Biased T-cell receptor usage is associated with allelic variation in the MHC class II peptide binding groove

Immunogenetics. 1999 Jun;49(6):532-40. doi: 10.1007/s002510050531.

Abstract

A comprehensive analysis was carried out of the tri-molecular complex of peptide, major histocompatibility class II molecule, and T-cell receptor (TcR) involved in the recognition of the promiscuous HA (306-318) peptide, restricted by one of two closely related HLA-DR alleles, HLA-DRB1*0101 and HLA-DRB1*0103. These two DR molecules differ by only three amino acids at positions 67, 70, and 71, in the third variable region of the DRB1 chain. None of the HA (306-318)-specific T-cell clones restricted by these two DR molecules tolerated amino acid substitution at the peptide-binding position 71, despite the fact that the substitution did not interfere with peptide binding. The majority of the DRB1*0103-restricted clones tolerated substitution of the amino acid at the TcR-contacting position 70, while the DRB1*0101-restricted T cells did not. Based usage of TRVA and TRVB segments was observed for the DRB1*0103-restricted clones; in contrast, apparently random usage was seen in the DRB1*0101-restricted T cells. Finally, limiting dilution analysis revealed a lower frequency of T cells reactive with the HA peptide in a DRB1*0103 compared with a DRB1*0101 individual. Taken together these data suggest that biased TcR gene usage may reflect a relatively low precursor frequency of T cells, and the need for clonal expansion of a limited set of high avidity T cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles*
  • Genetic Variation*
  • HLA-DR Antigens / immunology*
  • HLA-DRB1 Chains
  • Humans
  • Interleukin-2 / biosynthesis
  • Peptides / immunology
  • Receptors, Antigen, T-Cell, alpha-beta / genetics*
  • Receptors, Antigen, T-Cell, alpha-beta / immunology*
  • T-Lymphocytes / immunology*

Substances

  • HLA-DR Antigens
  • HLA-DRB1 Chains
  • Interleukin-2
  • Peptides
  • Receptors, Antigen, T-Cell, alpha-beta