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Research Article Free access | 10.1172/JCI114948

Phenotypic and functional characterization of T cells from patients with myasthenia gravis.

F Mokhtarian, M Pino, W Ofosu-Appiah, and D Grob

Department of Medicine, Maimonides Medical Center, Brooklyn, New York.

Find articles by Mokhtarian, F. in: JCI | PubMed | Google Scholar

Department of Medicine, Maimonides Medical Center, Brooklyn, New York.

Find articles by Pino, M. in: JCI | PubMed | Google Scholar

Department of Medicine, Maimonides Medical Center, Brooklyn, New York.

Find articles by Ofosu-Appiah, W. in: JCI | PubMed | Google Scholar

Department of Medicine, Maimonides Medical Center, Brooklyn, New York.

Find articles by Grob, D. in: JCI | PubMed | Google Scholar

Published December 1, 1990 - More info

Published in Volume 86, Issue 6 on December 1, 1990
J Clin Invest. 1990;86(6):2099–2108. https://doi.org/10.1172/JCI114948.
© 1990 The American Society for Clinical Investigation
Published December 1, 1990 - Version history
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Abstract

A study of cell surface phenotypes of PBL of myasthenia gravis (MG) patients showed that their T cells had a significantly higher percentage of 4B4+ T cells (the helper/inducer subset) than age- and sex-matched controls. The PBL of MG patients proliferated significantly higher than those of normal subjects (NS) in response to the purified alpha chain of the acetylcholine receptor (AChR). Anti-AChR antibody was present in sera of 88% of MG and none of the NS. The PBL B cells from MG only, when cultured with autologous T cells and stimulated with either pokeweed mitogen (69%), or AChR-alpha chain (38%), secreted antibody to AChR-alpha chain, whereas T and B cells alone secreted no antibody. T cells from PBL of MG patients were more readily cloned than T cells of NS, by limiting dilution, in the presence of recombinant IL-2 and in the absence of AChR-alpha chain. About 50% of T cell clones from MG patients, compared to none from NS, proliferated to AChR-alpha chain. This response was HLA-DR restricted. MG T cell clones did not display significant cytotoxic activity, as compared to control T cell clones. Our results indicate that in MG, 4B4+ regulatory T cells play their role in the pathogenesis of MG, not by cytotoxicity, but more likely by their ability to stimulate specific antibody production by B cells.

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