| First Author | Khalil M | Year | 2001 |
| Journal | J Immunol | Volume | 166 |
| Issue | 3 | Pages | 1667-74 |
| PubMed ID | 11160209 | Mgi Jnum | J:67103 |
| Mgi Id | MGI:1929845 | Doi | 10.4049/jimmunol.166.3.1667 |
| Citation | Khalil M, et al. (2001) T cell studies in a peptide-induced model of systemic lupus erythematosus. J Immunol 166(3):1667-74 |
| abstractText | We have previously reported that immunization with a peptide mimetope of dsDNA on a branched polylysine backbone (DWEYSVWLSN-MAP) induces a systemic lupus erythematosus-like syndrome in the nonautoimmune BALB/c mouse strain. To understand the mechanism underlying this breakdown in self tolerance, we examined the role of T cells in the response. Our results show that the anti-foreign and anti-self response induced by immunization is T cell dependent and is mediated by I-E(d)-restricted CD4(+) T cells of the Th1 subset. In addition, generation of the critical T cell epitope requires processing by APCs and depends on the presence of both DWEYSVWLSN and the MAP backbone. The breakdown in self tolerance does not occur through cross-reactivity between the T cell epitope of DWEYSVWLSN-MAP and epitopes derived from nuclear Ags. In this induced-model of SLE, therefore, autoreactivity results from the activation of T cells specific for foreign Ag and of cross-reactive anti-foreign, anti-self B cells. Despite the fact that tissue injury is mediated by Ab, the critical initiating T cell response is Th1. |
