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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chicken thymic nurse cells (TNC) were isolated and their plasma membrane antigens were characterized by immunofluorescence with a panel of allo-, hetero-, and monoclonal antibodies. Analogous to the murine system, chicken TNC are localized in the subcapsular region of the cortex and were strongly B-L and B-F positive (MHC Ia and H-2 D, K equivalents). The TNC were non-phagocytic and lacked fc receptors, but expressed an antigen specific for thymic epithelial cells, and their cytoplasm was stained by an anti-keratin antiserum. The internalized lymphocytes were all intact T cells of a distinct differentiation stage, their antigenic profile consistent with that of immature cortical thymocytes. To determine whether TNC may play a role in the activation of autoimmune disease, Obese strain chickens with spontaneous autoimmune thyroiditis were investigated. These chickens were found to have a twofold defect in their TNC content: the thymuses contained approximately one-half of the number of TNC found in normal chickens beginning as early as 17 days of embryogenesis, and the lymphocyte content of the Obese strain TNC was one-half that of the normals. The deficiency is specific for TNC and may be a major reason for the abnormal T cell differentiation in the Obese strain.
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PMID:Obese strain (OS) chickens with spontaneous autoimmune thyroiditis have a deficiency in thymic nurse cells. 636 Nov 33

In addition to thyroglobulin autoantibodies, some Obese strain (OS) chickens gave organ-specific reactions with the cytoplasm of thyroid acinar cells when the sera were tested by immunofluorescence. The staining pattern was similar to that seen with human antibodies to thyroid microsomes. A proportion stained the proventricular glands of the chicken stomach in a manner indistinguishable from that of pernicious anaemia sera containing parietal cell antibodies. Isolated examples of organ-specific reactions with adrenal and exocrine pancreas were also recorded. These findings strengthen the notion that the OS chicken represents an authentic model for human organ-specific autoimmune disease. The high incidence of non-organ specific reactions complicates but does not necessarily invalidate this view since normal chickens show a propensity to develop such antibodies. However the OS chicken appears to differ from the human in being hyper-responsive to antigens in general.
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PMID:Predisposition to organ-specific autoimmunity in Obese strain (OS) chickens: reactivity to thyroid, gastric, adrenal and pancreatic cytoplasmic antigens. 675 35

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 compared for their thyroiditis effector mechanisms. The OS B5B5 chickens, selected for high levels of serum thyroglobulin autoantibody, had correspondingly higher levels of thyroid-specific cytotoxic cells and also antibody dependent cellular cytotoxicity (ADCC) than the equivalent B5B5 line selected solely for the phenotypic trait of hypothyroidism. These results thus emphasize the importance of the non-MHC locus controlling immune responsiveness, in the 3 locus-model for this autoimmune disorder.
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PMID:Genetically-controlled severity of autoimmune thyroiditis in Obese strains (OS) chickens is expressed at both the humoral and cellular effector mechanism levels. 688 5

Obesity, high-fat diets, or excess lipids interact with infectious agents and immunocompetent cells in the following ways: Some infections and autoimmune diseases are enhanced in inbred mice. In man, surgical wound infections are increased; the risk of tubercular death is decreased; no data exist on the interaction of lipids and autoimmune disease. Certain fatty acids and cholesterol are potent modulators of T lymphocyte and phagocyte functions in laboratory animals and in leukocyte cultures. However, in humans, the modulation of immune function by dietary lipids is still uncertain. Precisely how lipids interact with the immune system opens an important and exciting area for future research.
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PMID:Obesity: does it modulate infectious disease and immunity? 702 62

