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Acetylcholine receptors in human thymic myoid cells in situ: An immunohistological study
Author(s) -
Schluep Myriam,
Willcox Nicholas,
Vincent Angela,
Dhoot Gurtej K.,
NewsomDavis John
Publication year - 1987
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410220205
Subject(s) - myasthenia gravis , acetylcholine receptor , monoclonal antibody , epitope , biology , polyclonal antibodies , immunohistochemistry , microbiology and biotechnology , immunofluorescence , antibody , receptor , endocrinology , medicine , immunology , biochemistry
Myoid cells were studied by double immunofluorescence in sections of thymus from 47 patients with myasthenia gravis and 15 control subjects, using polyclonal sheep anti–troponin T and monoclonal antibodies to troponin I, striated muscle myosin, and acetylcholine receptor (AChR). The myoid cells were rare and located mainly in the medulla, and most were clearly positive for AChR; labeling was similar with four individual monoclonal antibodies specific for extrajunctional AChR and five that also recognize endplate AChR. They were mostly keratin‐positive and consistently HLA–DR–negative. In the myasthenia gravis samples, the myoid cells were similar but largely confined to medullary epithelial areas; AChR labeling was slightly weaker, but otherwise they did not differ noticeably from those of control subjects. A preliminary finding was of even rarer AChR‐positive/HLA‐DR–positive antigen‐presenting (possibly) cells seen in 9 of 9 myasthenia gravis samples and in none of 9 control samples. Although myoid‐cell AChR appears antigenically similar to extrajunctional muscle AChR, and must therefore express the epitopes that myasthenics' antibodies recognize, these cells do not appear to be foci of immunological stimulation in myasthenia gravis.