| First Author | Lamhamedi-Cherradi SE | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 9 | Pages | 4886-92 |
| PubMed ID | 14568969 | Mgi Jnum | J:118907 |
| Mgi Id | MGI:3700626 | Doi | 10.4049/jimmunol.171.9.4886 |
| Citation | Lamhamedi-Cherradi SE, et al. (2003) Transcriptional regulation of type I diabetes by NF-kappa B. J Immunol 171(9):4886-92 |
| abstractText | Development of type I diabetes requires coordinated expression of myriad genes responsible for the initiation and progression of the disease. Expression of these genes are regulated by a small number of transcription factors including the Rel/NF-kappaB family. To determine the roles of the Rel/NF-kappaB family in type I diabetes, we studied multiple low-dose streptozotocin-induced diabetes in mice deficient in either c-Rel or NF-kappaB1. We found that mice deficient in each of these NF-kappaB subunits were resistant to streptozotocin-induced diabetes. However, the mechanisms of the disease resistance may differ in different cases. Deficiency in c-Rel selectively reduced Th1, but not Th2 responses, whereas NF-kappaB1 deficiency had little effect on T cell responses to anti-CD3 stimulation. Death of dendritic cells was accelerated in the absence of NF-kappaB1, whereas death of macrophages and granulocytes was affected primarily by c-Rel deficiency. Furthermore, Stat-1 expression was significantly reduced in macrophages deficient in NF-kappaB1, but not c-Rel. These results indicate that both c-Rel and NF-kappaB1are essential for the development of type I diabetes and that strategies targeting each of these subunits would be effective in preventing the disease. |
