| First Author | Gras S | Year | 2016 |
| Journal | Immunity | Volume | 45 |
| Issue | 4 | Pages | 749-760 |
| PubMed ID | 27717799 | Mgi Jnum | J:259203 |
| Mgi Id | MGI:6140347 | Doi | 10.1016/j.immuni.2016.09.007 |
| Citation | Gras S, et al. (2016) Reversed T Cell Receptor Docking on a Major Histocompatibility Class I Complex Limits Involvement in the Immune Response. Immunity 45(4):749-760 |
| abstractText | The anti-viral T cell response is drawn from the naive T cell repertoire. During influenza infection, the CD8(+) T cell response to an H-2D(b)-restricted nucleoprotein epitope (NP366) is characterized by preferential expansion of T cells bearing TRBV13(+) T cell receptors (TCRs) and avoidance of TRBV17(+) T cells, despite the latter dominating the naive precursor repertoire. We found two TRBV17(+) TCRs that bound H-2D(b)-NP366 with a 180 degrees reversed polarity compared to the canonical TCR-pMHC-I docking. The TRBV17 beta-chain dominated the interaction and, whereas the complementarity determining region-3 (CDR3) loops exclusively mediated contacts with the MHC-I, peptide specificity was attributable to germline-encoded recognition. Nevertheless, the TRBV17(+) TCR exhibited moderate affinity toward H-2D(b)-NP366 and was capable of signal transduction. Thus, the naive CD8(+) T cell pool can comprise TCRs adopting reversed pMHC-I docking modes that limit their involvement in the immune response. |
