期刊论文详细信息
BMC Immunology
All-trans retinoic acid attenuates airway inflammation by inhibiting Th2 and Th17 response in experimental allergic asthma
Zhenwei Xia1  Wenwei Zhong1  Qi Liu1  Yanjie Zhang1  Jinhong Wu1 
[1] Department of Pediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Ruijin 2nd Road 197, Shanghai 200025, China
关键词: Regulatory T cells;    Th17;    Th2;    All-trans retinoic acid;    Asthma;   
Others  :  1077782
DOI  :  10.1186/1471-2172-14-28
 received in 2012-12-18, accepted in 2013-06-18,  发布年份 2013
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【 摘 要 】

Background

Airway inflammation is mainly mediated by T helper 2 cells (Th2) that characteristically produce interleukin (IL)-4, IL-5, and IL-13. Epidemiological studies have revealed an inverse association between the dietary intake of vitamin A and the occurrence of asthma. Serum vitamin A concentrations are significantly lower in asthmatic subjects than in healthy control subjects. It has been reported that all-trans retinoic acid (ATRA), a potent derivative of vitamin A, regulates immune responses. However, its role in Th2-mediated airway inflammation remains unclear. We investigated the effects of ATRA in a mouse model of allergic airway inflammation.

Results

We found that ATRA treatment attenuated airway inflammation and decreased mRNA levels of Th2- and Th17-related transcription factors. The data showed that airway inflammation coincided with levels of Th2- and Th17-related cytokines. We also showed that ATRA inhibited Th17 and promoted inducible regulatory T-cell differentiation, whereas it did not induce an obvious effect on Th2 differentiation in vitro. Our data suggest that ATRA may interfere with the in vivo Th2 responses via T-cell extrinsic mechanisms.

Conclusions

Administration of ATRA dramatically attenuated airway inflammation by inhibiting Th2 and Th17 differentiation and/or functions. ATRA may have potential therapeutic effects for airway inflammation in asthmatic patients.

【 授权许可】

   
2013 Wu et al.; licensee BioMed Central Ltd.

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