Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-11-20
pubmed:abstractText
Wegener's granulomatosis is a granulomatous and vasculitic disease of unknown origin. Gene polymorphisms are known to affect phenotypes of numerous diseases. Polymorphisms within the angiotensin-converting enzyme (ACE), transforming growth factor-beta1 (TGF-beta1), and interleukin-10 (IL-10) genes are suspected to modify the course of granulomatous disorders. We examined whether the genotype frequencies of the named polymorphisms differ in Wegener's granulomatosis from those in healthy controls. Thirty-nine patients with Wegener's granulomatosis were genotyped for the deletion/insertion polymorphism in intron 16 of the ACE gene, a biallelic polymorphism in codon 25 of the TGF-beta1 gene and a biallelic polymorphism at position -1082 of the IL-10 gene and compared with healthy blood donors. For the ACE polymorphism no significant differences were detected neither in the allele frequencies nor in the genotype frequencies. For TGF-beta1 a trend to genotype CG was found. The most interesting result was the observed, significant shift to genotype AA of the IL-10 polymorphism in Wegener's granulomatosis. IL-10 and TGF-beta1, immunoregulatory cytokines capable of down-regulating T helper cell type 1 response, showed a significant shift or a trend, respectively towards genotypes associated with reduced cytokine release, leading to the hypothesis that different immunoregulatory cytokine patterns dependent on gene polymorphisms might be involved in the pathogenesis of Wegener's granulomatosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0946-2716
pubmed:author
pubmed:issnType
Print
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
665-70
pubmed:dateRevised
2011-7-8
pubmed:meshHeading
pubmed-meshheading:11715070-Adult, pubmed-meshheading:11715070-Alleles, pubmed-meshheading:11715070-Case-Control Studies, pubmed-meshheading:11715070-Codon, pubmed-meshheading:11715070-Cytokines, pubmed-meshheading:11715070-Down-Regulation, pubmed-meshheading:11715070-Female, pubmed-meshheading:11715070-Gene Deletion, pubmed-meshheading:11715070-Genotype, pubmed-meshheading:11715070-Humans, pubmed-meshheading:11715070-Interleukin-10, pubmed-meshheading:11715070-Introns, pubmed-meshheading:11715070-Male, pubmed-meshheading:11715070-Middle Aged, pubmed-meshheading:11715070-Peptidyl-Dipeptidase A, pubmed-meshheading:11715070-Polymerase Chain Reaction, pubmed-meshheading:11715070-Polymorphism, Genetic, pubmed-meshheading:11715070-T-Lymphocytes, pubmed-meshheading:11715070-Transforming Growth Factor beta, pubmed-meshheading:11715070-Transforming Growth Factor beta1, pubmed-meshheading:11715070-Wegener Granulomatosis
pubmed:year
2001
pubmed:articleTitle
Gene polymorphisms of immunoregulatory cytokines and angiotensin-converting enzyme in Wegener's granulomatosis.
pubmed:affiliation
Research Center Borstel, Medical Hospital, Parkallee 35, 23845 Borstel, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't