| First Author | Green EA | Year | 1998 |
| Journal | Immunity | Volume | 9 |
| Issue | 5 | Pages | 733-43 |
| PubMed ID | 9846494 | Mgi Jnum | J:51356 |
| Mgi Id | MGI:1315136 | Doi | 10.1016/s1074-7613(00)80670-6 |
| Citation | Green EA, et al. (1998) Local expression of TNFalpha in neonatal NOD mice promotes diabetes by enhancing presentation of islet antigens. Immunity 9(5):733-43 |
| abstractText | The relationship of inflammation to autoimmunity has been long observed, but the underlying mechanisms are unclear. Here, we demonstrate that islet-specific expression of TNFalpha in neonatal nonobese diabetic mice accelerated diabetes. In neonatal transgenic mice, disease was preceded by apoptosis of some beta cells, upregulation of MHC class I molecules on residual islet cells, and influx and activation of both antigen-presenting cells bearing MHC- islet peptide complexes and T cells. Infiltrating dendritic cells/macrophages, but not B cells, from neonatal islets activated islet-specific T cells in vitro. Thus, inflammation can trigger autoimmunity by recruiting and activating dendritic cells/macrophages to present self-antigens to autoreactive T cells. |
