ACUTE IMMUNE COMPLEX DISEASE IN RABBITS

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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Immune complexes: characteristics, clinical correlations, and interpretive approaches in the clinical laboratory.

Clinical Chemistry ◽

10.1093/clinchem/28.6.1259 ◽

1982 ◽

Vol 28 (6) ◽

pp. 1259-1271 ◽

Cited By ~ 25

Author(s):

S E Ritzmann ◽

J C Daniels

Keyword(s):

Immune Complex ◽

Lupus Erythematosus ◽

Immune Complexes ◽

Complex Disease ◽

Clinical Medicine ◽

Clinical Laboratory ◽

Therapeutic Monitoring ◽

Serum Samples ◽

Complement Components ◽

Antigen Antibody

Abstract Immune-complex-mediated injury is thought to play a role in diseases such as rheumatoid arthritis, systemic lupus erythematosus, serum sickness, various infectious diseases, and malignancies. With increased appreciation of the biological and pathological significance of circulating immune complexes has come efforts to develop appropriate techniques for identifying and measuring them. Common approaches exploit such phenomena as the attachment of complement components to antigen-antibody complexes, the presence of specialized receptors for immune complexes at the surface of cells, and the ability of rheumatoid factor to bind with immune complexes. This variety of assay systems for immune complexes has yielded abstruse results in numerous human pathological conditions. Unfortunately, these results seldom correlate with one another in a given disease. Thus, use of a panel of immune complex assays has been recommended. Indirect consequences of immune complex disease may still be appraised and evaluated with some confidence in clinical medicine: measurements of C3 and C4, cryoglobulins, serum viscosity, and turbidity of serum samples. Measurement of immune complexes may be useful in diagnosis, prognosis, and therapeutic monitoring, but it is the characterization of immune complexes that holds the greatest potential for better understanding of disease mechanisms.

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Complement, immune complexes and immune complex disease

Complement in Health and Disease ◽

10.1007/978-94-011-2214-6_7 ◽

1993 ◽

pp. 199-228 ◽

Cited By ~ 2

Author(s):

Y. C. Ng ◽

J. A. Schifferli

Keyword(s):

Immune Complex ◽

Immune Complexes ◽

Complex Disease ◽

Immune Complex Disease

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

International Archives of Allergy and Immunology ◽

10.1159/000234357 ◽

1987 ◽

Vol 83 (2) ◽

pp. 206-209 ◽

Cited By ~ 7

Author(s):

Madeleine E. Devey ◽

D.N. Hogben

Keyword(s):

Rheumatoid Factor ◽

Immune Complex ◽

Immune Complexes ◽

Complex Disease ◽

Immune Complex Disease

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Guinea pigs with inherited deficiencies of complement components C2 or C4 have characteristics of immune complex disease.

Journal of Clinical Investigation ◽

10.1172/jci112628 ◽

1986 ◽

Vol 78 (3) ◽

pp. 689-695 ◽

Cited By ~ 28

Author(s):

E C Böttger ◽

T Hoffmann ◽

U Hadding ◽

D Bitter-Suermann

Keyword(s):

Immune Complex ◽

Guinea Pigs ◽

Complex Disease ◽

Immune Complex Disease ◽

Complement Components

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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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