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Human IL-31 is induced by IL-4 and promotes TH2-driven inflammation.
J. Allergy Clin. Immunol. 132, 446-454 (2013)
BACKGROUND: The pruritic cytokine IL-31 has been shown to be expressed by murine activated effector T Lymphocytes of a TH2 phenotype. Like IL-17 and IL-22, IL-31 is a tissue-signaling cytokine the receptor of which is mainly found on nonimmune cells. An overabundance of IL-31 has been shown in patients with atopic disorders, including dermatitis, as well as asthma, and therefore represents a promising drug target, although its regulation in the context of the human TH2 clusters is not yet known. OBJECTIVE: We sought to address the gene regulation of human IL-31 and to test whether IL-31 possesses a similar proallergic function as members of the human TH2 cytokine family, such as IL-4, IL-5, and IL-13. METHODS: Polyclonal and purified protein derivative of tuburculin-specific T-cell clones were generated. TH phenotype was determined, and IL-31 was measured by means of ELISA. Gene expression of primary bronchial epithelial cells treated with IL-31 was also measured. RESULTS: IL-31 was expressed by all of the TH2 clones and not by TH1, TH17, or TH22. This expression was dependent on autocrine IL-4 expression from these clones because it could be reduced if blocking antibodies to IL-4 were present. Interestingly, TH1 clones were able to express IL-31 if IL-4 was added to culture. This IL-31 expression was transient and did not affect the phenotype of the TH1 clones. IL-31 was able to induce proinflammatory genes, such as CCL2 and granulocyte colony-stimulating factor. CONCLUSION: IL-31 is not a TH2 cytokine in the classical sense but is likely to be expressed by a number of cells in an allergic situation in which IL-4 is present and possibly contribute to the allergic reaction.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Allergic Airway Inflammation ; T(h)2 Cells ; Il-31 ; Il-4 ; Normal Human Bronchial Epithelial Cells ; Il-33 ; Chromatin Immunoprecipitation; T-cells ; Expression Patterns ; Epithelial-cells ; Human Genome ; Cytokine ; Interleukin-31 ; Protein ; Helper ; Activation ; Allergen
ISSN (print) / ISBN 0091-6749
Zeitschrift The journal of allergy and clinical immunology
Quellenangaben Band: 132, Heft: 2, Seiten: 446-454
Verlagsort Amsterdam [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Allergy Research (IAF)