Cell-mediated immunity is important in the pathogenesis of Graves' dis
ease. Activation of T cells is apparently associated with the release
of soluble CD8 (sCD8) and CD4 (sCD4) molecules from the corresponding
T cell subset. To test the possibility that the concentrations of thes
e molecules may be related to Graves' disease activity, we measured se
rum sCD8 and sCD4 concentration in 58 Graves' patients using ELISA tec
hnique before and after treatment with methimazole as well as in 10 pa
tients with toxic nodular goiter. sCD8 was significantly elevated in t
hyrotoxic patients [609.9 +/- 118 (SD) U/ml] compared to controls (264
.1 +/- 98.8, p < 0.001) and normalized when patients became euthyroid
as a result of methimazole treatment (278.7 +/- 89.1). The mean sCD8 c
oncentration in the patients with toxic nodular goiter was 302 +/- 28
U/ml, no different from control. The sCD4 level in the Graves' disease
group was not different from control values and did not change signif
icantly with treatment. Correlations were found between the levels of
serum thyroid hormone(s) and sCD8 concentration but not with anti-TSH
receptor antibodies in the 50 patients with Graves' disease. In additi
on, serum sCD8 studied prospectively in eight patients after discontin
uation of methimazole, increased before the rise in serum T-4, and wel
l before the clinical relapse of thyrotoxicosis. It is concluded that
sCD8 is a useful marker for the activation of CD8(+) cells in Graves'
disease.