| First Author | Amrani A | Year | 2002 |
| Journal | Immunity | Volume | 16 |
| Issue | 5 | Pages | 719-32 |
| PubMed ID | 12049723 | Mgi Jnum | J:76802 |
| Mgi Id | MGI:2180294 | Doi | 10.1016/s1074-7613(02)00315-1 |
| Citation | Amrani A, et al. (2002) CD154-dependent priming of diabetogenic CD4(+) T cells dissociated from activation of antigen-presenting cells. Immunity 16(5):719-32 |
| abstractText | We followed the fate of K(d)- or I-A(g7)-restricted beta cell-autoreactive T cells in monoclonal TCR-transgenic NOD mice expressing or lacking CD154. 8.3-NOD.RAG-2(-/-)/CD154(-/-) mice, which bear autoreactive CD8(+) T cells, developed diabetes with the same incidence and tempo as 8.3-NOD.RAG-2(-/-)/CD154(+) mice. Recruitment of CD154(-/-) 8.3-CD8(+) CTL was accelerated by CD154(+)CD4(+) T cells, by expression of a B7.1 transgene in beta cells or by treatment of the mice with CpG-DNA or an agonistic anti-CD40 antibody. In contrast, the autoreactive CD4(+) T cells maturing in 4.1-NOD.RAG-2(-/-) mice lost their diabetogenic potential if they lacked CD154, even in the presence of CD154(+)CD4(+) T cells, B7.1 molecules on beta cells, CpG-DNA treatment, or systemic CD40 ligation. These results demonstrate the existence of a novel, CD154-dependent pathway of CD4(+) T cell activation that is independent of CD40-mediated activation of APCs. |
