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Background   In vitro  studies have shown that the active form of vitamin D 3 , 1α,25-dihydroxyvitamin D3 (1,25(OH) 2 D 3 ), can regulate differentiation of CD4 +  T cells by inhibiting Th1 and Th17 cell differentiation and promoting Th2 and Treg cell differentiation. However, the serum concentration of 1,25(OH) 2 D 3  is far below the effective concentration of 1,25(OH) 2 D 3  found in  in vitro  studies, and it has been suggested that 1,25(OH) 2 D 3  must be produced locally from the inactive precursor 25-hydroxyvitamin D3 (25(OH)D 3 ) to affect ongoing immune responses  in vivo . Although it has been reported that activated T cells express the 25(OH)D-1α-hydroxylase CYP27B1 that converts 25(OH)D 3  to 1,25(OH) 2 D 3 , it is still controversial whether activated T cells have the capacity to produce sufficient amounts of 1,25(OH) 2 D 3  to affect vitamin D-responsive genes. Furthermore, it is not known how the vitamin D-binding protein (DBP) found in high concentrations in serum affects T cell responses to 25(OH)D 3 .    Results  We found that activated T cells express CYP27B1 and have the capacity to produce sufficient 1,25(OH) 2 D 3  to affect vitamin D-responsive genes when cultured with physiological concentrations of 25(OH)D 3  in serum-free medium. However, if the medium was supplemented with serum or purified DBP, DBP strictly inhibited the production of 1,25(OH) 2 D 3  and 25(OH)D 3 -induced T cell responses. In contrast, DBP did not inhibit the effect of exogenous 1,25(OH) 2 D 3 . Actin, arachidonic acid and albumin did not affect the sequestration of 25(OH)D 3  by DBP, whereas carbonylation of DBP did.    Conclusions  Activated T cells express CYP27B1 and can convert 25(OH)D 3  to 1,25(OH) 2 D 3  in sufficiently high concentrations to affect vitamin D-responsive genes when cultured in serum-free medium. However, DBP sequesters 25(OH)D 3  and inhibits the production of 1,25(OH) 2 D 3  in T cells. To fully exploit the immune-regulatory potential of vitamin D, future studies of the mechanisms that enable the immune system to exploit 25(OH)D 3  and convert it to 1,25(OH) 2 D 3  in vivo  are required.    Electronic supplementary material  The online version of this article (doi:10.1186/s12865-014-0035-2) contains supplementary material, which is available to authorized users.

Vitamin D-binding protein controls T cell responses to vitamin D