| First Author | Lenschow DJ | Year | 1996 |
| Journal | Immunity | Volume | 5 |
| Issue | 3 | Pages | 285-93 |
| PubMed ID | 8808683 | Mgi Jnum | J:35353 |
| Mgi Id | MGI:82802 | Doi | 10.1016/s1074-7613(00)80323-4 |
| Citation | Lenschow DJ, et al. (1996) CD28/B7 regulation of Th1 and Th2 subsets in the development of autoimmune diabetes. Immunity 5(3):285-93 |
| abstractText | CD28 ligation delivers a costimulatory signal important in T cell activation. This study demonstrates that the disruption of the CD28/B7 pathway early in the nonobese diabetic mouse strain, using CD28-/- and CTLA41g transgenic mice, promoted the development and progression of spontaneous autoimmune diabetes. Functional analyses of T cells isolated from CD28-deficient mice demonstrated that the GAD-specific T cells produced enhanced Th1-type cytokines (IL-2 and IFN gamma) and diminished Th2-type cytokine, IL-4. Moreover, there was a significant decrease in serum levels of anti-GAD antibodies of the IgG1 isotype consistent with a profound suppression of Th2-type responses in these animals. Thus, the early differentiation of naive diabetogenic T cells into the Th2 subset is dependent upon CD28 signaling and extends our understanding of the importance of Th1/Th2 balance in the regulation of this spontaneous autoimmune disease. |
