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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.

Acute Erythemal Ultraviolet Radiation Causes Systemic Immunosuppression in the Absence of Increased 25-Hydroxyvitamin D3 Levels in Male Mice