Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-8-24
pubmed:abstractText
Studies have shown the important roles of several regulatory and proinflammatory cytokines in insulin-dependent diabetes mellitus (IDDM). CC-chemokine receptors CCR2 and CCR5 bind chemokines that are involved in the trafficking of leukocytes in both basal and inflammatory states. A common 32-bp deletion mutation in the CCR5 gene (CCR5delta32) and a G-to-A nucleotide substitution in the CCR2 at position 190 (CCR2-64I) have recently been described. In the present study, we have determined the frequency of the CCR5delta32 and CCR2-64I alleles in children with IDDM [n = 115; age 1-14 (9.3+/-4.3) y] and in nondiabetic subjects [n = 280; age 1-14 (8.5+/-4.5) y]. The CCR5delta32 allele frequencies were 0.117 in children with IDDM and 0.111 in nondiabetic subjects, indicating that the deletion allele has no association with IDDM. The CCR2-64I allele frequency in children with IDDM was 0.226, which differed significantly from the allele frequency in controls (0.114, p = 0.001). The role of this mutation in IDDM cannot be explained yet, but, because CCR2 mediates the chemotaxis of CD4+ and CD8+ T cells to areas of inflammation and because these cells play important roles in insulitis, a mutation in the CCR2 gene may contribute to the susceptibility to the disease. Alternatively, the 64I allele could be a marker of a linked mutation through linkage disequilibrium. According to these results, the CCR2 gene may be a new candidate for the susceptibility locus of IDDM. However, because no IDDM locus has been identified near 3p21 until now, further investigations are needed to confirm this statement.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0031-3998
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
82-4
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10400139-Adolescent, pubmed-meshheading:10400139-Age of Onset, pubmed-meshheading:10400139-Alleles, pubmed-meshheading:10400139-Child, pubmed-meshheading:10400139-Child, Preschool, pubmed-meshheading:10400139-Diabetes Mellitus, Type 1, pubmed-meshheading:10400139-Female, pubmed-meshheading:10400139-Genotype, pubmed-meshheading:10400139-Humans, pubmed-meshheading:10400139-Infant, pubmed-meshheading:10400139-Male, pubmed-meshheading:10400139-Point Mutation, pubmed-meshheading:10400139-Polymorphism, Genetic, pubmed-meshheading:10400139-Receptors, CCR2, pubmed-meshheading:10400139-Receptors, CCR5, pubmed-meshheading:10400139-Receptors, Chemokine, pubmed-meshheading:10400139-Receptors, Cytokine, pubmed-meshheading:10400139-Reference Values, pubmed-meshheading:10400139-Sequence Deletion
pubmed:year
1999
pubmed:articleTitle
Chemokine receptor CCR2 and CCR5 polymorphisms in children with insulin-dependent diabetes mellitus.
pubmed:affiliation
Heim Pál Pediatric Hospital, Budapest, Hungary.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't