| First Author | Schuldt NJ | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 1 | Pages | 33-38 |
| PubMed ID | 28539428 | Mgi Jnum | J:250959 |
| Mgi Id | MGI:6099632 | Doi | 10.4049/jimmunol.1700406 |
| Citation | Schuldt NJ, et al. (2017) Cutting Edge: Dual TCRalpha Expression Poses an Autoimmune Hazard by Limiting Regulatory T Cell Generation. J Immunol 199(1):33-38 |
| abstractText | Despite accounting for 10-30% of the T cell population in mice and humans, the role of dual TCR-expressing T cells in immunity remains poorly understood. It has been hypothesized that dual TCR T cells pose an autoimmune hazard by allowing self-reactive TCRs to escape thymic selection. We revisited this hypothesis using the NOD murine model of type 1 diabetes. We bred NOD mice hemizygous at both TCRalpha and beta (TCRalpha(+/-) beta(+/-)) loci, rendering them incapable of producing dual TCR T cells. We found that the lack of dual TCRalpha expression skewed the insulin-specific thymocyte population toward greater regulatory T (Treg) cell commitment, resulting in a more tolerogenic Treg to conventional T cell ratio and protection from diabetes. These data support a novel hypothesis by which dual TCR expression can promote autoimmunity by limiting agonist selection of self-reactive thymocytes into the Treg cell lineage. |
