Circulating immune complexes and complement C4 null alleles in patients operated on for premature atherosclerotic peripheral vascular disease

Citation
S. Nityanand et al., Circulating immune complexes and complement C4 null alleles in patients operated on for premature atherosclerotic peripheral vascular disease, J CLIN IMM, 19(6), 1999, pp. 406-413
Citations number
48
Categorie Soggetti
Immunology
Journal title
JOURNAL OF CLINICAL IMMUNOLOGY
ISSN journal
02719142 → ACNP
Volume
19
Issue
6
Year of publication
1999
Pages
406 - 413
Database
ISI
SICI code
0271-9142(199911)19:6<406:CICACC>2.0.ZU;2-E
Abstract
Circulating immune complexes can lead to vascular inflammation and prematur e atherosclerosis and the fourth component of complement, C4, plays an impo rtant role in the removal of immune complexes. The objective of this study was to analyze the relation between circulating immune complexes and C4 nul l alleles in patients operated on for peripheral vascular disease before th e age of 50. The prevalence of circulating immune complexes and null allele s of C4 (C4Q0) was determined in 62 patients with peripheral atherosclerosi s requiring surgery before 50 years of age and in a matched control group. C4A and C4B null alleles (C4A*Q0, C4B*Q0) were determined by electrophoresi s of plasma, followed by immunofixation. C4A and C4B concentrations were me asured by ELISA. Circulating immune complexes were determined by sucrose de nsity gradient centrifugation and gel filtration. There was no difference i n the distribution of C4Q0 between patients and controls. The patients had higher prevalences and levels of circulating immune complexes. This was cor related with the presence of C4Q0, especially C4A*Q0. There was an inverse correlation of concentration of circulating immune complexes with C4A level s and with ratio of C4A/B levels. Thus, a significant proportion of patient s with premature peripheral atherosclerosis had circulating immune complexe s and C4A*Q0 enhanced the propensity to immune complex formation. This migh t represent one mechanism for vascular damage in this patient group.