The chicken MHC (B complex) initially described by Briles as controlling blood antigens, is now known to be composed of at least three regions, L, F and G. Two of these, F and G, were described on the basis of recombinants found in a study of over 10,000 chickens. On the basis of biochemical, tissue distribution and functional analyses, F corresponds to the murine H-2 K/D regions. The G region is unique to the chicken since the antigenic product is expressed only on erythrocytes and their progenitors. L was identified by serological studies and corresponds to the H-2 I region; the L antigen is expressed predominantly on B lymphocytes, monocytes and 10% of T lymphocytes, and differences in the L region result in variations in immune responsiveness. A number of functional similarities exist between the chicken MHC and that of other species such as regulation of graft rejection, graft-versus-host reaction (GVHR) and mixed lymphocyte reactions (MLR), mitogenic and immune responsiveness and resistance to RNA and DNA virus infection. The chicken MHC also controls the severity of autoimmune disease, as exemplified by the spontaneous thyroiditis of Obese strain (OS) chickens. It differs from mammalian MHC's by having of lower crossing-over frequency and no apparent gene duplication.
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PMID:Chicken major histocompatibility complex and disease. 704 23

Nonalcohol-induced fatty liver is widely believed to be a benign condition with little or no risk of disease progression. There have been occasional reports of progression to cirrhosis but none in the absence of preexisting fibrosis on the index biopsy specimen even when co-existing hepatitis was present (steatohepatitis). From our histological database (1978 to 1985), we identified 161 patients with fatty liver seen at our institution and traced the case notes of 156. One hundred five patients were initially excluded as having an alcohol-induced cause, and the remaining 51 either were seen in the clinic (37) or had died, in which cases copies of their death certificates were obtained (14). A further 7 patients were excluded after clinic attendance gave evidence of alcohol excess and another 4 after review of their initial biopsy showed the presence of fibrosis or steatohepatitis. The apparent cause of the steatosis in the 40 included patients with strictly nonalcohol-induced pure fatty liver was obesity in 12, diabetes in 4 (1 obese patient), and cachexia associated with extrahepatic malignancy in 6. Four of the remaining 19 had serological evidence of an autoimmune disorder, but none of these had any clinical or histological features of autoimmune liver disease. Nine patients had evidence of hyperlipidemia, 3 of whom were also obese. At a median follow-up of 11 years (7 to 16), 12 of 26 living patients had abnormal results of liver blood tests and had repeat liver biopsies performed. None had progressed to steatohepatitis or cirrhosis; 1 obese patient had developed mild fibrosis 9.8 years after her index biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The natural history of nonalcoholic fatty liver: a follow-up study. 748 79

Many important lessons have been learned from studies of autoimmune diseases in chicken models. It is now quite clear that both cellular and humoral immune responses are important in developing the final picture of autoimmune disease. In the case of the amelanosis of Smyth line (SL) chickens, antibody appears to play the primary role, whereas the sclerosis of University of California/Davis line-200 (UCD-200) birds is mainly mediated by T cells. Chronic thyroiditis of the OS chicken is due to both humoral and cellular effector mechanisms. The Obese strain (OS) chicken is particularly valuable for studies of genetics. Multiple genetic factors converge in producing maximal susceptibility to the development of autoimmune thyroiditis. They include MHC genes responsible for immune recognition; genes affecting thymus development, critical for regulation of the immune response; and genes that control thyroid function, influencing the vulnerability of the target organ to autoimmune attack. The importance of environmental factors, such as dietary iodine, is also strongly supported by studies in the OS chicken. Thus, the birds have provided valuable clues to our understanding of human autoimmune disorders in the past and are expected to do so in the future.
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PMID:Avian models of autoimmune disease: lessons from the birds. 793 87

