Degenerate TCR recognition and dual DR2 restriction of autoreactive T cells: implications for the initiation of the autoimmune response in multiple sclerosis

Eur J Immunol. 2008 May;38(5):1297-309. doi: 10.1002/eji.200737519.

Abstract

TCR degeneracy may facilitate self-reactive T cell activation and the initiation of an autoimmune response in multiple sclerosis (MS). MHC class II alleles of the DR2 haplotype DR2a (DRB5*0101) and DR2b (DRB1*1501) are associated with an increased risk for MS in Caucasian populations. In order to selectively expand and characterize T cells with a high degree of TCR degeneracy that recognize peptides in the context of disease-associated DR2 alleles, we developed DR2-anchored peptide mixtures (APM). We report here that DR2-APM have a high stimulatory potency and can selectively expand T cells with a degenerate TCR (TCR(deg)). Due to the low concentration of individual peptides in the mixtures, T cell clones' proliferative response to DR2-APM implies that multiple peptides stimulate the TCR, which is a characteristic of TCR(deg). The frequency of DR2-APM-reactive T cells is significantly higher in MS patients than in healthy controls, suggesting that they may play a role in the development of the autoimmune response in MS. DR2-APM-reactive cells have a dual DR2 restriction: they recognize DR2-APM in the context of both DR2a and DR2b molecules. The DR2-APM-reactive cells' IL-17 secretion, together with cross-reactivity against myelin peptides, may contribute to their role in the development of autoimmune response in MS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Amino Acid Sequence
  • Autoimmunity / immunology*
  • Clone Cells / immunology
  • Epitopes, T-Lymphocyte / immunology
  • HLA-DR2 Antigen / immunology*
  • Humans
  • Interferon-gamma / metabolism
  • Interleukin-17 / metabolism
  • Interleukin-4 / metabolism
  • Leukocytes, Mononuclear / immunology
  • Lymphocyte Activation / immunology
  • Middle Aged
  • Multiple Sclerosis, Relapsing-Remitting / immunology*
  • Myelin Basic Protein / immunology
  • Myelin Proteins
  • Myelin Proteolipid Protein / immunology
  • Myelin-Associated Glycoprotein / immunology
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments / immunology
  • Peptides / immunology
  • Receptors, Antigen, T-Cell / immunology*
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism

Substances

  • Epitopes, T-Lymphocyte
  • HLA-DR2 Antigen
  • Interleukin-17
  • MOG protein, human
  • Myelin Basic Protein
  • Myelin Proteins
  • Myelin Proteolipid Protein
  • Myelin-Associated Glycoprotein
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments
  • Peptides
  • Receptors, Antigen, T-Cell
  • Interleukin-4
  • Interferon-gamma