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Modulation of mast cell proteinase‐activated receptor expression and IL‐4 release by IL‐12
Author(s) -
Zhang Huiyun,
Yang Xiaoyu,
Yang Haiwei,
Zhang Zhongfang,
Lin Qing,
Zheng Yanshan,
Chen Shaoying,
Yang Pingchang,
He Shaoheng
Publication year - 2007
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/sj.icb.7100085
Subject(s) - tryptase , mast cell , cytokine , protease activated receptor 2 , microbiology and biotechnology , downregulation and upregulation , chemistry , biology , receptor , immunology , biochemistry , enzyme linked receptor , gene
It has been recognized that protease‐activated receptors (PARs), interleukin (IL)‐4 and IL‐6 are involved in the pathogenesis of allergic diseases, and that IL‐12 plays a role in adaptive immune response. However, little is known of the effect of IL‐12 on protease‐induced cytokine release from mast cells. In the present study, we examined potential influence of IL‐12 on mast cell PAR expression and IL‐4 and IL‐6 release. The results showed that IL‐12 downregulated the expression of PAR‐2 and upregulated expression of PAR‐4 on P815 cells. It also downregulated expression of PAR‐2 mRNA, and upregulated expression of PAR‐1, PAR‐3 and PAR‐4 mRNAs. However, IL‐12 enhanced trypsin‐ and tryptase‐induced PAR‐2 and PAR‐2 mRNA expression. It was observed that IL‐12 induced release of IL‐4, but reduced trypsin‐ and tryptase‐stimulated IL‐4 secretion from P815 cells. PD98059, U0126 and LY294002 not only abolished IL‐12‐induced IL‐4 release but also inhibited IL‐12‐induced phosphorylation of extracellular signal‐regulated kinase and Akt. In conclusion, IL‐12 may serve as a regulator in keeping the balance of Th1 and Th2 cytokine production in allergic inflammation.