We previously reported on an altered immune-endocrine feedback loop via the hypothalamo-pituitary-adrenal (HPA) axis in Obese strain (OS) chickens afflicted with spontaneous autoimmune thyroiditis. These animals are deficient in plasma corticosterone increase after antigenic challenge or application of cytokine-containing conditioned medium of mitogen-stimulated spleen cells (CM). To investigate whether the impaired ability to respond to cytokines with glucocorticoid-increasing factor (GIF) activity, e.g. interleukin 1 (IL 1), is restricted to OS chickens as a model for an organ-specific autoimmune disease, we extended our experiments to another autoimmune-prone animal strain, the chickens of the University of California at Davis line 200 (UCD-200). These animals develop an inherited inflammatory fibrotic disease that closely resembles human progressive systemic sclerosis (scleroderma). Application of GIF-containing CM to UCD-200 chickens leads to a transient increase in glucocorticoid serum levels within 1-2 hours comparable to that of controls. But, while corticosterone levels in the latter returned to normal baseline levels after 4 hours, they were still elevated in autoimmune chickens. Although the peak of the glucocorticoid hormone serum concentrations was equal to that of controls, UCD-200 had to secrete twice as much adrenocorticotropic hormone to achieve this corticosterone serum level due to an apparent hyporesponsiveness of the adrenal gland to this secretagogue. The altered cytokine-induced glucocorticoid secretion is found in early as well as in chronic, sclerotic stages of the disease. Cellular alterations in the peripheral blood of UCD-200 chickens during the prolonged elevated corticosterone section, i.e. between 2-4 hours after CM application, are characterized by a significant decrease in the percentage of CD4+ and CD8+ cells. Furthermore, a significant increase in B cells up to 24 hours with a maximum after 1 hour was found. The proliferative response to the mitogen concanavalin A of peripheral mononuclear cells was inversely correlated to the serum corticosterone level, showing a permanent decrease of 80-90% after 1-4 hours in autoimmune animals. This functional alteration in UCD-200 was accompanied by an 80% decrease in serum interleukin 2 (sIL 2) activity 4 hours after CM application. Twenty-four hours later an eight-fold increase in sIL 2 rebound activity was found, indicating that the inhibitory effect of corticosterone in UCD-200 chickens is not long-lasting.
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PMID:Effects of cytokine application on glucocorticoid secretion in an animal model for systemic scleroderma. 815 53

Autoimmune diseases have a multifactorial pathogenesis including essential genetic and nonessential modulatory factors. Among the essential factors, not only should genes coding for an abnormal reactivity of the immune system be considered, but we have, in addition, provided experimental evidence for the existence of genes responsible for a susceptibility of the target organ/structure for the autoimmune attack. Only when both sets of essential genes are present does an autoimmune disease develop at all. The modulatory factors then determine the final outcome in each case. The present contribution discusses the immunomodulating role of glucocorticoid and sex steroids focussing on the Obese Strain (OS) of chickens, a model for Hashimoto thyroiditis.
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PMID:Altered immunoendocrine dialogue in autoimmune disease. 846 66

According to our concept, the development of autoimmune disease depends on the presence of two sets of essential genes, one coding for an abnormal autoreactivity of the immune system, the other for a primary susceptibility of the target organ/structure for the immune attack. The final outcome of the disease in a given individual is then fine tuned by modulatory factors, such as diet or hormones. With regard to the latter, the immuno-endocrine interaction via the hypothalamo-pituitary-adrenal (HPA) axis has proven to be of special importance. Investigating the so-called Obese strain (OS) of chickens, an animal model with a spontaneously occurring Hashimoto-like autoimmune thyroiditis, we have first shown an impaired surge of glucocorticoid hormones after stimulation of the HPA axis by antigens or certain cytokines (glucocorticoid-increasing factors--GIFs). More recently, we have found a similar behavior in models with systemic autoimmune diseases, that is, murine lupus erythematosus and avian scleroderma. More detailed studies have, however, proven that the mechanisms underlying this altered immuno-endocrine communication via the HPA axis differs in different models. Finally, recent data point to the possibility that the classical pathways of glucocorticoid-T-cell interactions also take place in the thymus itself, which has been shown to be a site of steroid hormone production.
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PMID:Neuroendocrine-immune disturbances in animal models with spontaneous autoimmune diseases. 962 86


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