Stephensen C B
USDA Western Human Nutrition Research Center and Nutrition Department, University of California, Davis, California 95616, USA.
Annu Rev Nutr. 2001;21:167-92. doi: 10.1146/annurev.nutr.21.1.167.
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.
在食物中维生素A供应不足的人群中，传染病可通过减少摄入、降低吸收和增加排泄而促使维生素A缺乏。引发急性期反应的传染病还会通过短暂降低血清视黄醇浓度而损害对维生素A状态的评估。维生素A缺乏会阻碍受感染破坏的粘膜屏障的正常再生，并削弱中性粒细胞、巨噬细胞和自然杀伤细胞的功能，从而损害先天免疫。适应性免疫也需要维生素A，并在辅助性T（Th）细胞和B细胞的发育中发挥作用。特别是，维生素A缺乏会减少Th2细胞介导的抗体介导反应，尽管Th1介导的免疫的某些方面也会减弱。粘膜上皮再生和免疫功能的这些变化可能是当今世界许多地区维生素A缺乏的婴儿、幼儿和孕妇死亡率增加的原因。
