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  • Title: Differential activation of human autoreactive T cell clones by altered peptide ligands derived from myelin basic protein peptide (87-99).
    Author: Vergelli M, Hemmer B, Utz U, Vogt A, Kalbus M, Tranquill L, Conlon P, Ling N, Steinman L, McFarland HF, Martin R.
    Journal: Eur J Immunol; 1996 Nov; 26(11):2624-34. PubMed ID: 8921948.
    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.
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