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Differential activation of human autoreactive T cell clones by altered peptide ligands derived from myelin basic protein peptide (87-99) EUROPEAN JOURNAL OF IMMUNOLOGY Vergelli, M., Hemmer, B., Utz, U., Vogt, A., Kalbus, M., Tranquill, L., Conlon, P., Ling, N., Steinman, L., McFarland, H. F., Martin, R. 1996; 26 (11): 2624-2634

Abstract

We have examined the functional consequences induced by interaction of DR2a-restricted myelin basic protein (MBP) (87-99)-specific T cell clones (TCC) with altered peptide ligands (APL) derived from MBP peptide (87-99). The immunodominant MBP peptide (87-99) has been implicated as a candidate antigen in multiple sclerosis (MS) by several lines of evidence. In the present study, we have defined the T cell receptor (TCR) contact residues for DR2a-restricted, (87-99)-specific T helper type 1 T cells to design APL suitable to modify the functions of such T cells potentially relevant for the pathogenesis of MS. We show that neutral (L-alanine substitutions) or conservative exchanges of the primary and secondary TCR contact residues lead to various alterations of T cell function, ranging from differences in interleukin-2 receptor up-regulation to anergy induction and TCR antagonism. The potential usefulness of APL as an immunomodulating therapy for DR2+ MS patients is discussed.

View details for Web of Science ID A1996VT77500012

View details for PubMedID 8921948