Vitamin A, infection, and immune function

C. B. Stephensen

Research output: Contribution to journalArticle

471 Scopus citations

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 both T-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.

Original languageEnglish (US)
Pages (from-to)167-192
Number of pages26
JournalAnnual Review of Nutrition
Volume21
DOIs
StatePublished - 2001

Keywords

  • Acute phase response
  • Immunity
  • Retinoic acid
  • T-cells

ASJC Scopus subject areas

  • Medicine (miscellaneous)

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