Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured soluble interleukin 2 receptor, a part of the Tac protein (p55), in peripheral blood to study the immunological condition of the T cell in autoimmune thyroid disease. In 26 patients with untreated Graves' disease and 7 hyperthyroid patients with Hashimoto's thyroiditis, the mean levels of soluble IL-2 receptor were both significantly higher than in normal controls (1497 +/- 649 (mean +/- SD), 641 +/- 137 vs 221 +/- 63 10(3) U/l, p less than 0.001). There was good correlation between soluble IL-2 receptor levels and blood thyroxine levels (r = 0.684, p less than 0.001) in patients with untreated Graves' disease, but no correlation of soluble IL-2 receptor with TSH-inhibitory immunoglobulins, TS-ab, thyroidal autoantibodies to thyroglobulin and thyroidal microsomal antigen was found. We thought that the level of soluble IL-2 receptor is not dependent only on immunological conditions, but also on thyroid hormone status. When T3 was administered to subjects in remission from Graves' disease and in normal controls, the soluble IL-2 receptor levels significantly increased. Moreover, the mean level of soluble IL-2 receptor in patients with toxic multinodular goitre was also significantly higher than in normal controls (411 +/- 148 vs 221 +/- 63 10(3)U/l, p less than 0.05). We conclude that the soluble IL-2 receptor levels are higher in sera of subjects with elevated levels of thyroid hormone.
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PMID:Increased soluble interleukin 2 receptor levels in autoimmune thyroid disease. 168 85

Because of interest in IL-2, and IL-2-activated killer cell-induced hypothyroidism in humans, we attempted to study an in vitro system that might prove to illuminate this disorder. We have thus studied interleukin 2 (IL-2--0, 12.5, 25, or 50 U/mL) activated killer cell-mediated autologous thyrocyte lysis, as well as cytotoxic activity in IL-2-stimulated mononuclear cell supernatants in 7 patients with autoimmune thyroid disease (2 Graves' disease and 5 Hashimoto's thyroiditis) using the 51Cr release assay. Controls included 14 patients with nonautoimmune thyroid disease (3 nontoxic goiter, 8 follicular thyroid adenoma, 2 papillary thyroid carcinoma, and 1 medullary carcinoma of the thyroid). Soluble IL-2 receptor (sIL-2R) in supernatants of peripheral mononuclear cells stimulated by IL-2 from these patients also was measured. Whereas in the control preparations, IL-2-activated killer cell activity was increased in a dose-dependent fashion relative to the IL-2 concentration, as well as to the effector cell/target cell ratio, in preparations from patients with autoimmune thyroid disease, this activity was not elevated as the IL-2 concentration was increased. The susceptibility of thyrocytes to the lytic effect of IL-2-activated killer cells was higher in controls than that in autoimmune thyroid disease (at concentrations of IL-2 of 0, 12.5, 25, and 50 U/mL) (p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin 2-activated killer cells do not mediate autologous thyrocyte lysis in autoimmune thyroid disease in vitro. 182 61

In order to clarify the autoimmune mechanisms of anti-Tg antibody (anti-TgAb) in autoimmune thyroid disease (AITD), a series of examinations were conducted in patients with Graves' disease (n = 59), Hashimoto's thyroiditis (n = 63) and healthy controls (n = 38). Our findings can be summarized as follows: 1) The distribution of anti-TgAb was measured by IgG subclass ELISA. IgG1 and/or IgG4 antibodies formed the major anti-Tg response, but in some patients, IgG2 anti-Tg tend to be the predominant response. We used ELISA to determine an IgG1 anti-Tg bound to Tg that had already interacted with IgG2 Tg-antibody (and vice versa). The results substantiated the view that TgAb of a different IgG subclass interact with different epitopes on Tg. 2) Human antiidiotypic (anti-Id) antibodies to anti-Tg antibody occur spontaneously in the AITD. These anti-Id antibodies can be divided into two categories based on properties of their binding sites. One type acts like a 'internal image' of Tg antigen which shown Ab2 beta activity. Another type has Ab2 alpha activity that recognizes Id determinants in the framework region common among anti-Tg antibody. 3) We also examined the competitive binding assay between TgAb and TgAb F(ab')2 fragments, and demonstrated differences in the TgAb repertoires between patients. 4) Soluble IL-2 receptor (IL-2R) of patients significantly increased as compared with normal subjects and IL-2R values in GD were higher than those in HT (p < 0.001). Therefore, IL-2R is regarded as a useful marker for disease activity.
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PMID:Studies on autoimmune mechanisms of thyroglobulin autoantibody in autoimmune thyroid disease. 801 70

Recent studies have confirmed that polymorphisms in several genes confer susceptibility for the development of autoimmune thyroid disease, and that of these HLA-DR alleles, and the genes encoding CTLA-4, PTPN22, FCRL3, and probably the IL-2 receptor all have associations with other autoimmune disorders, indicating that they provide a lowering of the background threshold for the development of autoimmunity. Other factors (the TSHR and possibly Tg genes, HLA-C alleles, and environmental factors) determine that the type of disease which results from this background propensity specifically targets the thyroid. We also now appreciate much better how complex these disorders are in their pathogenesis: multiple genes influencing multiple immunological pathways are involved in pathogenesis, but are not involved in every patient. Any individual patient with thyroid autoimmunity has their own cluster of genetic (and environmental) susceptibility factors, only very partially shared with other patients who have the same diagnostic and clinical label. The interplay of forces that cause autoimmune thyroid disease in an individual patient are more subtle than previously imagined and there is at present no obvious upper limit on the number of genes which may be involved.
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PMID:The genetics of autoimmune thyroid disease. 1934 17