期刊
SCIENCE
卷 343, 期 6169, 页码 432-437出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1247606
关键词
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资金
- Division of Intramural Research of the National Institute of Allergy and Infectious Diseases (NIAID), NIH
- Office of Dietary Supplements, NIH
- NIH [F30 DK094708]
- Human Frontier Science Program
- U.S. Department of Agriculture-Agricultural Research Service [1254-32000-094-00D]
- Damon Runyon Cancer Research Foundation
How the immune system adapts to malnutrition to sustain immunity at barrier surfaces, such as the intestine, remains unclear. Vitamin A deficiency is one of the most common micronutrient deficiencies and is associated with profound defects in adaptive immunity. Here, we found that type 3 innate lymphoid cells (ILC3s) are severely diminished in vitamin A-deficient settings, which results in compromised immunity to acute bacterial infection. However, vitamin A deprivation paradoxically resulted in dramatic expansion of interleukin-13 (IL-13)-producing ILC2s and resistance to nematode infection in mice, which revealed that ILCs are primary sensors of dietary stress. Further, these data indicate that, during malnutrition, a switch to innate type 2 immunity may represent a powerful adaptation of the immune system to promote host survival in the face of ongoing barrier challenges.
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