Literature DB >> 6221141

Characterization of inflammatory cells in autoimmune tubulointerstitial nephritis in rats.

F M Mampaso, C B Wilson.   

Abstract

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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Year:  1983        PMID: 6221141     DOI: 10.1038/ki.1983.41

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  17 in total

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Authors:  A Giménez; F Leyva-Cobián; C Fierro; M Río; T Bricio; F Mampaso
Journal:  Clin Exp Immunol       Date:  1987-09       Impact factor: 4.330

5.  Inhibition of experimental autoimmune tubulointerstitial nephritis in Brown-Norway rats by (15S)-15-methyl prostaglandin E1. Analysis of the effect of prostaglandin E1 on the induction of the humoral immune response and the elicitation of humorally mediated inflammation.

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7.  Passive dual immunization against tumour necrosis factor-alpha (TNF-alpha) and IL-1 beta maximally ameliorates acute aminonucleoside nephrosis.

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Review 8.  Glomerular antigens in glomerulonephritis.

Authors:  T J Neale; C B Wilson
Journal:  Springer Semin Immunopathol       Date:  1982

9.  IL-1-like production in adriamycin-induced nephrotic syndrome in the rat.

Authors:  T Bricio; A Molina; J Egido; E Gonzalez; F Mampaso
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10.  Retinoids as a potential treatment for experimental puromycin-induced nephrosis.

Authors:  V Moreno-Manzano; F Mampaso; J C Sepúlveda-Muñoz; M Alique; S Chen; F N Ziyadeh; M C Iglesias-de la Cruz; J Rodríguez; E Nieto; J M Orellana; P Reyes; I Arribas; Q Xu; M Kitamura; F J Lucio Cazana
Journal:  Br J Pharmacol       Date:  2003-06       Impact factor: 8.739

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