ArticleThe Journal of allergy and clinical immunology2016
IL-4 production by group 2 innate lymphoid cells promotes food allergy by blocking regulatory T-cell function.
Article in The Journal of allergy and clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.
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Who cites it
142 citing papers in PubMed, 246 citations in OpenAlex.
- Interleukin-4-producing type 2 innate lymphoid cells in the lymph node promote proallergic Tfh13 cell differentiation.Immunity · 2026Article
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- A Case for Anti-IgE Vaccination.Allergy · 2026Review
- Type 2 conventional dendritic cells and regulatory T cells form a barrier tissue circuit to control allergic inflammation.bioRxiv : the preprint server for biology · 2026Article
- Mouse Models of Food Allergies: Where Do They Take Us?Clinical reviews in allergy & immunology · 2026Review
- Bioengineering Interventions to Enhance the Capacity of the Gut Microbiota in Controlling Food Allergies.Life (Basel, Switzerland) · 2026Review
- Early Combination Antiretroviral Therapy Initiation During Primary HIV Infection Restricts HIV Reservoirs and Gut-Driven Inflammation but Fails to Rewire the Systemic Cytokine Landscape.Open forum infectious diseases · 2026Article
- Modulating the Allergen-Specific Immune Response to Achieve Remission of Food Allergy Through Oral Immunotherapy.Advances in experimental medicine and biology · 2026Review
- The shifting balance: innate lymphoid cell plasticity in chronic gut diseases.Frontiers in immunology · 2026Review
- Context-dependent roles of the gut microbiome in food allergy tolerance versus sensitization.Gut microbes · 2025Review
- Gut mucosal immune responses - Implications for celiac disease and food allergy.Seminars in immunology · 2025Review
- Article
- S. aureus exposure during cutaneous antigen sensitization causes basophil- and interleukin-4-dependent exaggerated food anaphylaxis.Immunity · 2025Article
- Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.Journal of inflammation (London, England) · 2025Review
- Skin damage signals mediate allergic sensitization to spatially unlinked antigen.Science immunology · 2025Article
- A Phenotypically Distinct Human Th2 Cell Subpopulation Is Associated With Development of Allergic Disorders in Infancy.Allergy · 2025Article
- Interleukin-4 and Atopic Dermatitis: Why Does it Matter? A Narrative Review.Dermatology and therapy · 2025Review
- The Etiology of IgE-Mediated Food Allergy: Potential Therapeutics and Challenges.International journal of molecular sciences · 2025Review
- Rocaglamide Suppresses Allergic Reactions by Regulating IL-4 Receptor Signaling.Molecules (Basel, Switzerland) · 2025Article
- Review
82 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundFood allergy is a major health issue, but its pathogenesis remains obscure. Group 2 innate lymphoid cells (ILC2s) promote allergic inflammation. However their role in food allergy is largely unknown.
objectiveWe sought to investigate the role of ILC2s in food allergy.
methodsFood allergy-prone mice with a gain-of-function mutation in the IL-4 receptor α chain (Il4raF709) were orally sensitized with food allergens, and the ILC2 compartment was analyzed. The requirement for ILC2s in food allergy was investigated by using Il4raF709, IL-33 receptor-deficient (Il1rl1(-/-)), IL-13-deficient (Il13(-/-)), and IL-4-deficient (Il4(-/-)) mice and by adoptive transfer of in vitro-expanded ILC2s. Direct effects of ILC2s on regulatory T (Treg) cells and mast cells were analyzed in coculture experiments. Treg cell control of ILC2s was assessed in vitro and in vivo.
resultsIl4raF709 mice with food allergy exhibit increased numbers of ILC2s. IL-4 secretion by ILC2s contributes to the allergic response by reducing allergen-specific Treg cell and activating mast cell counts. IL-33 receptor deficiency in Il4raF709 Il1rl1(-/-) mice protects against allergen sensitization and anaphylaxis while reducing ILC2 induction. Adoptive transfer of wild-type and Il13(-/-) but not Il4(-/-) ILC2s restored sensitization in Il4raF709 Il1rl1(-/-) mice. Treg cells suppress ILC2s in vitro and in vivo.
conclusionIL-4 production by IL-33-stimulated ILC2s blocks the generation of allergen-specific Treg cells and favors food allergy. Strategies to block ILC2 activation or the IL-33/IL-33 receptor pathway can lead to innovative therapies in the treatment of food allergy.
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