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Autor(en) / Beteiligte
Titel
Human IL-31 is induced by IL-4 and promotes TH 2-driven inflammation
Ist Teil von
  • Journal of allergy and clinical immunology, 2013, Vol.132 (2), p.446-454.e5
Erscheinungsjahr
2013
Link zum Volltext
Quelle
Alma/SFX Local Collection
Beschreibungen/Notizen
  • Background The pruritic cytokine IL-31 has been shown to be expressed by murine activated effector T Lymphocytes of a TH 2 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 TH 2 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 TH 2 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 TH 2 clones and not by TH 1, TH 17, or TH 22. 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, TH 1 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 TH 1 clones. IL-31 was able to induce proinflammatory genes, such as CCL2 and granulocyte colony-stimulating factor. Conclusion IL-31 is not a TH 2 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.
Sprache
Englisch
Identifikatoren
ISSN: 0091-6749
eISSN: 1097-6825
DOI: 10.1016/j.jaci.2013.03.050
Titel-ID: cdi_elsevier_clinicalkeyesjournals_1_s2_0_S0091674913005964
Format
Schlagworte
Allergy and Immunology

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