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NEUROLOGY 1991;41:1809
© 1991 American Academy of Neurology

T cells in myasthenia gravis specific for embryonic acetylcholine receptor

Maria Pia Protti, MD, Angelo A. Manfredi, MD, James F. Howard, Jr., MD and Bianca M. Conti-Tronconi, MD

Department of Biochemistry (Drs. Protti, Manfredi, and Conti-Tronconi), College of Biological Sciences, University of Minnesota, St. Paul, MN, and the Department of Neurology (Dr. Howard), University of North Carolina at Chapel Hill, Chapel Hill, NC.

In myasthenia gravis (MG) there is an autoimmune response against muscle acetylcholine receptor (AChR). Embryonic and adult muscles express different AChRs; embryonic AChR contains a {gamma} subunit, instead of the homologous {varepsilon} subunit that contributes to form adult AChR. We report propagation from the blood of MG patients of T helper (TH) cell lines specific for human embryonic AChR, by cycles of stimulation with a pool of synthetic peptides corresponding to the complete sequence of the {gamma} subunit ({gamma} pool). The TH lines strongly recognized AChR from embryonic mammalian muscle, and reacted less or not at all with adult muscle AChR. The existence of TH cells specific for embryonic AChR strongly suggests that the primary anti-AChR sensitization in MG occurs in a tissue other than the innervated skeletal muscle. This may be within the thymus, which expresses an AChR similar or identical to embryonic muscle AChR.

Address correspondence and reprint requests to Dr. Bianca M. Conti-Tronconi, Department of Biochemistry, CBS, University of Minnesota, 1479 Gortner Ave., St. Paul, MN 55108.

Supported by the NINCDS grant NS 29919 and a grant from the Muscular Dystrophy Association of America (to B.M.C.-T.). M.P.P. is a recipient of the MDA Sidney Blackmer Fellowship. A.A.M. is a recipient of a MDA Postdoctoral fellowship.

Received February 11, 1991. Accepted for publication in final form May 6, 1991.






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