Technical Abstract: Vitamin A deficiency increases the risk of death from infectious diseases in infants and young children in areas of the world where vitamin A deficiency is common. This increased risk apparently results from impaired innate and adaptive immune function. Retinoic acid is the major metabolite of vitamin A produced by immune cells. In particular, dendritic cells produce retinoic acid that acts to regulate gene expression in cells of the immune system. Innate immune cells, such as neutrophils, develop in the bone marrow in response to locally produced retinoic acid. Neutrophil function is impaired by vitamin A deficiency in that their ability to kill bacteria is compromised, thus increasing the risk of invasive bacterial infections. Natural Killer (NK) cells are active against viruses and other intracellular bacteria and their numbers and activity are decreased by vitamin A deficiency. Antigen-presenting cells, particularly intestinal dendritic cells, produce retinoic acid and thereby regulate the development of both B and T lymphocytes, the major effector cells of adaptive immunity. In particular, retinoic acid enhances the development of some T helper (Th) cell phenotypes, including Th2 cells and inducible T regulatory (iTreg) cells, regulates the development of B cells that produce antibodies such as immunoglobulin A (IgA), and promotes trafficking of lymphocytes to the intestine and other mucosal sites by inducing expression of chemokine receptor 9 and a4ß7 integrin. Retinoic acid thus is particularly active in boosting mucosal immunity and vitamin A deficiency thus particularly impairs protection against mucosal infections, such as diarrheal pathogens.