Journal
IMMUNITY
Volume 45, Issue 4, Pages 749-760Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.09.007
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Funding
- Australian National Health and Medical Research Council (NHMRC)
- Australian Research Council (ARC)
- University of Melbourne Faculty Research Scholarship
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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.
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