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Complement factor B allotypes in the susceptibility and severity of coeliac disease in patients and relatives
Author(s) -
Da Rosa Utiyama S. R.,
Da Silva Kotze L. M.,
De Messias Reason I. T.
Publication year - 2005
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.2005.00529.x
Subject(s) - coeliac disease , allotype , autoantibody , enteropathy , medicine , antibody , complement factor b , first degree relatives , pathogenesis , immunology , immunopathology , endocrinology , biology , complement system , disease , family history
Summary The alternative pathway of complement plays an important role in the pathogenesis of coeliac disease (CD), where factor B (BF) is central to its activation. CD is a gluten‐sensitive enteropathy that results from a complex interplay between genetic, immunologic, and environmental factors. In this study we evaluated the association of BF allotypes with the susceptibility and severity of CD, and with the presence of autoantibodies. Seventy‐six non‐related patients (56 female; 20 male; 2–77 years) and 150 first‐degree relatives (87 female, 63 male; 2–75 years) were investigated. As controls, 97 healthy individuals were included (67 female;, 30 male; 1–71 years). The BF allotypes were determined by high‐voltage agarose gel electrophoresis, followed by specific immunofixation. Disease severity was evaluated by anti‐endomisial antibody (IgA‐EmA) titres and histological findings of intestinal mucosa, which showed a high correlation ( r = 0.8; P < 0.00001) in samples collected simultaneously. IgA‐EmA was detected in all CD patients ingesting gluten, and in 13.3% of the relatives. The IgA‐EmA, smooth muscle, mitochondrial, liver‐kidney microsomal, nuclear, gastric parietal cells, and thyroid microsome antibodies were tested by indirect immunofluorescence. A significant decrease in BF S ( P = 0.026) and an increasing tendency in BF SF allotype ( P = 0.06) were observed in CD patients when compared to their relatives. On the other hand, BF S frequency was increased ( P = 0.001 RR = 2.32) and BF SF ( P = 0.002) decreased in the relatives when compared to the controls. No differences were observed in the distribution of BF phenotypes amongst the CD patients and the control group, and no association was found with CD severity or with the presence of autoantibodies. These results suggest BF SF as a CD susceptibility marker, and BF S as a protection marker of the disease amongst CD families in the Brazilian population.