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A Z Barabas

Publications and source records attributed to A Z Barabas.

At least 19 recordsLinked to original sources
PubMed1989

Immunoregulation in Heymann nephritis. I. Cell marker studies.

Immunoregulation was examined in rats with Heymann nephritis (HN), an established model of membranous glomerulonephropathy (MGN). There is little known of the cellular immune events for the induction and maintenance of the autoimmune response in HN. The cell marker studies utilized fluorescein (FITC)-labelled monoclonal antibodies directed to B cells (Mark-I), and T cell subsets: pan T (ER-I), helper/inducer T (ER-2) and suppressor/cytotoxic T (ER-3). Lymphoid subsets were compared in spleen, lymph nodes, peripheral blood and bone marrow, of normal and diseased rats. Animals were investigated during the induction and chronic phases of disease. The induction of HN was associated with an early, significant, but transient increase of the non-specific myeloid component of the defence system. Subsequently, a significant increase was seen in the number of cells of the B lymphocyte lineage in HN animals, which coincided well with the overall increased humoral immune responsiveness. No alterations in the T lymphocyte subsets were noted during the development of this experimental autoimmune disease.

Animals↗
PubMed1989

Immunoregulation in Heymann nephritis. II. Functional studies.

In this study, the functional properties of the cells involved in the immunoregulation of Heymann nephritis (HN) have been investigated. HN is a disease model in the rat where the pathology closely resembles membranous glomerulonephropathy (MGN) in man. This autoimmune model is induced by injection of renal tubular antigen (RTA) incorporated in Freund's complete adjuvant (FCA). The strong B cell and plasma cell response in the chronic phase of HN, as determined by cell marker analyses, is predominantly antigen-non-specific. The secondary response pattern found was not only to RTA upon repeated immunization, but also to non-related antigen (SRBC). Although cell marker studies have indicated no major quantitative changes in the T cell population throughout the development of HN, a severe deregulation of the cellular immune response is observed especially during the induction period of HN. This was shown by a strong decrease of the mitogen-induced proliferative response and IL-2 production. This phenomenon is caused by both defective cellular components and inhibitory serological factors. Finally, in the chronic phase, these aberrations gradually return to normal.

Animals↗
PubMed1986

Effect of cationic proteins on the glomerular deposition of anionic proteins and immune complexes.

When 3 mg of cationized human IgG (cIgG, pI greater than 9) was injected intravenously into mice and followed 15 min later by 3 mg anionized bovine serum albumin (aBSA, pI = 4), deposits were detected along the capillary loops and in the mesangium. Additional infusion of immunoaffinity-purified rabbit anti-BSA antibodies 1 h later led to their deposition at the same location. Intravenous injection of an equivalent amount of preformed BSA-anti-BSA or aBSA-anti-BSA immune complexes into mice with glomerular planted cIgG gave rise to few deposits. Similarly, the perfusion of preformed aBSA-anti-BSA complexes in isolated rat kidneys with planted cIgG led to granular deposition of both, but the intensity of staining was less than when sequential perfusions were used. Cationic macromolecules bound to the glomerulus may lead to the deposition of anionic macromolecules and anionic immune complexes.

Animals↗
PubMed1986

Stimulation of circulating autoantibody levels in the rat with established progressive passive Heymann nephritis.

Rats with established progressive passive Heymann nephritis (PPHN) were stimulated with tubular nephritogenic antigen derived from rat kidney fraction 3 (rKF3) or heterologous antibody to the eKF3 antigen. Rats stimulated with antigen had elevated levels of circulating autoantibody and increased amounts of rat IgG in a beaded pattern around the glomerular capillaries. The brush border (BB) region of the proximal convoluted tubules also stained for rat IgG. Rats stimulated with antibody had similar changes, but in addition the injected antibody was demonstrated in the glomerular deposits and in the BB region of the proximal convoluted tubules. Proteinuria was markedly increased in the antibody injected rats. This study indicates that the cells of the 'primed' immune system of rats with PPHN can be stimulated by 'additional' rKF3 antigen or antibody to it, to produce increased levels of circulating autoantibody. It is suggested that the progression of PPHN is dependent on the availability and access of the nephritogenic autoantigen to the immune system and that autoantigen may be released by autoantibody.

Animals↗
PubMed1986

Passive Heymann nephritis in pre- and post-natal rats.

