Cited by 447IL-33, ST2, and ILC PathwaysT-cell and B-cell ImmunologyImmune responses and vaccinations

Adaptation of Innate Lymphoid Cells to a Micronutrient Deficiency Promotes Type 2 Barrier Immunity

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Spencer, S. P., Wilhelm, C., Yang, Q., Hall, J. A., Bouladoux, N., Boyd, A., Nutman, T. B., Urban, J. F. +5 more·2014·Science

Abstract

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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  • Depletion of vitamin A, in the adult, led to a decrease of Th1, Th17, and ILC3 responses, an effect which is counteracted through time.

    “the depletion of vitamin A, in the adult, led to a decrease of Th1, Th17, and ILC3 responses (a synonym of lowered immunity to bacterial infection), an effect which is counteracted through time127.”

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  1. [15]Spits H Innate lymphoid cells--a proposal for uniform nomenclature Nature reviews. Immunology 13 145 149 2013 23348417

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Authors
Spencer, S. P., Wilhelm, C., Yang, Q., Hall, J. A., Bouladoux, N., Boyd, A., Nutman, T. B., Urban, J. F., Wang, J., Ramalingam, T. R., Bhandoola, A., Wynn, T. A., & Belkaid, Y.
Affiliations
  • National Institutes of Health (US)
  • University of Pennsylvania (US)
  • Helminth Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, NIH, Bethesda, MD 20892, USA.
  • Beltsville Human Nutrition Research Center (US)
  • University of California, Berkeley (US)
Corresponding author
  • Spencer, S. P.
  • Wilhelm, C.
  • Belkaid, Y.
Venue
Science
Published
2014-01-24
Volume
343
Issue
6169
Pages
432-437
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1999696784
Cited by
447
References
38
Citations by year
2026: 14 · 2025: 23 · 2024: 25 · 2023: 31 · 2022: 33 · 2021: 24 · 2020: 29 · 2019: 44 · 2018: 36 · 2017: 43 · 2016: 40 · 2015: 56 · 2014: 48 · 2012: 1
FWCI
28.46
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (Z99 AI999999)
  • National Institute of Diabetes and Digestive and Kidney Diseases (F30DK094708)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
Keywords
innate lymphoid cells, vitamin A deficiency, micronutrient deficiency, malnutrition, Th2 immune response, ILC3, ILC2, IL-13, intestinal immunity, barrier immunity, nematode infection, acute bacterial infection, immune adaptation
MeSH terms
Animals, Enterobacteriaceae Infections, Immunity, Innate, Lymphocytes, Mice, Inbred C57BL, Mice, Mutant Strains, Vitamin A, Vitamin A Deficiency, Homeodomain Proteins, Interleukin-13, Micronutrients, Citrobacter rodentium, Mice, Adaptive Immunity

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