Activation of Classical Pathway Complement in Chronic Inflammation
Elevated Levels of Circulating C3d and C4d Split Products in Rheumatoid Arthritis and Crohn`s Disease
NIELS ERIK PETERSEN, JENS ELMGREEN, B0RGE TEISNER and SVEN-ERIK SVEHAG
From the Institute of Medical Microbiology, University of Odense, Odense and Medical Department TIA, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
ABSTRACT. Petersen NE, Elmgreen J, Teisner B, Svehag S*E (Institute of Medical Microbiology, University of Odense, Odense and Medical Department TTA, Rigshospita let, University of Copenhagen, Copenhagen, Denmark). Activation of classical pathway complement in chronic inflammation. Elevated levels of circulating C3d and C4d split products in rheumatoid arthritis and Crohn`s disease. Acta Med Scand 1988; 223:557--60.
Split products of complement component 3 (C3) and complement component 4 (C4) derived from activation of the alternative and classical complement pathways were meas ured 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 in creased in both groups of patients. C3d concentrations correlated positively with C4d levels Crs=0.51--0.56, p<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. Key U)()rds: Crohn` s disease, rheumatoid arthritis, chronic inflammation, complement C3, complement C4.
Normal or even increased levels of complement factor 3 (C3) (1), complement factor 4 (C4) and factor B (2) in sera of patients with rheumatoid arthritis and Crohn` s disease may reflect increased synthesis compensating for enhanced catabolism (3-5). Immune com plexes may be demonstrated in both conditions (6), but neither the site of complement activation nor the etiological factor(s) have been identified. The nature of the antigenic component of immune complexes found in Crohn`s disease remains unidentified.
The aim of the present study was to define the pathway responsible for elevated levels of the d split product of C3 (C3d) inpatients with Crohn`sdisease. For comparison C3d and the d split product of C4 (C4d) were also measured in patients with definite rheumatoid arthritis.
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