Passive Heymann nephritis (PHN) was induced in pre- and post-natal rats by a single intra-peritoneal injection of 0.2 ml of a rabbit anti-rat kidney fraction 3 (rKF3) antibody. Immune complex formation occurred only in those glomeruli or parts of glomeruli which were open to the circulation. Double staining of kidney sections for the glomerular nephritogenic antigen and rabbit IgG, 2 days after the injection of the antibody showed an identical distribution of both components in the glomeruli. In rats killed more than 4 days after the injection of the anti-rKF3 antibody, the nephritogenic antigen could be demonstrated in the subcapsular glomeruli, in the absence of rabbit IgG; and the same applied when the kidneys had reached maturity. When the injected antibody was expected to be present in the circulation, no nephritogenic antigen was demonstrated in the glomeruli in the absence of the heterologous IgG. These observations indicate that the nephritogenic antigen appears in the glomerulus at the same time as the glomerular capillary loops open to the circulation. Unlike PHN in the adult rat, the immune complexes in the glomeruli of neonatal rats do not persist longer than 84 days.

Aging↗
PubMed1985

Passive Heymann-like nephritis in the rabbit.

Rabbits injected with a guinea-pig anti-rabbit kidney fraction 3 antiserum developed immune complex deposition in the glomerulus which disappeared by the sixth day. The distribution of the glomerular deposits was similar to those of passive Heymann nephritis in the rat. A glomerular fixed antigen was not demonstrated in normal rabbit kidneys after perfusion with the guinea-pig anti-tubular antiserum. When tubular antigen was injected intraperitoneally in saline it could be detected in the glomeruli and after injection of the anti-tubular antiserum the deposits stained with increased intensity. Addition of a small amount of anti-GBM antiserum to the anti-tubular antiserum enhanced the size and number of glomerular deposits and increased their survival time. It is concluded that there is no pre-existing tubular antigen in the rabbit glomerulus and that the injected heterologous anti-tubular antiserum releases antigen from an extraglomerular source, probably the proximal tubules, and this released antigen becomes trapped in the glomerulus.

Animals↗
PubMed1985

Progressive passive Heymann nephritis: induction of autologous antibodies to rat brush border by multiple injections of heterologous antiserum.

Multiple i.v. injection of a heterologous anti-rat kidney fraction 3 antiserum and guinea pig anti-rabbit F3 into rats produced a progressive immune complex glomerulonephritis. The kidney disease was characterized by diffuse beaded deposition of rat gammaglobulin along the glomerular capillaries and proteinuria. Gammaglobulin eluted from the kidneys reacted with the brush border region of normal rat kidney frozen sections. Control animals did not develop the progressive disease. It appears that multiple i.v. injections of the heterologous antisera are capable of inducing an autoimmune kidney disease which is similar to Heymann nephritis.

Animals↗
PubMed1983

The effect of pre-injection of rat kidney F3 antigen on the development of passive Heymann nephritis.

The effect of repeated i.p. injections of a small dose of rat kidney F3 antigen, in an aqueous solution, on the development of passive Heymann nephritis in the rat has been investigated. The test animals receiving the antigen before the i.v. injection of the heterologous antibody developed more numerous and larger immune complexes on the epithelial side of the glomerular basement membrane than the control rats. It is suggested that the injected antigen is trapped in the glomerular basement membrane at sites where the pre-existing nephritogenic antigen is present making it possible for the more numerous and larger deposits to form.

Animals↗
PubMed1982

Progressive passive Heymann nephritis in the rat.

Progressive passive Heymann nephritis was produced in rats by simultaneous intravenous injections of heterologous antirat glomerular basement membrane antiserum and heterologous antirat kidney tubular fraction 3 antibody. The animals were killed at 16 weeks by which time approximately one-half of them were severely proteinuric. The glomeruli showed beaded immune deposits around the capillaries by immunofluorescence, and on electron microscopy osmiophilic deposits were noted in the subepithelial zones and within the glomerular basement membrane. The lesion resembled that of severe Heymann nephritis. gamma-Globulin eluted from the kidneys contained an autologous IgG that reacted with the brush border region of the renal proximal tubules of normal rats. This component was present in proteinuric and nonproteinuric animals. It is concluded that the progression results from the development of autoantibodies to the tubular nephritogenic antigen and the proteinuria is related to increasing deposition of immune complexes in the glomeruli.

