title: Analysis of IL-2 and IL-6 binding to peripheral blood lymphocytes in Graves disease: relationship with disease activity.
abstract: Growing evidence points to the 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 = 0.565, P < 0.05) and to IL-6 (r = 0.653), P = 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 = 0.720, P < 0.01 and r = 0.783, P < 0.002, respectively) as well as with the absolute numbers of circulating T cells binding IL-6 (r = 0.671, P < 0.02 and r = 0.626, P < 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 = 0.586, P < 0.05) and to IL-6 (r = 0.757, P < 0.001). These findings suggest that IL-2 and IL-6 may play a role in the pathogenesis of GD.
authors.affiliation: Departamento de Medicina, Hospital Clínico Universitario, Salamanca, Spain.
authors.forename: J J
authors.initials: JJ
authors.lastname: Corrales
authors.forename: A
authors.initials: A
authors.lastname: Orfao
authors.forename: A
authors.initials: A
authors.lastname: López
authors.forename: M T
authors.initials: MT
authors.lastname: Mories
authors.forename: J M
authors.initials: JM
authors.lastname: Miralles
authors.forename: J
authors.initials: J
authors.lastname: Ciudad
mesh_terms: D000328:Adult; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D006111:Graves Disease / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism*; D016131:Lymphocyte Subsets / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011971:Receptors, Immunologic / Q000378:metabolism; D015375:Receptors, Interleukin-2 / Q000378:metabolism*; D018709:Statistics, Nonparametric; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D013963:Thyroid Hormones / Q000378:metabolism; D013972:Thyrotropin / Q000378:metabolism
chemical_list: D007376:Interleukin-2; D015850:Interleukin-6; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2; D013963:Thyroid Hormones; D013972:Thyrotropin