Authors:
Gorman S; Scott NM; Tan DHW; Weeden CE; Tuckey RC; Bisley JL; ... Hart PH
Authors notes:
PLoS ONE. 2012;7(9):e46006
Keywords:
Vitamin D, Ultraviolet irradiation, Immunosupression, Male Mice
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 D3-deficient mice were established by dietary vitamin D3 restriction.
In comparison to vitamin D3>-replete mice, vitamin D3-deficient mice had significantly reduced serum levels of 25-hydroxyvitamin D3 (25(OH)D3, 20 nmol.L−1) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D, 20 pmol.L−1).
Following either acute erythemal UVR, or chronic sub-erythemal UVR (8 exposures over 4 weeks) treatment, serum 25(OH)D3 levels significantly increased in vitamin D3-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)D3 after UVR.
Erythemal UVR (≥4 kJ/m2) 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 D3-deficient mice.
Thus, in male mice, UVR-induced 25(OH)D3 is not essential for mediating the immunosuppressive effects of erythemal UVR.