An important role of tumor necrosis factor receptor-2 on natural killer T cells on the development of dsRNA-enhanced Th2 cell response to inhaled allergens.
SCIE
SCOPUS
- Title
- An important role of tumor necrosis factor receptor-2 on natural killer T cells on the development of dsRNA-enhanced Th2 cell response to inhaled allergens.
- Authors
- Choi, JP; Kim, YM; Choi, HI; Choi, SJ; Park, HT; Lee, WH; Gho, YS; Jee, YK; Jeon, SG; Kim, YK
- Date Issued
- 2014-02
- Publisher
- John Wiley & Sons, Inc.
- Abstract
- BackgroundRecent evidence indicates that TNF- is a key mediator of the development of dsRNA-enhanced Th2 cell response to inhaled allergens. Natural killer T (NKT) cells may be a candidate source of Th2-polarizing cytokines. ObjectiveThe objective of this study was to evaluate the role of lung NKT cells on the development of TNF--mediated Th2 cell response. MethodsA virus-associated asthma mouse model was generated by the administration of ovalbumin (OVA, 75g) and poly[I:C] (0.1g). Role of NKT and type I NKT cells was evaluated using CD1d- and J18-deficient mice. TNF- receptors (TNFRs) were antagonized by using TNFR blocking peptides. ResultsThe number of infiltrated NKT cells was increased in a virus-associated asthma mouse model. Increase in Th2 and Th17 cytokine levels in wild-type mice were abolished in both CD1d- and J18-deficient mice. In vitro co-culture experiments with alveolar macrophages and NKT cells showed that TNF- produced by macrophages in the presence of poly[I:C] acts on NKT cells, inducing production of Th2-polarizing cytokines. Moreover, the induction of Th2-polarizing cytokines by poly[I:C] or recombinant TNF- was impaired in both CD1d- and J18-deficient mice and that the above effect was reversed by a TNF- receptor-2 (TNFR2) blocking peptide, but not by a TNFR1 blocker. ConclusionsThese findings suggest that NKT cells play a key role in the development of Th2 cell response to inhaled allergens and that TNF- produced by alveolar macrophages induces Th2 cell response, via TNFR2 on NKT cells.
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/13890
- DOI
- 10.1111/ALL.12301
- ISSN
- 0105-4538
- Article Type
- Article
- Citation
- Allergy, vol. 69, no. 2, page. 186 - 198, 2014-02
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