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The IL‐10 gene is not involved in the predisposition to inflammatory bowel disease
Author(s) -
Klein Wolfram,
Tromm Andreas,
Griga Thomas,
Fricke Harald,
Folwaczny Christian,
Hocke Michael,
Eitner Klaus,
Marx Michaela,
Runte Maren,
Epplen Jörg Thomas
Publication year - 2000
Publication title -
electrophoresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.666
H-Index - 158
eISSN - 1522-2683
pISSN - 0173-0835
DOI - 10.1002/1522-2683(200011)21:17<3578::aid-elps3578>3.0.co;2-z
Subject(s) - inflammatory bowel disease , genetic predisposition , ulcerative colitis , haplotype , exon , single strand conformation polymorphism , allele , gene , coding region , immunology , pathogenesis , genetics , biology , disease , medicine
Although genetic predisposition for inflammatory bowel disease (IBD) is well established, little is known about the accountable genes. The pathogenesis of IBD is characterized by an imbalanced activation of Th 1 ‐ and Th 2 ‐lymphocytes. IL‐10 represents an anti‐inflammatory cytokine which downregulates the production of Th 1 ‐derived cytokines. To evaluate the role of the IL‐10 gene in IBD, two polymorphisms in the promoter region (G/A at position —1082 and C/A at position —592) were genotyped in 142 patients with Crohn's disease (CD), 104 patients with ulcerative colitis (UC), and 400 healthy controls. Significant differences were not apparent, neither in the allele frequencies of either polymorphism, nor in the haplotype frequencies. Screening of the coding region of the IL‐10 gene by polymerase chain reaction — single strand conformation polymorphism (PCR‐SSCP) analysis revealed a rare sequence variation in exon 1 leading to an amino acid exchange (G→A; G15R) in two patients with CD and five healthy controls. Therefore, polymorphisms of the IL‐10 gene are not demonstrably involved in the predisposition of IBD in our cohorts of patients.