Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Different forms of cellular cytotoxicity that may constitute potential effector mechanisms in the spontaneous autoimmune thyroiditis (SAT) arising in Obese strain (OS) chickens have been investigated. A microcytotoxicity assay (MCA) employing 51Cr-labelled-, thyroglobulin (Tg) coated-chicken red blood cells (Tg-CRBC) was used to detect cells mediating Tg-specific direct cellular cytotoxicity (DCC). Tg-CRBC presensitized with anti-Tg autoantibody (Tg-AAB) obtained from high titer OS sera served as targets for antibody-dependent cell-mediated cytotoxicity (ADCC). Tannic acid-only treated CRBC (TA-CRBC) were used simultaneously as specificity controls for DCC and also as targets for cells eliciting spontaneous cellular cytotoxicity (SCC) to surface-modified normal cells. The results demonstrated that Tg-specific cytotoxic cells exist in the OS and thus represent an effector mechanism in SAT, in addition to the previously well-documented role of antibody. This DCC appears to be unrelated to the presence and titer of circulating Tg-AAb. It is present in highest levels in the peripheral blood of OS chickens, but in only 55% of the animals tested, indicating either a secondary importance to humoral immunity in the disease process or the possibility of different effector mechanisms prevailing in different birds. There were no overall differences in ADCC between OS and normal chickens when the two strains were considered as a whole. Chronological analysis, however, revealed very low ADCC in the peripheral blood of young OS birds, followed by a later elevation above that in the normal control chickens. Destruction of the gland by ADCC may be initiated via maternally-derived of in situ-produced anti-Tg antibody. No overall significant differences in SCC were observed between OS and normal chickens.
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PMID:Effector mechanisms in the spontaneous autoimmune thyroiditis of obese strain (OS) chickens: analysis of cytotoxic cells. 698 71

A 51chromium (51Cr)release microcytotoxicity assay has been established for studying cell-mediated immunity in chickens to a potentially wide variety of antigens. The system investigated in detail uses thyroglobulin-coated chicken red blood cells (Tg-CRBC) to analyse effector cell mechanisms operative in spontaneous autoimmune thyroiditis in Obese strain (OS) chickens. A variety of technical parameters were investigated in order to optimise reliable, reproducible target cell preparation and to minimise spontaneous 51Cr-release. The final method adopted used tannic acid for coupling antigen to carefully selected donor erythrocytes of uniform MHC genotype. For the study of antibody dependent, cell-mediated cytotoxicity, Tg-CRBC were pre-sensitised with OS serum containing high titre Tg-autoantibody. Tannic acid-treated CRBC (TA-CRBC) served simultaneously as controls for the Tg specificity of direct cellular cytotoxicity (DCC) to Tg-CRBC, and also as target cells for natural, or spontaneous cellular cytotoxicity (SCC). With such an assay, cells capable of mediating Tg-specific DCC were demonstrated in the OS, but not in normal chickens. No differences in ADCC or SCC were observed when the two strains were considered as a whole, i.e. regardless of age, sex, MHC genotype or extent of disease.
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PMID:Killer cells in the chicken: a microcytotoxicity assay using antigen-coated erythrocytes as targets. 740 May 85

Tannic acid is a hydrolyzable tannin that exists in many widespread edible plants with a variety of biological activities. In this study, we found that tannic acid potently inhibited the activity of fatty acid synthase (FAS) in a concentration-dependent manner with a half-inhibitory concentration value (IC50) of 0.14 microM. The inhibition kinetic results showed that the inhibition of FAS by tannic acid was mixed competitive and noncompetitive manner with respect to acetyl-CoA and malonyl-CoA, but uncompetitive to NADPH. Tannic acid prevented the differentiation of 3T3-L1 pre-adipocytes, and thus repressed intracellular lipid accumulation. In the meantime, tannic acid decreased the expression of FAS and down-regulated the mRNA level of FAS and PPARgamma during adipocyte differentiation. Further studies showed that the inhibitory effect of tannic acid did not relate to FAS non-specific sedimentation. Since FAS was believed to be a therapeutic target of obesity, these findings suggested that tannic acid was considered having potential in the prevention of obesity.
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PMID:Inhibitory effects of tannic acid on fatty acid synthase and 3T3-L1 preadipocyte. 2404 66