ArticleAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology2017
Regulation of Th2 responses by different cell types expressing the interleukin-31 receptor.
Article in Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- IL-31: State of the Art for an Inflammation-Oriented Interleukin.International journal of molecular sciences · 2022Pooled it
- A Hot-Spring Water Improves Inflammatory Conditions in an Injury-Induced Atopic Dermatitis Mouse Model by Regulating Skin Barrier Function.Biomedicines · 2025Article
- Analyzing the Antinociceptive Effect of Interleukin-31 in Mice.International journal of molecular sciences · 2023Article
- Interleukin-31 Receptor A Expression in the Dorsal Root Ganglion of Mice with Atopic Dermatitis.International journal of molecular sciences · 2023Article
- Genetic association of IL2RA, IL17RA, IL23R, and IL31RA single nucleotide polymorphisms with alopecia areata.Saudi journal of biological sciences · 2022Article
- Comparative Transcriptomics of IBD Patients Indicates Induction of Type 2 Immunity Irrespective of the Disease Ideotype.Frontiers in medicine · 2021Article
- IL-31 plays dual roles in lung inflammation in an OVA-induced murine asthma model.Biology open · 2019Article
- Bleomycin Aggravates Atopic Dermatitis via Lung Inflammation in 2,4-Dinitrochlorobenzene-Induced NC/Nga Mice.Frontiers in pharmacology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin-31 (IL-31) is a recently identified cytokine produced by Th2 cells that is involved in the development of atopic dermatitis-induced skin inflammation and pruritus. Its receptor, IL-31RA, is expressed by a number of cell types, including epithelial cells, eosinophils, and activated monocytes and macrophages. To date, however, the regulation of Th2 responses by distinct cell types and tissues expressing IL-31RA has not been well studied.
methodsIn this study, Cry j 2, one of the major allergens of Japanese cedar pollen, was administered to IL-31RA-deficient or wild-type (WT) mice via nasal or intraperitoneal injection for induction of specific Th2 responses.
resultsAfter nasal administration of Cry j 2, IL-31RA-deficient mice showed lower Cry j 2-specific CD4+ T cell proliferation, Th2 cytokine (IL-5 and IL-13) production, and Th2-mediated (IgE, IgG1, and IgG2b) antibody responses than WT mice. In contrast, IL-31RA-deficient mice administered Cry j 2 intraperitoneally showed stronger Th2 immune responses than WT mice.
conclusionsThese results indicate that IL-31R signaling positively regulates Th2 responses induced by nasal administration of Cry j 2, but negatively regulates these responses when Cry j 2 is administered intraperitoneally. Collectively, these data indicate that the induction of antigen-specific Th2 immune responses might depend on tissue-specific cell types expressing IL-31RA.
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