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TNF-α enhance Th2 and Th17 immune responses regulating by IL23 during sensitization in asthma model.
- Source :
-
Cytokine . Mar2016, Vol. 79, p23-30. 8p. - Publication Year :
- 2016
-
Abstract
- Background TNF-α has been postulated to be a critical mediator contributing to airway inflammation. The purpose of this study was to evaluate the role of TNF-α in the induction of Th17 and Th2 cells related to asthma pathogenesis. Objective To evaluate detailed mechanisms for the modulation of IL-23 by TNF-α in sensitization period. Methods During sensitization period, 10 μg of rat anti-mouse TNF-α mAb was intravenously administrated one hour before the application of OVA and 0.1 μg of LPS. To see the relation between TNF-α and associated effectors cytokine, we replenished TNF-α KO mice with IL-23 during sensitization period. To assess cellular resources, CD11c+ cells isolated from lung tissue after sensitization were treated with anti-TNF-α Ab. Results Treatment of anti-TNF-α mAb during sensitization period significantly reduced airway eosinophilia, serum OVA-specific IgE levels and methacholine AHR compared to isotype Ab. Anti-TNF-α mAb treated mice showed significant reduction in the levels of IL-23 after sensitization in bronchoalveolar lavage fluid (BALF) as well as IL-17A, IL-4 levels in BALF after challenge compared with isotype Ab treated mice. Supplementation of IL-23 in TNF-α KO mice resulted in complete restoration of eosinophilic airway inflammation, AHR, and IL-17A and IL-4 expression in CD4+ T cells. Anti-TNF-α mAb treatment after sensitization significantly diminished the population of IL-23p19-secreting CD11c+ cells in lung. Conclusion TNF-α plays an important role in the development of airway inflammation by enhancing IL-23/Th17 and Th2 immune responses. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10434666
- Volume :
- 79
- Database :
- Academic Search Index
- Journal :
- Cytokine
- Publication Type :
- Academic Journal
- Accession number :
- 112630527
- Full Text :
- https://doi.org/10.1016/j.cyto.2015.12.001