Vitamin D Receptor Agonists Target CXCL10: New Therapeutic Tools for Resolution of Inflammation

Figure 1

Effects of vitamin D on different immune system cells. Vitamin D regulates several immune system cell functions. It stimulates monocyte proliferation and differentiation towards macrophage-like cells, by self-increasing VDR, CYP27B, and IL-1 expressions; this “fast-forward” autocrine mechanism seems to be the basis for the subsequent maturation into macrophages, which does not take place in vitamin D deficient conditions; macrophage specific surface antigen expression is also enhanced. Vitamin D prevents T cells from proliferation, maturation, and releasing Th1-type molecules, such as IFN𝛾, IL-2, and IL-17, whereas it promotes Treg development. Vitamin D treatment prevents DCs from maturation and differentiation as well, by MHC class II, costimulatory factors, and interleukin downregulation. Vitamin D-induced protolerogenic DCs seem to be the key event for suppressive effects on immune system cells. Downregulation of B cell proliferation and maturation seems to be an indirect consequence of the suppressive effect exerted by vitamin D on T cells and APC. (+) and (−) indicate induction or inhibition.