| First Author | Falcone M | Year | 2001 |
| Journal | Clin Immunol | Volume | 98 |
| Issue | 2 | Pages | 190-9 |
| PubMed ID | 11161975 | Mgi Jnum | J:127661 |
| Mgi Id | MGI:3764583 | Doi | 10.1006/clim.2000.4979 |
| Citation | Falcone M, et al. (2001) IL-4 triggers autoimmune diabetes by increasing self-antigen presentation within the pancreatic Islets. Clin Immunol 98(2):190-9 |
| abstractText | Several findings have recently questioned the long held hypothesis that cytokines belonging to the Th2 pathway are protective in T-cell-mediated autoimmunity. Among them, there is our previous report that pancreatic expression of IL-4 activated islet antigen-specific BDC2.5 T cells and rendered them able to trigger insulin-dependent diabetes mellitus in ins-IL-4/BDC2.5 mice (Mueller et al., Immunity, 7, 1997). Here we analyze the mechanisms underlying IL-4-mediated activation of the self-reactive BDC2.5 T cells. IL-4 is mainly known as the Th2-driving cytokine. However, IL-4 is also critical for DC maturation and upregulation of antigen uptake and presentation by macrophages. In our model, we found that pancreatic expression of IL-4 activated self-reactive BDC2.5 T cells by increasing islet antigen presentation by macrophages and dendritic cells. IL-4 could have triggered self-antigen presentation within the pancreatic islets both by driving maturation of DC from a tolerizing to a priming state and by increasing self-antigen uptake by macrophages. |
