The T cell suppressor defect in autoimmune thyroiditis: evidence for a high set 'autoimmunostat'.

We examined T cell function in patients with autoimmune thyroiditis in relation to mitogen-stimulated thyroglobulin autoantibody secretion and used total IgG and IgM secretion as a measure of non-specific polyclonal activation. Control subjects (n = 8) showed enhanced immunoglobulin secretion (both IgG and IgM) in the presence of increasing autologous T cells up to a ratio of 4:1 T:non-T followed by suppression of such secretion when the number of T cells was increased still further (the T cell suppressor effect). Patients (n = 8) demonstrated similar enhancement of immunoglobulin secretion when compared to normals but the T cell suppressor effect was markedly reduced. Autoantibodies to human thyroglobulin antigen, measured by specific ELISA techniques, were detected in cultures from five patients and demonstrated a similar pattern of enhancement but reduced suppression as observed with the immunoglobulin assays. However, normal suppression of immunoglobulin and thyroglobulin autoantibody secretion in such patients was obtained with the use of allogeneic normal T cells. These data confirm the presence of a T cell suppressor defect in autoimmune thyroiditis but indicate that the abnormality is not restricted to the control of thyroid autoantibodies. Such T cell dysfunction may allow the abnormal amplification of a distinct and separate primary event and may be viewed as an abnormal set point for a hypothetical 'autoimmunostat'.