T‐CELL SENSITIZATION TO AUTOLOGOUS THYROID CELLS AND NORMAL NON‐SPECIFIC SUPPRESSOR T‐CELL FUNCTION IN GRAVES' DISEASE

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Abstract
A syngeneic system utilizing thyroid cell monolayers initiated following thyroid surgery co-cultured with autologous T cells was employed to demonstrate T cell autosensitization in patients with Graves'' disease. Antigen-induced blastogenesis was monitored using 24 h [3H]thymidine uptake. Control experiments with 5 d [day] cultured normal human thyroid cells from tissue around benign adenomata showed no evidence of syngeneic T cell autosensitization. Human thyroid cells alone were unable to incorporate [3H]thymidine in the presence of b [bovine] TSH. In 3 of 4 experiments with Graves'' thyroid cells there was significant induction of autologous T cell blastogenesis with a mean stimulation index of 220%. In parallel experiments we explored the non-specific helper and suppressor T cell function of these and similar patients with Graves'' disease. In normal controls(n = 6) increasing numbers of T cells added to a constant number of B cells (consisting of a T cell depleted peripheral mononuclear cell preparation) showed a marked helper effect measured as increasing IgG secretion. As the ratio of T:B cells increased above 4:1 there was a suppression of IgG secretion. One of 2 hyperthyroid Graves'' patients was observed to have deficient T cell function as demonstrated by lack of IgG suppression. The remaining 5 patients (all but one of whom were euthyroid at the time of testing) had results similar to the control indicating normal suppressor T cell function in this disease. Patients with Graves'' disease possessed circulating T cells which exhibited autosensitization to syngeneic thyroid cell surface antigens, a phenomenon not demonstrable in control individuals. This specific T cell autosensitization did not interfere with non-specific T cell function as judged by its influence on IgG secretion.