title: Vitamin A, infection, and immune function.
abstract: In populations where vitamin A availability from food is low, infectious diseases can precipitate vitamin A deficiency by decreasing intake, decreasing absorption, and increasing excretion. Infectious diseases that induce the acute-phase response also impair the assessment of vitamin A status by transiently depressing serum retinol concentrations. Vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells. Vitamin A is also required for adaptive immunity and plays a role in the development of T both-helper (Th) cells and B-cells. In particular, vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished. These changes in mucosal epithelial regeneration and immune function presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.
authors.affiliation: USDA Western Human Nutrition Research Center and Nutrition Department, University of California, Davis, California 95616, USA. cstephensen@ucdavis.edu
authors.forename: C B
authors.initials: CB
authors.lastname: Stephensen
mesh_terms: D000210:Acute-Phase Reaction; D019587:Dietary Supplements; D006801:Humans; D007109:Immunity; D007239:Infections / Q000276:immunology / Q000503:physiopathology; D009752:Nutritional Status; D014801:Vitamin A / Q000008:administration & dosage / Q000502:physiology*; D014802:Vitamin A Deficiency / Q000276:immunology
chemical_list: D014801:Vitamin A