Myasthenia gravis: T and B cell reactivities to the β-bungarotoxin binding protein presynaptic membrane receptor

• Published in: Journal of the neurological sciences Vol. 109; no. 2; pp. 173 - 181
• Main Authors: Link, Hans, Sun, Jia-Bin, Lu, Chuan-Zhen, Xiao, Bao-Guo, Fredrikson, Sten, Höjeberg, Bo, Olson, Tomas
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 01.06.1992; Elsevier Science
• Subjects: Adult; Aged; alpha7 Nicotinic Acetylcholine Receptor; Animals; Antibody secreting cells; B-Lymphocytes - metabolism; Biological and medical sciences; Bungarotoxins - metabolism; Cattle; Diseases of striated muscles. Neuromuscular diseases; Female; Humans; In Vitro Techniques; Interferon-γ; Male; Medical sciences; Middle Aged; Muscles - metabolism; Myasthenia gravis; Myasthenia Gravis - metabolism; Myelin Sheath - metabolism; Neurology; Peripheral Nerves - metabolism; Receptors, Cholinergic - drug effects; Receptors, Cholinergic - metabolism; Receptors, Nicotinic; Synapses - metabolism; T cell reactivities; T-Lymphocytes - metabolism; β-Bungarotoxin binding protein; Antibody secreting cells; Myasthenia gravis; β-Bungarotoxin binding protein; Interferon-γ; T cell reactivities; Human; Immunopathology; Nervous system diseases; Antibody; Autoimmune disease; Exploration; Binding protein; Striated muscle disease; Cholinergic receptor; T-Lymphocyte; Serum; Gamma interferon; Biological receptor
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/0022-510X(92)90165-H

Antibodies against acetycholine receptor (AChR) can be detected in most patients with myasthemia gravis (MG) and are considered to be involved in the immunopathogenesis of this disease. AChR are isolated from crude receptor preparations by binding to α-bungarotoxin (α-BuTx). Patients with MG have also antibodies against a second protein tentatively named presynaptic membrane receptor (PsmR), which has been isolated from crude receptor utilizing β-bungarotoxin (β-BuTx). PsmR could represent another antigen besides AChR relevant for the development of MG. We have now evaluated the T cell reactivity to PsmR in MG and controls by analyzing the frequencies of cells which in response to PsmR in short-term cultures secreted interferon-gamma (IFN-γ). The B cell response to PsmR was analysed in parallel by counting cells secreting anti-PsmR antibodies. Most patients with MG had PsmR reactive T cells in blood with a median number of about 1 per 44 000 mononuclear cells. Cells secreting anti-PsmR antibodies belonging to the IgG and IgA isotypes, less frequently of the IgM isotype were detected in most MG patients. A positive correlation was found between T cells reactive with PsmR and anti-PsmR IgG antibody secreting cells. PsmR reactive T and B cells were also detected in control patients, but at much lower numbers. Our results indicate that MG is accompanied by T as well as B cell responses to PsmR, in addition to the previously recognized responses to AChR. It remains to be shown whether these PsmR reactivities are of pathogenetic importance in MG.