Comparison of peptide and superantigen-induced anergy in a peptide-specific polyclonal human T cell line

• Published in: International immunology 1995-07, Vol.7 (7), p.1057-1063
• Main Authors: Chu, N. Randall, Quaratino, Sonia, Feldmann, Marc, Londei, Marco
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; autoimmunity; Bacterial Toxins; Base Sequence; Cell Line; Clonal Anergy; Clostridium tetani; Dose-Response Relationship, Immunologic; Enterotoxins - immunology; Epitopes; Humans; Immune Tolerance; Lymphocyte Activation; Molecular Sequence Data; Peptide Fragments - immunology; Peptide Fragments - pharmacology; Receptor-CD3 Complex, Antigen, T-Cell - immunology; Staphylococcus aureus - immunology; superantigen; Superantigens - pharmacology; T-Lymphocytes - immunology; Tetanus Toxin - immunology; tolerance
• ISSN: 0953-8178; 1460-2377
• DOI: 10.1093/intimm/7.7.1057

T cells recognizing tetanus toxin peptide ‘p2’ (sequence 830–844) raised in HLA DR6 individuals preferentially express Vβ2 in the TCR. A p2-specific T cell line (60% Vβ2+) was used to compare peptide and superantigen [toxic shock syndrome toxin-1 (TSST-1)]-induced clonal anergy. Many experiments consistently revealed that the degree of ‘tolerance’ or ‘clonal anergy’ induced by peptide was greater than with the superantigen TSST-1. These results are of interest in a number of contexts. First they suggest that using superantigens or anti-Vβ to delete the majority population of T cells may not be sufficient to diminish an autoimmune response. Secondly, the results indicate that induction of anergy of a large proportion of peptide-specific T cells does not lead to a suppressive bystander effect on the remaining responsive T cells. These results emphasize the need to define the dominant autoantigenic epitopes in human autoimmune diseases, since peptide based therapy such as the use of peptide analogues to induce anergy or a change in cytokine profile, is possibly more effective in controlling undesired immune responses than the use of non-antigen, TCR-directed approaches such as superantigens.