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)

Serum complement (C) and C components were examined during a systemic graft versus host (GVH) reaction in the rat. In our series of experiments (Lewis times Brown Norway) F-1 hybrid rats (60-80g) were given 200 times 10-6 or 400 times 10-6 Lewis spleen cells intravenously. Clinical GVH disease appeared 5-7 days after cell injection. Five of six rats in the experimental groups had a fall in levels of serum C2 (20-76%) and C4 (75-98%). Only one of six rats in the control group had a significant fall in C components. In a subsequent experiment (Fisher 344 times Brown Norway) F-1hybrid rats (60g) were given 400 times 10-6 Fischer 344 spleen cells or 200 times 10-6 Fischer 344 Ficoll-Hypaque separated spleen lymphocytes. Clincal GVH disease in this instance appeared on day 10. As in the previous experiments C2 and C4 fell markedly, 20-60% and 60-8-%, respectively, from baseline titers. The control groups did not have a significant fall in C2 or C4. Further examination showed reduction in C3, C5, C6,AND C8 suggesting a sequential activation of the C system via the classical pathway. We have postulated that the cells undergoing blast transformation may be activating the C system through membrane changes during the GVH reaction. Furthermore, the deficiency of C AND C components during GVH disease may contribute to the increased susceptibility of the host to infection and sepsis.
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PMID:Complement in graft versus host disease: IL Depletion of complement components during a systemic graft versus host reaction in the rat (38499). 23 66

Doses of as little as 50 micrograms of a soluble chaotropic extract of bovine tubular basement membrane (Bov-KBr-TBM) with adjuvants induced anti-TBM antibodies and tubulointerstitial nephritis (TIN) in Brown Norway (BN) rats. The lesion was shown by renal histology, by deposition of IgG and C3 along TBM, and in terms of the humoral and cellular immune responses to compare to that produced by the standard immunization (particulate bovine TBM) for this model of TIN in BN rats. More than half of the mononuclear cells in kidneys of BN rats with TIN bore various T-cell antigens (monoclonal antibodies W3-13, W3-25, and OX-8), and most of the infiltrating cells were positive for Ia (monoclonal antibody OX-6) by indirect immunofluorescence. Purified suspensions of these mononuclear infiltrates were prepared by using Ficoll-Hypaque gradients and the fluorescence-activated cell sorter (FACS) to eliminate renal tubular epithelial cells. The purified mononuclear cells, cultured for 5 days, incorporated thymidine in response to concanavalin A (Con A), Mycobacterium tuberculosis purified protein derivative, and Bov-KBr-TBM but not in response to a variety of autologous renal antigens. After culture for 5 days in Bov-KBr-TBM and Con A supernatant, lymph node cells (LNC) from Bov-KBr-TBM-immunized BN rats passively transferred TIN to naive BN rats. Although no cells reactive with autologous renal antigens were detected in the renal infiltrates, the transfer of disease with propagated LNC suggests that elements of the cellular immune system, in addition to anti-TBM antibody, contribute to the generation of this BN-TIN.
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PMID:Tubulointerstitial nephritis induced in the brown Norway rat with chaotropically solubilized bovine tubular basement membrane: the model and the humoral and cellular responses. 400 24

Brown Norway rats immunized with bovine tubular basement membrane (TBM) antigens develop tubulointerstitial nephritis. The composition of the inflammatory cell infiltrate was characterized in kidney tissue sections and cell suspensions obtained from affected kidneys. Anti-TBM antibody deposition in the kidney began 8 days after immunization and was followed on days 8 to 10 by C3 deposits and infiltration of polymorphonuclear leukocytes (PMN). After day 13, the infiltrate became almost exclusively mononuclear in character. On day 13, the inflammatory mononuclear cells recovered by Ficoll-Hypaque centrifugation contained 10% Ig+ cells (B cells), 60% W3/25+ cells (T helper cells), 9% OX8+ cells (T suppressor cells), 9% esterase+ cells (monocytes/macrophages), 4% renal cells, and 8% other unidentified cells. Monocytes/macrophages were prominent only at the latest stages of the disease. The ratio of W3/25+ to OX8+ cells was higher in the kidney than in the spleen or peripheral blood. The sequential accumulation of T cells and then monocytes/macrophages after an initial antibody, complement, and PMN lesion suggests a role for the T cells (selective prevalence of the helper T cell population over that of suppressor T cells) both as inflammatory cells and in progression and regulation of the subsequent stages of injury.
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PMID:Characterization of inflammatory cells in autoimmune tubulointerstitial nephritis in rats. 622 Nov 41