PubMed Health⌕ Search

Biomedical subjects

M Milgrom

Publications and source records attributed to M Milgrom.

43 records · Page 3Linked to original sources
PubMed1980

Tissue deposition of immune complexes in mice receiving daily injections of bovine serum albumin.

The daily intraperitoneal injection of 0.3 mg of 0.5 mg BSA into preimmunized mice produced chronic serum sickness (CSS) within several weeks. The glomerulonephritis which developed was characterized in most cases (74%) by the deposition of immune complexes in the glomerular capillary wall. Associated pathological changes included crescent formation, hypercellularity, capillary occlusion and exudative and degenerative lesions in the glomeruli. In other animals (26%) a less severe renal disease developed in which immune complex deposition and histological abnormalities were limited to the glomerular mesangium. Mice with membranoproliferative immune complex glomerulonephritis had deposits of immune complexes in many other organs besides the kidney. A model of CSS in mice opens the possibility of studying the cellular basis of the immune response and genetic determinants in experimentally induced systemic immune complex disease.

Animals↗
PubMed1979

Experimental chronic serum sickness in rats. A model of immune complex glomerulonephritis and systemic immune complex deposition.

This article describes a method of immunization that produces chronic serum sickness in rats within a relatively short time. Fisher rats, which were immunized subcutaneously three times with bovine serum albumin (BSA) in adjuvant, responded with high titers of antibodies to BSA. 2 weeks after the third subcutaneous immunization, daily increasing amounts of BSA were injected either intraperitoneally or intravenously. When an intravenous dose of 2mg of BSA was reached, the rats were given daily intravenous injections of BSA for several weeks. This procedure, which avoided death from anaphylaxis, induced severe proliferative glomerulonephritis in all the rats and produced deposition of antigen-antibody complexes in many other organs besides the kidney. This highly reproducible model of experimental chronic serum sickness in inbred animals may have applications for the study of the mechanisms of immune complex disease.

Animals↗
PubMed1979

Structural observations on epithelioid and giant cells in experimental autoimmune tubulointerstitial nephritis in guinea pigs.

In order to analyze the role of phagocytic cells in experimental antitubular basement membrane (TBM) antibody-mediated nephritis, Hartley guinea pigs (GP) were immunized with rabbit tubular basement membrane (TBM) in complete Freund's adjuvant and pertussis vaccine. Renal tissue was obtained 10 to 15, 15 to 25, and 25 to 35 days after the start of immunization. Severe renal tubulointerstitial (RTI) nephritis developed in 95% of the animals. Linear deposits of IgG and C3 along TBM were seen 10 days after initial immunization. A few days later, monocytes and macrophages infiltrated the interstitium and subsequently differentiated into epithelioid and foreign body-type giant cells (GC). The GC were most actively involved in the destruction of the TBM: Cytoplasmic pseudopodia of the GC adhered to the TBM; the areas of membrane apposition were several microns in length; no evidence of specialization was found in the plasma membrane adjoining the TBM; no cellular organelles, except for abundant microfilaments, were seen in the contact regions. The initial contact was followed by lysis of plasma membrane of the GC and TBM, perforation of TBM, and phagocytosis of TBM fragments. Concomitantly, fluorescent staining for IgG along the TBM became discontinuous or disappeared. Destruction of TBM was accompanied by degeneration of tubular epithelial cells and collapse of tubular architecture. The morphologic observations are consistent with the hypothesis that, in GP, autoimmune RTI nephritis damage of TBM results from the cooperation of humoral and cellular mechanisms, probably akin to those of antibody-mediated lymphocytotoxicity.

Animals↗