| First Author | Chapoval SP | Year | 2003 |
| Journal | Clin Immunol | Volume | 106 |
| Issue | 2 | Pages | 83-94 |
| PubMed ID | 12672399 | Mgi Jnum | J:82789 |
| Mgi Id | MGI:2655035 | Doi | 10.1016/s1521-6616(03)00002-0 |
| Citation | Chapoval SP, et al. (2003) CD28 costimulation is critical for experimental allergic asthma in HLA-DQ8 transgenic mice. Clin Immunol 106(2):83-94 |
| abstractText | The objective of this study was to investigate the contribution of the CD28 costimulatory molecules to allergen-induced primary and chronic inflammatory responses. To this end, we have developed and characterized a short ragweed allergen-induced asthma model involving sensitization of HLA-DQ transgenic mice followed by intranasal challenge with allergen. Forty-eight hours after primary challenge, sensitized DQ8 mice developed pulmonary eosinophilic inflammation, airway hyperreactivity, Th2 cytokines, and IgE/IgG1 Ab. This allergic inflammatory response was absent in H-2Abeta(0) and DQ8/CD28(0) mice. Secondary rechallenge with allergen 4 weeks later induced even greater inflammatory changes in the airways of DQ8 mice with eosinophils being the predominant inflammatory cells while only pulmonary lymphocytosis was observed in DQ8/CD28(0) mice. No inflammation was detected in H-2Abeta(0) mice. Proliferation and cytokine profile studies demonstrated that CD28 regulates T-cell activation and effector function. Therefore, CD28 is essential for the extrinsic asthma and can be a target for immunotherapy. |
