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Normal Suppressive T Cell Function of Epstein-Barr Virus-Induced B Cell Activation in Graves' Disease

INSERM U. 283, Hôpital Cochin (A.K., J.C.) 75674 Paris Cedex 14
Service d'Endocrinologie, Hôpital H. Mondor (J.-P.L.) Créteil, France

Address all correspondence and requests for reprints to: A. Kahan, INSERM U.283, Hôpital Cochin, 27 rue du Fg. St. Jacques 75674, Paris Cedex 14, France.

Several studies have demonstrated abnormalities of T cell regulation of Epstein-Barr virus (EBV)-induced B cell activation in systemic autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. To investigate whether this abnormality is a common feature of other autoimmune diseases, we studied 10 EBV-immune normal subjects and 22 EBV-immune patients with Graves' disease (GD); 11 had newly diagnosed hyperthyroidism, and 11 had received carbimazole treatment for hyperthyroidism for at least 6 months. Peripheral B lymphocytes infected with EBV were cultured for 20 days in the presence or absence of autologous T cells at different ratios. Immunoglobulins M and G secretion into the supernatants was determined using an enzyme-linked immunosorbent assay. The extent of suppression when T cells were added, as measured by a suppression ratio, was not significantly different in normal subjects and newly diagnosed GD patients (0.65 vs. 0.63 on the 16th day and 0.77 vs. 0.72 on the 20th day of culture, respectively). In carbimazole-treated patients, the appearance of functional suppressor T cells was delayed slightly, but the overall suppression ratios on the 16th and 20th days were normal. Thus, a T cell regulation abnormality of EBV-induced B cell activation could not be demonstrated in patients with untreated hyperthyroid GD, suggesting that the autoimmune reactivity in such patients is probably dependent upon a specific thyroid suppression defect rather than a generalized suppression defect.

Received January 29, 1987.