Activation of classical pathway complement in chronic inflammation. Elevated levels of circulating C3d and C4d split products in rheumatoid arthritis and Crohn's disease.

Split products of complement component 3 (C3) and complement component 4 (C4) derived from activation of the alternative and classical complement pathways were measured in untreated outpatients, 20 with Crohn's disease and 19 with rheumatoid arthritis. Elevated levels of the d split product of C4 (C4d) were observed in 12 of 19 patients with rheumatoid arthritis and in 9 of 20 patients with Crohn's disease. Levels of the d split product of C3 (C3d) were increased in 14 of 19 patients with rheumatoid arthritis and in 6 of 20 Crohn's disease patients. The median values of C4d and C3d were significantly increased in both groups of patients. C3d concentrations correlated positively with C4d levels (rs = 0.51-0.56, p less than 0.005). The complement activation was not reflected in reduced plasma levels of native C3 and C4. The data indicate activation of the classical complement pathway in both rheumatoid arthritis and Crohn's disease.

[1]  J. Elmgreen,et al.  Hypercatabolism of complement in Crohn's disease--assessment of circulating C3c. , 2009, Acta medica Scandinavica.

[2]  J. Elmgreen,et al.  Subnormal sensitivity of neutrophils to complement split product C5a in rheumatoid arthritis: relation to complement catabolism and disease extent. , 1985, Annals of the rheumatic diseases.

[3]  J. Elmgreen.  Subnormal activation of phagocytes by complement in chronic inflammatory bowel disease? Neutrophil chemotaxis to complement split product C5a. , 1984, Gut.

[4]  S. Kreiner,et al.  Incidence and prevalence of ulcerative colitis and Crohn's disease in the County of Copenhagen, 1962 to 1978. , 1982, Gastroenterology.

[5]  D. Vergani,et al.  Correlation in rheumatoid arthritis of concentrations of plasma C3d, serum rheumatoid factor, immune complexes and C-reactive protein with each other and with clinical features of disease activity. , 1982, Clinical and experimental immunology.

[6]  I. Brandslund,et al.  Double-decker rocket immunoelectrophoresis for direct quantitation of complement C3 split products with C3d specificities in plasma. , 1981, Journal of immunological methods.

[7]  K. Skubitz,et al.  Reversal of hemodialysis granulocytopenia and pulmonary leukostasis: A clinical manifestation of selective down-regulation of granulocyte responses to C5adesarg. , 1981, The Journal of clinical investigation.

[8]  H. Müller-Eberhard,et al.  Activation of the fourth component of complement (C4): assessment by rocket immunoelectrophoresis and correlation with the metabolism of C4. , 1980, Journal of immunology.

[9]  D. Jewell,et al.  Humoral immune system in inflammatory bowel disease: I. Complement levels. , 1977, Gut.

[10]  R. Zubler,et al.  Circulating complement breakdown products in patients with rheumatoid arthritis. Correlation between plasma C3d, circulating immune complexes, and clinical activity. , 1977, The Journal of clinical investigation.

[11]  S. Kaplan,et al.  The alternate complement pathway in inflammatory bowel disease. Quantitation of the C3 proactivator (factor B) protein. , 1976, Gastroenterology.

[12]  M. Eastwood,et al.  Proceedings: Serum complement components C3 and C4 in inflammatory bowel disease. , 1974, Gut.

[13]  C. Laurell,et al.  Quantitative estimation of proteins by electrophoresis in agarose gel containing antibodies. , 1966, Analytical biochemistry.

[14]  G. A. Bennett,et al.  1958 REVISION of diagnostic criteria for rheumatoid arthritis. , 1959, Arthritis and rheumatism.

[15]  J. Folkersen,et al.  Immunoelectrophoretic analysis of C4 split products expressing D but not C epitopes: influence of storage, Ca2+ and Ca2+-chelating agents. , 1985, Complement.

[16]  K. Whaley,et al.  Molecular aspects of complement activation , 1981 .