Autoantibodies as Predictive and Diagnostic Markers of Idiopathic Inflammatory Myopathies

The purpose of the present study was to determine whether patients with euthyroid Graves’ exophthal-mopathy have an impaired NK cell function compared to patients with Graves’ hyperthyroidism and healthy controls.

The NK cell activity measured against K562 target cells was significantly suppressed (p < 0.01) in patients with euthyroid Graves’ ophthalmopathy, whereas the NK cell activity of patients with Graves’ hyperthyroidism was not. Although interferon-α, interleukin-2 and indomethacin significantly enhanced (p < 0.01) the NK cell activity in all three groups, none of these agents fully restored the defective NK cell activity in euthyroid Graves’ ophthalmopathy. The concentrations in the blood of large granular lymphocytes and CD 16 positive cells did not differ between the three groups, furthermore an immunosuppressive serum factor was not detected. The number of effector/target cell conjugates did not differ between patients and controls, whereas the interferon-α -induced production of a soluble natural killer cytotoxic factor (NKCF) with specificity for NK sensitive target cells was suppressed in patients with Graves’ euthyroid ophthalmopathy. We conclude that one of the mechanisms underlying the defective NK cell activity in patients with euthyroid ophthalmopathy may be an impairment of the release of NKCF from the NK cells.