Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although both the T and B cells of the Lewis rat have immunoglobulin receptors for basic protein (BP) of myelin, and both cell types are required for antibody production to BP, the present results demonstrate that the T cells are the only cells required for the induction of experimental allergic encephalomyelitis (EAE). Both EAE and anti-BP were readily induced in thymectomized, irradiated Lewis rats reconstituted with normal thymus and bone marrow cells and challenged with BP in complete Freund's adjuvant. If the thymus cells were first treated with BP heavily labeled with 125I so as to eliminate (sucide) specific T cells, the recipients neither develop EAE nor produce antibody to BP. On the other hand, if the thymus cells were untreated and the specific B cells of bone marrow were eliminated by treatment with 125I-BP, EAE was not inhibited, although no antibody was produced. These results strongly suggest that the T cell is responsible for the induction of EAE although both the T and B cells are competent to respond to BP. Evidence was presented which suggests that neither suppressor T cells nor circulating antibody are involved in the inhibition of EAE by injection of Lewis rats with nonencephalitogenic preparations of BP. The immune status of T and B cells of the Lewis rat to BP was compared with the immune status of these cells in other species to thyroglobulin, where only the B cells appear to be competent. In this context, Brown Norway rats, which are resistant to the induction of EAE, also appear to lack T cells reactive to BP, although competent B cells are present.
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PMID:Cellular events in the induction of experimental allergic encephalomyelitis in rats. 6 Apr 61

The ability of mouse peritoneal macrophages to hydrolyze and excrete cytoplasmic cholesteryl ester droplets was studied. The macrophages were loaded with cholesteryl esters by incubation with acetylated low density lipoprotein (acetyl-LDL), which is internalized by adsorptive endocytosis. The cholesteryl esters of acetyl-LDL are hydrolyzed within lysosomes and the liberated cholesterol is re-esterified in the cytoplasm where it accumulates as cytoplasmic cholesteryl ester droplets. Hydrolysis and excretion of these stored cholesteryl esters were quantified by gas-liquid chromatographic measurement of the content of free and esterified cholesterol in cells and in medium. After removal of acetyl-LDL from the culture medium, the cytoplasmic cholesteryl esters were rapidly hydrolyzed and large amounts of free cholesterol were excreted from the cells. Hydrolysis and excretion required a cholesterol acceptor in the culture medium. The following agents were shown to be effective as cholesterol acceptors: high density lipoprotein (HDL), whole serum, the density > 1.215 g/ml fraction of whole serum, intact erythrocytes, casein, and thyroglobulin. The following agents did not promote the hydrolysis and excretion of cholesteryl esters under these experimental conditions: LDL, serum albumin, serum gamma-globulins, and phosphatidylcholine/sphingomyelin liposomes. The results indicate that net hydrolysis of cytoplasmic cholesteryl esters in macrophages is coupled to the process of cholesterol excretion and that net hydrolysis does not occur unless an effective cholesterol acceptor is present in the culture medium.-Ho, Y. K., M. S. Brown, and J. L. Goldstein. Hydrolysis and excretion of cytoplasmic cholesteryl esters by macrophages: stimulation by high density lipoprotein and other agents.
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PMID:Hydrolysis and excretion of cytoplasmic cholesteryl esters by macrophages: stimulation by high density lipoprotein and other agents. 738 31

Repeated exposure of Brown Norway (BN) rats to relatively low doses of HgCl2 induces autoantibodies to renal antigens (e.g., laminin) and a membranous glomerulonephropathy characterized by proteinuria. In contrast, Lewis (LEW) rats are "resistant" to the autoimmune effects of mercury and, when exposed to this metal, are protected against experimental autoimmune encephalomyelitis (EAE) and Heymann's nephritis. To date, there is no information on "suppressive" effects of mercury in naturally occurring (so-called "spontaneous") rat models of autoimmune disease. Therefore, we have administered HgCl2 to diabetes-prone (DP) BB rats, animals that spontaneously develop both insulin-dependent diabetes mellitus (IDDM) and thyroiditis. We found that DP rats treated with mercury or water for a period of 40-125 days developed autoantibodies to thyroglobulin, with a higher incidence in HgCl2-injected animals (92% vs. 56% in H2O-injected controls). A novel finding of our study was the detection of autoantibodies to laminin in the same rats, again with an increased incidence after HgCl2 treatment (83% vs. 44%). IgG2a was the most frequently detected isotype of antibodies to laminin, followed by IgG1, IgG2b and IgG2c. The IgG isotype profile suggests that treatment with HgCl2 may activate both Th1 and Th2 lymphocytes in BB rats. In spite of these stimulatory effects on autoantibody responses, we found that there was no difference in the incidence of IDDM and thyroiditis between HgCl2-treated and control animals. We conclude that the suppressive effects of mercury previously observed in EAE and Heymann's nephritis of LEW rats do not occur in "spontaneous" autoimmune IDDM and thyroiditis of BB rats. Therefore, immune suppression caused by HgCl2 cannot be considered a common phenomenon, but may be a genetically determined characteristic of LEW rats, possibly related to a specific or unique cytokine profile of this particular rat strain. In contrast, while mercury does not seem to recruit, induce or rescue regulatory T cell function in DP rats, it does stimulate autoantibody responses in these animals.
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PMID:Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes-prone (DP) BB rats. 955 Feb 85