| First Author | Sprouse ML | Year | 2018 |
| Journal | J Immunol | Volume | 200 |
| Issue | 3 | Pages | 909-914 |
| PubMed ID | 29282307 | Mgi Jnum | J:257850 |
| Mgi Id | MGI:6112913 | Doi | 10.4049/jimmunol.1700156 |
| Citation | Sprouse ML, et al. (2018) Cutting Edge: Low-Affinity TCRs Support Regulatory T Cell Function in Autoimmunity. J Immunol 200(3):909-914 |
| abstractText | Regulatory T cells (Tregs) use a distinct TCR repertoire and are more self-reactive compared with conventional T cells. However, the extent to which TCR affinity regulates the function of self-reactive Tregs is largely unknown. In this study, we used a two-TCR model to assess the role of TCR affinity in Treg function during autoimmunity. We observed that high- and low-affinity Tregs were recruited to the pancreas and contributed to protection from autoimmune diabetes. Interestingly, high-affinity cells preferentially upregulated the TCR-dependent Treg functional mediators IL-10, TIGIT, GITR, and CTLA4, whereas low-affinity cells displayed increased transcripts for Areg and Ebi3, suggesting distinct functional profiles. The results of this study suggest mechanistically distinct and potentially nonredundant roles for high- and low-affinity Tregs in controlling autoimmunity. |
