| First Author | Stephens LA | Year | 2005 |
| Journal | Proc Natl Acad Sci U S A | Volume | 102 |
| Issue | 48 | Pages | 17418-23 |
| PubMed ID | 16287973 | Mgi Jnum | J:104376 |
| Mgi Id | MGI:3611725 | Doi | 10.1073/pnas.0507454102 |
| Citation | Stephens LA, et al. (2005) CD4+CD25+ regulatory T cells limit the risk of autoimmune disease arising from T cell receptor crossreactivity. Proc Natl Acad Sci U S A 102(48):17418-23 |
| abstractText | The molecular-mimicry theory proposes that immune crossreactivity between microbial and self-antigen is the initiating event in the activation of autoaggressive immune responses leading to autoimmune disease. In support of this possibility, it is now accepted that T cell recognition of antigen is highly degenerate. However, it is to be expected that the immune system would have evolved mechanisms to counter such a potential danger. We studied the influence of CD4(+)CD25(+) regulatory T cells (Treg) on the ability of suboptimal T cell receptor ligands to provoke autoimmunity. By using CD4(+) T cell-driven experimental autoimmune encephalomyelitis as a model, it was found that depletion of CD4(+)CD25(+)Foxp3(+) Treg allowed pathology to develop in response to suboptimal T cell stimulation. These data demonstrate the importance of Treg in raising the threshold of triggering of autoreactive T cell responses, thus limiting the risk of autoimmune disease due to molecular mimicry. |
