Linked Life Data

11929587

Source:http://linkedlifedata.com/resource/pubmed/id/11929587

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-4-3
pubmed:abstractText
We investigated the allelic distributions of single nucleotide polymorphisms (SNPs) of the TNFA, TNFB and IKBL genes, 3 microsatellites within the tumor necrosis factor (TNF) region of HLA locus, and the HLA phenotypes as well as the TLR4 gene in Chromosome 9 in 26 healthy Caucasian volunteers. These individuals were also assessed as ultraviolet B (UVB)-susceptible (S) or UVB-resistant (R). Our results identified 12 UVB-S and 14 UVB-R individuals. Attempts to correlate particular HLA-A, -B, -C, and -DR antigens with the UVB phenotypes failed. Similarly, attempts to correlate SNP at the NcoI-RFLP within intron 1 of the TNFB, IKBL and TLR4 gene with UVB phenotypes also failed. However, microsatellite analyses of TNFa, TNFc, and TNFd markers revealed a significant increase in the frequencies of TNFa2 in UVB-S individuals (P=0.00032) and of TNFd3 in UVB-R individuals (P=0.012). Moreover, DNA sequencing analyses of 5 SNPs of the TNFA promoter region revealed a significant increase in the frequency of the allele B of the TNFA gene (TNFApB) representing the nucleotide A at position -863 and C at position -1031 (P=0.015). Since it is known that TNFa2 and TNFApB is a high TNF-alpha responder, whereas TNFd3 is a TNF-alpha low responder, we propose that the TNF region of HLA contains polymorphic genes that confer susceptibility and resistance to the deleterious effects of UVB radiation on the induction of contact hypersensitivity. This proposal is consistent with previous reports that a unique microsatellite region of the Tnfa gene in mice contains alleles that dictate the UVB-dependent phenotypes in mice, and implicate TNF-alpha as the primary mediator of the immune-damaging effects of UVB radiation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0001-2815
pubmed:author
pubmed:issnType
Print
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
369-78
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11929587-Dermatitis, Contact, pubmed-meshheading:11929587-Drosophila Proteins, pubmed-meshheading:11929587-Gene Frequency, pubmed-meshheading:11929587-Histocompatibility Antigens Class II, pubmed-meshheading:11929587-Histocompatibility Testing, pubmed-meshheading:11929587-Humans, pubmed-meshheading:11929587-Immune System, pubmed-meshheading:11929587-Membrane Glycoproteins, pubmed-meshheading:11929587-Microsatellite Repeats, pubmed-meshheading:11929587-Phenotype, pubmed-meshheading:11929587-Polymorphism, Restriction Fragment Length, pubmed-meshheading:11929587-Polymorphism, Single Nucleotide, pubmed-meshheading:11929587-Promoter Regions, Genetic, pubmed-meshheading:11929587-Receptors, Cell Surface, pubmed-meshheading:11929587-Toll-Like Receptor 4, pubmed-meshheading:11929587-Toll-Like Receptors, pubmed-meshheading:11929587-Tumor Necrosis Factor-alpha, pubmed-meshheading:11929587-Ultraviolet Rays
pubmed:year
2001
pubmed:articleTitle
Polymorphisms in the tumor necrosis factor (TNF) genes are associated with susceptibility to effects of ultraviolet-B radiation on induction of contact hypersensitivity.
pubmed:affiliation
Department of Dermatology, Clinical Research Institute, National Tokyo Medical Center, 2-5-1 Higeshi-ga-oka, Meguro, Tokyo 152-8902, Japan. hniizeki@ntmc.hosp.go.jp
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.