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In vitro production of interferon‐gamma by peripheral blood from patients with Graves' disease, Hashimoto's thyroiditis and rheumatoid arthritis

The production of interferon‐gamma (IFN‐γ) by peripheral blood mononuclear cells (PBMC), CD4 cells, or CD8 cells in response to interleukin‐2 (IL‐2) stimulation has been studied; the samples were obtained from 12 healthy control subjects, 19 patients with Graves' disease (10 hyperthyroid and nine euthyroid), 13 patients with Hashimoto's thyroiditis (four hypothyroid and nine euthyroid), and 15 patients with rheumatoid arthritis (11 active and four inactive). A dose of IL‐2 (25 U/ml) was utilized to induce IFN‐γ by PBMC from all four groups. The incremental increase in IFN‐γ values (with IL‐2 stimulation minus without stimulation) was significantly less in PBMC from patients with Graves' disease, Hashimoto's thyroiditis, and rheumatoid arthritis than that in PBMC from control subjects. The values from PBMC in patients with Graves' disease in a euthyroid state were below normal but greater than those from patients with Graves' disease in a hyperthyroid state. The incremental increase in IFN‐γ values from Graves' disease PBMC correlated with the serum TSH values (r=0.622, P < 0.01), but not with thyroid autoantibodies (anti‐thyroid microsomal antibodies, anti‐thyroid microsomal antibodies, nor TSH‐binding inhibitory immunoglobulin activities). The incremental increase in IFN‐γ from PBMC from both control subjects and Graves* disease was correlated with that from CD4 cells (r=0.711, P < 0.01), but not with that from CD8 cells. The production of IFN‐γ in response to IL‐2 from PBMC in Graves' disease correlated inversely with thyroid function, appearing to reflect the very effect of hyperthyroidism in this process. The precise explanation of these phenomena remains unclear. The decreased response of IFN‐γ to IL‐2 stimulation by PBMC from patients with Graves' disease, Hashimoto's thyroiditis, and rheumatoid arthritis seems to be a non‐specific phenomenon occurring in both organ specific autoimmune disease and systemic autoimmune disease. It may be due to a down‐regulation in autoimmune disease of CD4 cells in response to IL‐2, a decreased level of IL‐2 cellular receptors or a decreased receptor affinity, associated increased soluble IL‐2 receptors, or a defect of the intra‐CD4 cellular IL‐2 signal to produce or release IFN‐γ in the conditions studied.