The Effect of Rheumatoid Factor on the Clearance of Endogenous Immune Complexes Formed in Low-Affinity Mice during the Induction of Immune Complex Disease

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.

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INFECTIOUS VIRUS-ANTIBODY COMPLEXES: INTERACTION WITH ANTI-IMMUNOGLOBULINS, COMPLEMENT, AND RHEUMATOID FACTOR

Journal of Experimental Medicine ◽

10.1084/jem.134.3.41 ◽

1971 ◽

Vol 134 (3) ◽

pp. 41-51 ◽

Cited By ~ 38

Author(s):

Abner Louis Notkins

Keyword(s):

Rheumatoid Factor ◽

Immune Complex ◽

Complex Disease ◽

Infectious Virus ◽

Immune Complex Disease ◽

Virus Antibody ◽

Extensive Coverage ◽

Antiviral Antibody

Interaction of antiviral antibody with the virion can result in the formation of infectious VA complexes. These complexes have been recovered from the blood of chronically infected animals and have been produced in vitro. Incubation of infectious VA complexes with specific anti-immunoglobulins or the purified first and fourth components of complement resulted in neutralization. With subneutralizing concentrations of the first and fourth components of complement, neutralization was enhanced by the addition of the second and third components of complement. RF attached to infectious VA complexes but failed to produce neutralization. The attachment of RF to VA complexes, however, increased the susceptibility of these complexes to neutralization by complement. These findings support the hypothesis that anti-immunoglobulins and complement result in neutralization by more extensive coverage of the surface of the virion than occurs with antiviral antibody alone. Other experiments showed that antiviral antibody increased the sedimentation of radio-labeled virus and that rate-zonal centrifugation could be used to purify VA complexes and to study factors which influence the association and dissociation of these complexes. Our experiments suggest that in vivo the attachment of accessory factors to infectious VA complexes might enhance virus neutralization and play a role in the pathogenesis of virus-induced immune complex disease.

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AUTOLOGOUS IMMUNE COMPLEX NEPHRITIS INDUCED WITH RENAL TUBULAR ANTIGEN

Journal of Experimental Medicine ◽

10.1084/jem.127.3.573 ◽

1968 ◽

Vol 127 (3) ◽

pp. 573-588 ◽

Cited By ~ 78

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.

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