| First Author | King C | Year | 1998 |
| Journal | Immunity | Volume | 8 |
| Issue | 5 | Pages | 601-13 |
| PubMed ID | 9620681 | Mgi Jnum | J:136448 |
| Mgi Id | MGI:3796323 | Doi | 10.1016/s1074-7613(00)80565-8 |
| Citation | King C, et al. (1998) TGF-beta1 alters APC preference, polarizing islet antigen responses toward a Th2 phenotype. Immunity 8(5):601-13 |
| abstractText | TGF-beta1, expressed in the pancreatic islets, protects the nonobese diabetic (NOD) mouse from insulin-dependent diabetes mellitus (IDDM). The islet antigen-specific T cell response of ins-TGF-beta1 mice relied on different antigen-presenting cells (APC) from those used by NOD T cells. T cells from NOD mice utilized B cells to present islet antigen, whereas T cells from ins-TGF-beta1 mice utilized macrophages. In addition, the islet antigen-specific T cell repertoire of ins-TGF-beta1 mice was distinct and deviated toward an IL-4-producing Th2 phenotype. When ins-TGF-beta1 mice were treated with anti-iL-4 antibody, islet antigen-specific IFNGamma-producing Th1 cells were unleashed, and the incidence of diabetes increased to the level of NOD mice. This suggests active suppression of a diabetogenic T cell response. This study describes a novel mechanism in which expression of TGF-beta1 in the context of self-antigen shifts APC preference, deviating T cell responses to a Th2 phenotype, preventing IDDM. |
