B7-H3 participates in the development of Asthma by augmentation of the inflammatory response independent of TLR2 pathway.
B7-H3 participates in the development of Asthma by augmentation of the inflammatory response independent of TLR2 pathway.
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B7-H3 通过增强独立于 TLR2 通路的炎症反应参与哮喘的发展
DOI：
10.1038/srep40398
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发表时间：
2017-01-17
影响因子：
4.6
通讯作者：
Ji W
中科院分区：
文献类型：
--
作者：
Gu W;Zhang X;Yan Y;Wang Y;Huang L;Wang M;Shao X;Chen Z;Ji W
B7-H3是B7超家族的一个新成员，同时作为T细胞共刺激因子和共抑制因子。最近的研究发现B7-H3在哮喘的发展中起着关键作用。但确切的机制尚不清楚。在这项研究中，我们进一步报告说，B7-H3参与的发展，卵蛋白诱导的哮喘小鼠模型。并通过体内外实验研究其作用机制。B7-H3的外源性给药在体外和体内强烈放大了炎症反应并增强了促炎细胞因子。这些B7-H3相关的促炎作用不依赖于TLR 2信号传导，因为在给予重组小鼠B7-H3后，TLR 2缺陷小鼠中的气道炎症、嗜酸性粒细胞浸润和细胞因子（IL-4、IL-5、IL-13和IFN-γ）增加仍然被放大。这些结果表明B7-H3在哮喘小鼠模型中Th 1和Th 2细胞的发育中起重要作用，并且其促炎作用不依赖于TLR 2信号传导。
B7-H3, a new member of the B7 superfamily, acts as both a T cell costimulator and coinhibitor. Recent studies identified B7-H3 plays a critical role in the development of asthma. But the definitive mechanism is not clear. In this study, we further report that B7-H3 participates in the development of OVA-induced asthma in a murine model. And study its mechanism through the vitro and vivo experiment. Exogenous administration of B7-H3 strongly amplified the inflammatory response and augmented proinflammatory cytokines in vitro and vivo. These B7-H3–associated proinflammatory effects were not dependent on TLR2 signaling, as airway inflammation, eosinophils infiltration and cytokins (IL-4, IL-5, IL-13 and IFN-gamma) augment were still amplified in TLR2-deficient mice after administrated recombinant mouse B7-H3. These results indicated an important role for B7-H3 in the development of Th1 and Th2 cells in a murine model of asthma and its proinflammatory effects are not dependent on TLR2 signaling.