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Fas/Fas Ligand Pathway, Apoptosis, and Clonal Anergy Involved in Systemic Acetylcholine Receptor T Cell Epitope Tolerance¹

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555

The cellular mechanisms of high dose systemic acetylcholine receptor (AChR) T cell epitope, 146–162 peptide-induced tolerance in experimental myasthenia gravis were examined. CD4 cells are the prime target for 146–162 peptide-induced tolerance. The expression of CD69, Fas, and B7.2 molecules on AChR-immune lymphocytes was enhanced within 4–12 h after tolerance induction. A high dose of 146–162 peptide in IFA failed to suppress T cell proliferation and/or clinical myasthenia gravis in lpr and gld mice deficient in Fas and Fas ligand, respectively. A high dose of 146–162 peptide in IFA in AChR-immunized mice induced apoptosis of BV6 cells. Further, reconstitution of IL-2 in vitro-recovered 146–162 peptide tolerized T cell proliferation, IFN-, and IL-10 production. The findings implicate the possible role of Fas-/Fas ligand-mediated apoptosis and the resulting clonal anergy as the mechanisms of high dose AChR 146–162 peptide-induced tolerance on CD4 cells.

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