| First Author | Nagashima O | Year | 2008 |
| Journal | J Immunol | Volume | 181 |
| Issue | 6 | Pages | 4062-71 |
| PubMed ID | 18768862 | Mgi Jnum | J:139095 |
| Mgi Id | MGI:3807317 | Doi | 10.4049/jimmunol.181.6.4062 |
| Citation | Nagashima O, et al. (2008) B7-h3 contributes to the development of pathogenic th2 cells in a murine model of asthma. J Immunol 181(6):4062-71 |
| abstractText | B7-H3 is a new member of the B7 family. The receptor for B7-H3 has not been identified, but it seems to be expressed on activated T cells. Initial studies have shown that B7-H3 provides a stimulatory signal to T cells. However, recent studies suggest a negative regulatory role for B7-H3 in T cell responses. Thus, the immunological function of B7-H3 is controversial and unclear. In this study, we investigated the effects of neutralizing anti-B7-H3 mAb in a mouse model of allergic asthma to determine whether B7-H3 contributes to the development of pathogenic Th2 cells and pulmonary inflammation. Administration of anti-B7-H3 mAb significantly reduced airway hyperreactivity with a concomitant decrease in eosinophils in the lung as compared with control IgG-treated mice. Treatment with anti-B7-H3 mAb also resulted in decreased production of Th2 cytokines (IL-4, IL-5, and IL-13) in the draining lymph node cells. Although blockade of B7-H3 during the induction phase abrogated the development of asthmatic responses, B7-H3 blockade during the effector phase did not inhibit asthmatic responses. These results indicated an important role for B7-H3 in the development of pathogenic Th2 cells during the induction phase in a murine model of asthma. |
