVR-induced 25(OH)D(3) is not essential for mediating the immunosuppressive effects of erythemal UVR.

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