concanavalin a/obezita

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Suppression of concanavalin A-induced responses in splenic lymphocytes by activated macrophages in the non-obese diabetic mouse.

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Spleen cells from non-obese diabetic mice were found to generate low interleukin 2 production and cell proliferation in response to concanavalin A. However, some of non-obese diabetic mice maintained in the same environment preserved their responsiveness to this T cell mitogen. Non-obese diabetic

T cell hyperproliferation in autoimmunity prone obese strain (OS) chickens is independent of abnormal mitogen binding in vitro and can be demonstrated in vivo.

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In contrast to systemic autoimmunity, spontaneous autoimmune thyroiditis of Obese strain (OS) chickens is associated with a marked T cell hyperreactivity in vitro, i.e. an increased proliferation and interleukin 2 (IL 2) secretion in response to Concanavalin A (ConA). In the present study we report

Analysis of lymphocytes infiltrating the thyroid gland of Obese strain chickens.

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Lymphocytes were isolated from the infiltrated thyroid glands of 2- to 5-wk-old Obese strain (OS) chickens with spontaneous autoimmune thyroiditis (SAT). Immunofluorescence analysis performed by using a panel of monoclonal and polyclonal antibodies revealed that 60% of thyroid infiltrating

Obesity minimizes the immunopotentiation of food restriction in ob/ob mice.

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The objective of this study was to investigate food restriction-related changes in several indices of immune competence in young (11 wk old) and adult (33 wk old) female lean (+/?) and obese (ob/ob) C57BL/6J mice. Body weight accumulation, tail length accretion and organ weights were more severely

Ingested interferon alpha suppresses type I diabetes in non-obese diabetic mice.

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Type I diabetes mellitus is a chronic disorder that results from autoimmune destruction of the insulin-producing pancreatic beta cell. The non-obese diabetic mouse is a model of the human autoimmune disease Type I diabetes [1-3]. We have previously shown that ingested type 1 interferon inhibits

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

Effect of thyroxine and chicken growth hormone on immune function in autoimmune thyroiditis (obese) strain chicks.

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The effect of thyroxine (T4) and/or recombinant chicken growth hormone (rcGH) supplementation on immune function and on immune cell maturation was examined in Obese strain chickens. Day-old Obese strain chicks received the control treatments or were treated with either T4 (supplemented in the diet),

T-cell repopulation following neonatal injection of non-obese diabetic (NOD) mice with anti-T-cell antibodies.

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Non-obese diabetic (NOD) mice injected with CD3 antibody as newborns have a reduced incidence of diabetes, raising the possibility that the neonatal injection caused a long-lasting change in circulating T cells. The present study shows that NOD and BALB/c mice injected with soluble CD3 antibody in

Neonatal injections of cyclosporin enhance autoimmune diabetes in non-obese diabetic mice.

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Since the modulation of the immune system at birth may influence the course of insulin-dependent (type 1) diabetes, we investigated whether neonatal injections of cyclosporin (CsA) to newborn non-obese diabetic (NOD) mice influence diabetes during later life. Two groups of 90 mice (45 female, 45

Genetically obese mice: resistance to metastasis of B16 melanoma and enhanced T-lymphocyte mitogenic responses.

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The metastasis of B16 melanoma cells differed significantly in obese (ob/ob) and lean (+/?) female mice of strain C57BL/6J. When the mice were inoculated subcutaneously with melanoma cells at 10 to 11 months of age, the primary tumor grew more slowly in obese than in lean littermates and the

Lymphocyte vaccination prevents spontaneous diabetes in the non-obese diabetic mouse.

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The aim of this study was to investigate whether lymphocyte vaccination can prevent diabetes occurring in the non-obese diabetic (NOD) mouse, an animal model of human insulin-dependent diabetes mellitus (IDDM). The lymphocyte vaccine was composed of lymphocytes isolated from the spleens of diabetic

Cytokine production in patients with anorexia nervosa, bulimia nervosa, and obesity.

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OBJECTIVE We previously reported elevated serum levels of the cytokines interleukin-6 (IL-6) and transforming growth factor-beta (TGF-beta) in patients with anorexia nervosa (AN). We investigated the cellular production of these two cytokines and of interferon-gamma (IFN-gamma), interleukin-1alpha

Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences.

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BACKGROUND Interleukin-22 (IL-22), a cytokine with important functions in anti-microbial defense and tissue repair, has been recently suggested to have beneficial effects in obesity and metabolic syndrome in some but not in other studies. Here, we re-examined the effects of IL-22 on obesity, insulin

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

Incomplete Freund's adjuvant reduces diabetes in the non-obese diabetic mouse.

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As the study of type 1 diabetes moves towards preventive therapy, the role of adjuvants needs to be addressed. Incomplete Freund's adjuvant (IFA) is thought of as "immunologically inert" as, unlike complete FA (CFA), it has no components designed to provoke an immune response. We investigated the

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