scholarly journals AUTOLOGOUS IMMUNE COMPLEX NEPHRITIS INDUCED WITH RENAL TUBULAR ANTIGEN

1968 ◽  
Vol 127 (3) ◽  
pp. 573-588 ◽  
Author(s):  
Richard J. Glassock ◽  
Thomas S. Edgington ◽  
J. Ian Watson ◽  
Frank J. Dixon
Keyword(s):  
Immune Complex ◽  
Immune Complexes ◽  
Complex Disease ◽  
Membranous Glomerulonephritis ◽  
Immune Complex Disease ◽  
Pathogenetic Mechanism ◽  
Glomerular Deposits ◽  
Circulating Antibodies ◽  
Renal Tubular ◽  
Experimental Allergic

The pathogenetic mechanism involved in a form of experimental allergic glomerulonephritis induced by immunization of rats with renal tubular antigen has been investigated. A single immunization with less than a milligram of a crude renal tubular preparation, probably containing less than 25 µg of the specific nephritogenic antigen, is effective in the induction of this form of chronic membranous glomerulonephritis. In the nephritic kidney autologous nephritogenic tubular antigen is found in the glomerular deposits along with γ-globulin and complement. When large amounts of antigen are injected during induction of the disease the exogenous immunizing antigen can also be detected in the glomerular deposits. It appears that this disease results from the formation of circulating antibodies capable of reacting with autologous renal tubular antigen(s) and the deposition of these antibodies and antigen(s) plus complement apparently as immune complexes in the glomeruli. This pathogenetic system has been termed an autologous immune complex disease and the resultant glomerulonephritis has been similarly designated.

scholarly journals AUTOLOGOUS IMMUNE COMPLEX NEPHRITIS INDUCED WITH RENAL TUBULAR ANTIGEN

1968 ◽  
Vol 127 (3) ◽  
pp. 555-572 ◽  
Author(s):  
Thomas S. Edgington ◽  
Richard J. Glassock ◽  
Frank J. Dixon
Keyword(s):  
Plasma Membrane ◽  
Immune Complex ◽  
Rat Kidney ◽  
Specific Antigen ◽  
Membranous Glomerulonephritis ◽  
Antigenic Specificity ◽  
Normal Rat ◽  
Renal Tubular ◽  
Capillary Walls ◽  
Experimental Allergic

The nephritogenic antigen, responsible for the immunogenic stimulus in experimental allergic glomerulonephritis induced with tubular antigen, has been identified as a renal tubular epithelial (RTE)-specific antigen and has been isolated in a relatively purified form. This antigen, RTE-α5, is a distinct and antigenically specific lipoprotein of high density which is derived primarily from the brush border of proximal convoluted tubular epthelium of the rat kidney. It has been suggested that this molecule may be a plasma membrane subunit. Immunization of rats with as little as 3 µg N of RTE-α5 in complete Freund's adjuvant has effectively induced this form of membranous glomerulonephritis. RTE-α5 is not a constituent of normal rat glomeruli; however, with the onset of autologous immune complex nephritis it is deposited in a granular fashion along glomerular capillary walls indistinguishable from the deposits of γ-globulin and complement. The antigenic specificity of this antigen and its tissue derivation has been explored, and the observations support the autologous immune complex pathogenesis of the glomerulonephritis induced in rats by immunization with renal tubular antigen.

scholarly journals ACUTE IMMUNE COMPLEX DISEASE IN RABBITS

1971 ◽  
Vol 133 (3) ◽  
pp. 554-571 ◽  
Author(s):  
P. M. Henson ◽  
C. G. Cochrane
Keyword(s):  
Immune Complex ◽  
Immune Complexes ◽  
Complex Disease ◽  
Immune Complex Disease ◽  
Neutrophil Accumulation ◽  
Blood Leukocytes ◽  
Complement Components ◽  
Arterial Lesions ◽  
Immunological Reactions ◽  
Independent Reaction

By depletion of C3 from rabbits undergoing acute experimental immune complex disease with an anticomplementary factor in cobra venom, it has been possible to demonstrate that deposition of the complexes in arteries and glomeruli does not require the complement components reacting after C2. Immunological reactions, in which platelets release their vasoactive amines, have been examined in rabbits undergoing immune complex disease. A correlation was obtained between the presence of a complement-independent reaction which required blood leukocytes, antigen and platelets, the deposition of immune complexes, and the induction of glomerulonephritis. C3 depletion did, however, have a marked alleviating effect on the severity of the arterial lesions. Neutrophil accumulation and the subsequent necrotizing arteritis were prevented. In contrast, the character and severity of the glomerulonephritis was not altered by depletion of later-acting complement components.

scholarly journals DISEASE ACCOMPANYING IN UTERO VIRAL INFECTION

1972 ◽  
Vol 135 (4) ◽  
pp. 827-838 ◽  
Author(s):  
Michael B. A. Oldstone ◽  
Frank J. Dixon
Keyword(s):  
Viral Infection ◽  
Immune Complex ◽  
Infected Mouse ◽  
Complex Disease ◽  
In Utero ◽  
Immune Complex Disease ◽  
Immune Complex Glomerulonephritis ◽  
Viral Antibody ◽  
Glomerular Deposits ◽  
Antiviral Antibody

Early, after in utero infection with LCM virus, SWR/J and HA/ICR mice developed manifestations of immune complex disease. Observations based on nursing such mice with virus-infected, immune, or noninfected mouse mothers indicated that maternal antiviral antibody was responsible for the early immune complex glomerulonephritis. Despite comparable viral persistance, in utero-infected offspring failed to develop glomerulonephritis when nursed by noninfected mouse mothers, but did when suckled by virus-infected mouse mothers. Nursing by mouse mothers carrying high titers of anti-LCM viral antibody markedly enhanced the Ig glomerular deposits and the resultant nephritis.

scholarly journals C1q nephropathy: a true immune complex disease or an immunologic epiphenomenon?

2009 ◽  
Vol 2 (4) ◽  
pp. 285-291
Author(s):  
M. Muorah ◽  
M. D. Sinha ◽  
C. Horsfield ◽  
P. J. O'Donnell
Keyword(s):  
Immune Complex ◽  
Complex Disease ◽  
Immune Complex Disease ◽  
C1q Nephropathy
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