Animals↗
PubMed1981

Immune-complex nephritis in the rabbit produced by injections of rat renal tubular fraction 3 antigen.

Rabbits used for the production of anti-rat kidney tubular fraction 3 antibody developed a form of immune-complex glomerulonephritis which was characterized by the deposition of immune complexes in the glomerular basement membrane and in the mesangium. The deposits were composed of the injected rat kidney antigen and rabbit antibody to the injected antigen. Eluted gamma-globulin obtained from the diseased rabbit kidneys reacted only with the brush-border region of the proximal convoluted tubules of normal rat kidney sections but not with normal rabbit kidney sections, in an indirect fluorescent antibody test. The developing kidney disease does not appear to have an autoimmune component.

Animals↗
PubMed1981

Unilateral Masugi nephritis in the rat.

In unilateral nephritis produced in rats by clamping one kidney, injecting heterologous Masugi antiserum prepared from homogenates of cortex, and releasing the clamp after 30 to 60 minutes, nephritis develops in the unclamped kidney. In the clamped kidney, although nephritis does not occur, the injected heterologous antibody can be demonstrated in the glomeruli with immunofluorescence techniques, and the intensity increases with time. Antirat glomerular basement membrane antisera and antirat tubular fraction 3 antisera were raised separately in rabbits. Rats with one kidney pedicle clamped were injected with antirat raised separately in rabbits. Rats with one kidney pedicle clamped were injected with antirat glomerular basement membrane antiserum alone, antirat tubular fraction 3 alone, or a mixture of both. The clamp was released after 1 hour. Frozen sections of the kidney were stained at intervals for the presence of rabbit IgG and rat IgG. When antirat glomerular basement membrane was injected alone, faint linear fluorescence was noted at 24 hours in the clamped kidney, and this did not increase over 4 weeks. Antirat tubular fraction 3 antiserum injected alone showed fine granular deposits around the capillary walls at 24 hours, and the intensity of fluorescence increased with time. When a mixture of antirat glomerular basement membrane and antirat tubular fraction 3 was injected, in the clamped kidney, there was initially faint linear fluorescence. By the 8th day, a granular pattern was noted superimposed on a linear background. By 32 days, the granular pattern was evident. The presence of subepithelial deposits was confirmed by electron microscopy. It is deduced that the slow reacting factor in Masugi antiserum prepared from homogenates of cortex is partly a "contaminating" antitubular antibody and that injections of Masugi antiserum may produce two superimposed types of immunologic glomerular lesions.

Animals↗
PubMed1980

Irreversible attachment of immunoglobulins and F(ab')2 fragments to their specific cell membrane antigens.

Antiserum was raised in sheep against rat kidney glomerular basement membrane, and the antibodies and their F(ab')2 fragments were prepared. These were reacted with one arm of the bifunctional reagent toluene diisocyanate at pH 7.5 and injected into the tail vein of rats. Kidney sections were taken from the rats and, after washing, incubated at pH 8.5 to permit the other arm of the toluene diisocyanate to become reactive. This procedure resulted in the specific irreversible attachment of the antibodies and their F(ab')2 fragments to their corresponding glomerular basement membrane antigens.

Animals↗
PubMed1977

IgA nephropathy.

This presentation attempts to define the criteria for diagnosis of the suggested clinicopathologic entity of IgA nephropathy. Of 250 patients in whom renal biopsies with immunofluorescence, light and electron microscopic, and clinical data were available, 12 patients (4.8 per cent) showed predominance of IgA with localization mainly in the mesangium, a variable degree of mesangial cell proliferation, and increased mesangial matrix on light microscopy. Electron densities were restricted to the mesangium and paramesangial areas. IgA was accompanied by C3 only in two patients, by IgG and C3 in five, and by IgG, IgM, and C3 in five. Properdin was found in 11 of these 12 cases. There was a marked male predominance. All showed gross or microscopic hematuria and variable proteinuria. Ten had had normal renal function tests at the time of presentation, and there was no significant worsening of renal function in the 11 patients followed for six to 84 months after biopsy. No morphologic change was detected in two repeat biopsies six and seven years after the initial biopsies. These 12 patients appear to form a distinct clinicopathologic entity. They can only be separated from other glomerular disorders with IgA when the morphologic and clinical findings are considered in combination with the finding of diffuse IgA predominance on renal biopsy.

Complement C3↗