IMMUNOGLOBULIN-G SUBCLASS DISTRIBUTION OF ANTIENDOTHELIAL CELL ANTIBODIES (AECA) IN PATIENTS WITH ULCERATIVE-COLITIS OR CROHNS-DISEASE

Citation
D. Aldebert et al., IMMUNOGLOBULIN-G SUBCLASS DISTRIBUTION OF ANTIENDOTHELIAL CELL ANTIBODIES (AECA) IN PATIENTS WITH ULCERATIVE-COLITIS OR CROHNS-DISEASE, Digestive diseases and sciences, 42(11), 1997, pp. 2350-2355
Citations number
31
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01632116
Volume
42
Issue
11
Year of publication
1997
Pages
2350 - 2355
Database
ISI
SICI code
0163-2116(1997)42:11<2350:ISDOAC>2.0.ZU;2-T
Abstract
Anti-endothelial cell antibodies have been described in sera from pati ents with inflammatory bowel disease. The aim of this study was to det ermine, by ELISA, the IgG subclass distribution of anti-endothelial ce ll antibodies, in patients with ulcerative colitis (N = 28) or Crohn's disease (N = 82) as compared with blood donors (N = 95). Thirty-six p ercent of ulcerative colitis and 23% of Crohn's disease patients were positive for at least one of the IgG anti-endothelial cell subclasses. Interestingly, the pattern of IgG anti-endothelial cell subclass obse rved in the two inflammatory bowel diseases differs. In Crohn's diseas e, the IgG(1) anti-endothelial cell antibody level was significantly i ncreased (P < 0.05) while IgG(2) and IgG(4) anti-endothelial cell anti body levels were decreased (P < 0.0001 and P < 0.01, respectively) as compared to ulcerative colitis patients. The immunoglobulin G(3) anti- endothelial cell antibody level was decreased in both ulcerative colit is and Crohn's disease patients as compared to healthy blood donors. N o relationship was detected between disease activity of ulcerative col itis or Crohn's disease patients and anti-endothelial cell IgG subclas ses. Finally, the disparity of IgG anti-endothelial cell subclass dist ribution in these two inflammatory bowel diseases suggests that the ab ility to activate effector mechanisms is not identical, and hence, dea ls with the concept of distinctive pathogenetic mechanisms in these tw o diseases.