| First Author | Smith SS | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 7 | Pages | 3897-905 |
| PubMed ID | 15778344 | Mgi Jnum | J:97982 |
| Mgi Id | MGI:3576843 | Doi | 10.4049/jimmunol.174.7.3897 |
| Citation | Smith SS, et al. (2005) Transgenic Ly-49A inhibits antigen-driven T cell activation and delays diabetes. J Immunol 174(7):3897-905 |
| abstractText | Activation of islet-specific T cells plays a significant role in the development of type 1 diabetes. In an effort to control T cell activation, we expressed the inhibitory receptor, Ly-49A, on islet-specific mouse CD4 cells. Ag-mediated activation of Ly-49A T cells was inhibited in vitro when the Ly-49A ligand, H-2D(d), was present on APCs. Ag-driven T cell proliferation, cytokine production, and changes in surface receptor expression were significantly reduced. Inhibition was also evident during secondary antigenic challenge. Addition of exogenous IL-2 did not rescue cells from inhibition, suggesting that Ly-49A engagement does not lead to T cell anergy. Importantly, in an adoptive transfer model, Ly-49A significantly delays the onset of diabetes. Together these results demonstrate that the inhibitory receptor Ly-49A effectively limits Ag-specific CD4 cell responses even in the presence of sustained autoantigen expression in vivo. |
