Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: Relationship with disease activity
✍ Scribed by J. J. Corrales; A. Orfao; A. López; M. T. Mories; J. M. Miralles; J. Ciudad
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 66 KB
- Volume
- 30
- Category
- Article
- ISSN
- 0196-4763
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✦ Synopsis
Growing evidence points to the possible involvement of cytokines in the pathogenesis of some autoimmune diseases. To investigate the possible role of interleukin 2 (IL-2) and interleukin 6 (IL-6) on the pathogenesis of Graves disease (GD), the binding of both exogenous IL-2 and IL-6 and the expression of the IL-2 receptor subunit p55 (CD25) were evaluated by flow cytometry in peripheral blood T and B cells from 70 GD patients, in different states of the disease, and from 19 age-and sex-matched healthy volunteers. Serum levels of total T3 and T4, of free T4, and of anti-TSH receptor antibodies were also simultaneously determined. All GD patients displayed significantly increased numbers of B cells bound to IL-2. Hyperthyroid untreated GD patients had significantly higher numbers of T and B cells expressing the IL-2 receptor subunit p55 as compared to euthyroid patients in long-term remission. In addition, serum anti-TSH receptor antibody levels were directly correlated with the absolute numbers of T cells bound to IL-2 (r 5 0.565, P F 0.05) and to IL-6 (r 5 0.653, P 5 0.02) in the hyperthyroid untreated patients, but not in long-term remission euthyroid GD patients or in patients treated with methimazole. The serum levels of total T3 and free T4 were significantly correlated with the absolute numbers of circulating T cells binding IL-2 (r 5 0.720, P F 0.01 and r 5 0.783, P F 0.002, respectively) as well as with the absolute numbers of circulating T cells binding IL-6 (r 5 0.671, P F 0.02 and r 5 0.626, P F 0.02, respectively). The serum levels of total T3 were also correlated with both the absolute numbers of B cells binding to IL-2 (r 5 0.586, P F 0.05) and to IL-6 (r 5 0.757, P F 0.001). These findings suggest that IL-2 and IL-6 may play a role in the pathogenesis of GD. Cytometry 30:118-123, 1997.