Purpose of review: The role of vitamin D extends well beyond that of regulating calcium homeostasis. One of these areas is immune function. Immunity is both adaptive and innate, and vitamin D signaling is operative in both. This review will examine these actions of vitamin D, in particular the role of vitamin D in host defense against infection.
Recent findings: This review will consider two examples of vitamin D-regulated innate immunity that have been recently explored: the role of vitamin D signaling within macrophages to enable them to respond to and kill Mycobacterium tuberculosis organisms, and the role of vitamin D signaling in the keratinocytes of the epidermis to enable them to respond to disruption of their barrier function. Potential application to periodontal disease will then be considered.
Summary: Both adaptive and innate immune processes are two edged: beneficial and harmful. Although suppression of adaptive immunity may be beneficial in a number of self-destructive diseases, such suppression may predispose to infection. Enhancement of innate immunity is clearly beneficial in diseases like tuberculosis, but potentiation of proinflammatory processes can increase tissue destruction as in bone loss in periodontal disease. The balance, however, favors adequate vitamin D nutrition in host defense against infection.