| First Author | Okazaki T | Year | 2001 |
| Journal | J Immunol | Volume | 167 |
| Issue | 4 | Pages | 1977-81 |
| PubMed ID | 11489978 | Mgi Jnum | J:120414 |
| Mgi Id | MGI:3706496 | Doi | 10.4049/jimmunol.167.4.1977 |
| Citation | Okazaki T, et al. (2001) Impairment of bleomycin-induced lung fibrosis in CD28-deficient mice. J Immunol 167(4):1977-81 |
| abstractText | Lung fibrosis is an important pulmonary disease with a high mortality rate, but its pathophysiological mechanism has not been fully clarified. Various types of cells have been implicated in the development of lung fibrosis, including T cells. However, the contribution of functional molecules expressed on T cells to the development of lung fibrosis remains largely unknown. In this study, we determined whether costimulation via CD28 on T cells was crucial for the development of lung fibrosis by intratracheally administering bleomycin into CD28-deficient mice. Compared with wild-type mice, the CD28-deficient mice showed markedly impaired lung fibrosis after injection with low doses of bleomycin, as judged by histological changes and hydroxyproline content in the lungs. In addition, bleomycin-induced T cell infiltration into the airways and production of several cytokines and chemokines including IL-5 were also impaired in the CD28-deficient mice. Furthermore, adoptive transfer of CD28-positive T cells from wild-type mice recovered the impaired bleomycin-induced lung fibrosis in CD28-deficient mice. These findings suggest that the CD28-mediated T cell costimulation plays a critical role in the development of lung fibrosis, possibly by regulating the production of cytokines and chemokines in the lung. Thus, manipulation of the CD28-mediated costimulation could be a potential therapeutic strategy for the prevention of lung fibrosis. |
