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,
VAS V. ROW and
ROBERT VOLPÉ
Department of Medicine, University of Toronto, and the Endocrinology Research Laboratory, The Wellesley Hospital Toronto, Ontario, Canada
Address requests for reprints to: Dr. R. Volpé, Endocrinology Research Laboratory, The Wellesley Hospital, 160 Wellesley Street East, Toronto, Ontario M4Y 1J3 Canada.
The involvement of cell-mediated immunity in the pathogenesis of Graves disease (GD) and Hashimotos thyroiditis (HT) was investigated by employing a modified migration inhibition factor test using preparations of isolated T-lymphocytes. The migration of T-lymphocytes from patients with GD and HT in response to crude human thyroid antigen was significantly inhibited compared to the migration of T-lymphocytes from normal subjects. This response was organ specific. When normal T-lymphocytes were mixed with GD or HT Tlymphocytes in ratios varying from 1:9 to 1:1, the migration inhibition activity of the GD or HT T-lymphocytes in response to thyroid antigen was abolished, but was not abolished when two different GD or HT T-lymphocyte preparations were mixed.
Mitomycin C inhibited this suppressive effect of normal T-lymphocytes in vitro, but did not influence the migration inhibition activity of the antigen-sensitized GD or HT T-lymphocytes. On the other hand, the migration inhibition of GD and HT T-lymphocytes was prevented by puromycin. There thus appears to be activity in normal T-lymphocytes which can suppress the ability of GD and HT T-lymphocytes to respond to the thyroid antigen, which is lacking in the GD and HT T-lymphocytes themselves.
Our results are consistent with the hypothesis that there is a defect in suppressor T-lymphocyte function in GD and HT.
* Presented in part at the International Thyroid Congress, Sydney, Australia, February 4–8, 1980. This work was supported by a grant (MT-859) from the Medical Research Council of Canada.
Fellow of the Wellesley Hospital Research Foundation.
Received June 20, 1980.
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