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T‐Cell Epitopes on the Human Acetylcholine Receptor α‐Subunit Residues 10‐84 in Myasthenia Gravis
Author(s) -
ÅHLBERG R.,
YI Q.,
ENG H.,
PIRSKANEN R.,
LEFVERT A. K.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb02958.x
Subject(s) - myasthenia gravis , acetylcholine receptor , epitope , t cell , stimulation , acetylcholine , receptor , protein subunit , cell , microbiology and biotechnology , antigen , biology , chemistry , endocrinology , immunology , biochemistry , immune system , gene
In myasthenia gravis the production of anti‐acetylcholine receptor antibodies is modulated by acetylcholine receptor‐specific T cells. Most B‐and T‐cell epitopes are located on the α‐subunit of the receptor. In order to map the fine specificity of the antigen‐specific T cells in myasthenia gravis, T‐cell stimulation in response to 70 hexapeptides was studied in 24 patients and 24 healthy individuals. The hexapeptides overlapped with one amino acid and represented residues 10‐84 of the NH 2 ‐terminal part of the α‐subunit of the receptor. The IFN‐γ secretion from single T cells was used to detect T‐cell stimulation. A significanl difference in the T‐cell response to several of the peptides was found between patients and healthy controls. The majority of the hexapeptides induced T‐cell stimulation in at least one of the patients. Peptidc‐induced T‐cell stimulation was evident in all but one of the patients. The results indicate that different epitopes and multiple T‐cell clones are involved in the T‐cell recognition of the acetylcholine receptor.