thyroiditis/ожирение

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Prevention of lymphocytic thyroiditis in iodide-treated non-obese diabetic mice lacking interferon regulatory factor-1.

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OBJECTIVE Interferon regulatory factor-1 (IRF-1) is a critical regulator of interferon-gamma(IFNgamma)-mediated immune responses. To determine whether IRF-1 is involved in the pathogenesis of thyroiditis in animal models, we evaluated the incidence of iodide-induced lymphocytic thyroiditis (LT) in

Spontaneous lymphocyt ic thyroiditis in interferon regulatory factor-1 deficient non-obese diabetic mice.

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Interferon regulatory factor-1 (IRF-1) is a transcription factor involved in interferon-mediated immune reaction, CD8+ T cell differentiation and development of T helper 1 immune reaction. We have recently demonstrated that IRF-1 is pivotal in iodine-induced lymphocytic thyroiditis (LT) in non-obese

Disturbed immune-endocrine communication in autoimmune disease. Lack of corticosterone response to immune signals in obese strain chickens with spontaneous autoimmune thyroiditis.

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Antigenic challenge as well as injection of lymphokine-containing media lead to a transient increase of serum glucocorticoids, a phenomenon that has been implicated in the regulation of the specificity of immune responses. In the present study we examined the dialogue between the immune and the

Antioxidants delay the onset of thyroiditis in obese strain chickens.

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Dietary iodine has been shown to be important in the induction of thyroiditis in susceptible chicken strains although the underlying mechanism remains unknown. Iodine may exert its effects through the formation of reactive oxidative radicals which would cause thyroidal injury and initiate

Enhanced response to Con A and production of TCGF by lymphocytes of obese strain (OS) chickens with spontaneous autoimmune thyroiditis.

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The mitogenic response to Con A and the production of T cell growth factor or interleukin 2 (IL 2) by splenic and peripheral blood lymphocytes of obese strain (OS) chickens with spontaneous autoimmune thyroiditis have been investigated. By using an optimized method with Con A-coated chicken

Electron-dense deposits in the follicular basal lamina of obese strain chickens with spontaneous hereditary autoimmune thyroiditis. An electron microscopic study.

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Thyroid glands of 36 chickens of the obese strain with hereditary spontaneous autoimmune thyroiditis were examined by electron microscopy at 1, 3, 5, 7, 10, and 14 weeks of age with particular emphasis on basal lamina changes. All chickens were of the B1B1 genotype. The electron microscopic results

Effect of cyclosporin A on spontaneous autoimmune thyroiditis of Obese strain (OS) chickens.

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The spontaneous autoimmune thyroiditis (SAT) which develops in the Obese strain (OS) of chickens depends on an intact B-dependent portion of immune system. T helper cells have been shown to be required for the production of thyroglobulin autoantibodies (Tg-AAb), but a possible contribution of

Effect of growth hormone and thyroid hormone on autoimmune thyroiditis in obese chickens.

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The effect of thyroxine (T4) and recombinant (rcGH) or purified pituitary-derived (pcGH) chicken growth hormone on the development of spontaneous autoimmune thyroiditis (SAT) was examined in the Obese strain (OS) chicken. Day-old OS chicks were randomly assigned to a control or 1.0 ppm T4

Genetically-controlled severity of autoimmune thyroiditis in Obese strains (OS) chickens is expressed at both the humoral and cellular effector mechanism levels.

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Two lines of Obese strain (OS) chickens of identical MHC (B) genotype, B5B5, bred over 10 years with different selection parameters, differ in their severity of spontaneous autoimmune thyroiditis. To determine whether alterations in immune responsiveness underly this discrepancy, the two lines were

Materno-embryonally transferred antibodies precipitate autoimmune thyroiditis in obese strain (OS) chickens.

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In Obese strain (OS) chickens the role of maternal antibodies, passively transferred through the egg to the developing chick, was evaluated as a causative factor in the early development of spontaneous autoimmune thyroiditis (SAT). In the egg, passive antibody titers were highest in the yolk and

Sex steroid and glucocorticoid receptors in the bursa of Fabricius of obese strain chickens spontaneously developing autoimmune thyroiditis.

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The female sex develops autoimmune disease far more often than the male. This is claimed to be due to differences in peripheral sex steroid levels. We have examined in the bursa of Fabricius of Obese strain (OS) chickens, which spontaneously develop autoimmune thyroiditis, as well as in their

Immunogenetic analysis of spontaneous autoimmune thyroiditis of obese strain chickens.

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A variety of immunological, endocrinological, and virological abnormalities have been implicated in the etiopathogenesis of spontaneous autoimmune thyroiditis (SAT) of Obese strain (OS) chickens, e.g., a general T cell hyperreactivity, an increased uptake of iodine into the thyroid gland, a

Inhibition of the development of spontaneous autoimmune thyroiditis in the obese strain (OS) chickens by in vivo treatment with anti-CD4 or anti-CD8 antibodies.

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The involvement of CD4+ and CD8+ T cells in pathogenesis of spontaneous autoimmune thyroiditis (SAT) in obese strain (OS) chickens has not been studied in depth until now. We depleted CD4+ or CD8+ T cells in OS chickens by treatment with murine monoclonal anti-CD4 or anti-CD8 antibodies at 3 day

Requirement of T cells for the development of spontaneous autoimmune thyroiditis in obese strain (OS) chickens.

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A combination of neonatal thymectomy and intensive treatment with a highly specific turkey anti-chicken T cell serum effectively abrogates the spontaneous development of thyroiditis and thyroglobulin autoantibodies in the Obese strain chicken. Thus, in addition to a restraining influence of

The induction of tolerance to thyroglobulin significantly reduces the severity of thyroiditis in obese strain chickens.

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Obese strain chickens develop severe spontaneous autoimmune thyroiditis several weeks after hatching, characterized by mononuclear cell infiltration and antibodies to thyroglobulin (Tg). The presence of antibodies to Tg suggests that Tg is an important antigen in this disease, but it does not

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