{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T23:24:42Z","timestamp":1792452282846,"version":"4.5.0"},"reference-count":39,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6169","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2014,1,24]]},"abstract":"<jats:p>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\u2013deficient settings, which results in compromised immunity to acute bacterial infection. However, vitamin A deprivation paradoxically resulted in dramatic expansion of interleukin-13 (IL-13)\u2013producing 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.<\/jats:p>","DOI":"10.1126\/science.1247606","type":"journal-article","created":{"date-parts":[[2014,1,23]],"date-time":"2014-01-23T14:21:55Z","timestamp":1390486915000},"page":"432-437","source":"Crossref","is-referenced-by-count":437,"title":["Adaptation of Innate Lymphoid Cells to a Micronutrient Deficiency Promotes Type 2 Barrier Immunity"],"prefix":"10.1126","volume":"343","author":[{"given":"S. P.","family":"Spencer","sequence":"first","affiliation":[{"name":"Immunity at Barrier Sites Initiative, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda 20892, USA."},{"name":"Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda, MD 20892, USA."},{"name":"Department of Pathology and Laboratory Medicine, Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Wilhelm","sequence":"additional","affiliation":[{"name":"Immunity at Barrier Sites Initiative, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda 20892, USA."},{"name":"Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Q.","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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B.","family":"Nutman","sequence":"additional","affiliation":[{"name":"Helminth Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda, MD 20892, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"J. F.","family":"Urban","sequence":"additional","affiliation":[{"name":"U.S. Department of Agriculture, Beltsville Human Nutrition Research Center, Diet, Genomics, and Immunology Laboratory, Beltsville, MD 20705, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Wang","sequence":"additional","affiliation":[{"name":"Program in Metabolic Biology, Nutritional Science and Toxicology, University of California, Berkeley, CA 94720, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. 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