| First Author | Gu W | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 40398 | PubMed ID | 28094276 |
| Mgi Jnum | J:312654 | Mgi Id | MGI:6791792 |
| Doi | 10.1038/srep40398 | Citation | Gu W, et al. (2017) B7-H3 participates in the development of Asthma by augmentation of the inflammatory response independent of TLR2 pathway. Sci Rep 7:40398 |
| abstractText | 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. |
