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Effects of a Single Nucleotide Polymorphism on the Expression of Human Tumor Necrosis Factor‐alpha
Author(s) -
Lv K.,
Chen R.,
Cai Q.,
Fang M.,
Sun S.
Publication year - 2006
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2006.01786.x
Subject(s) - tumor necrosis factor alpha , genotype , allele , proinflammatory cytokine , promoter , biology , microbiology and biotechnology , pathogenesis , single nucleotide polymorphism , gene , lipopolysaccharide , cytokine , activator (genetics) , gene expression , immunology , genetics , inflammation
Abstract Tumor necrosis factor (TNF)‐ α plays a prominent role in inflammations and is a proinflammatory cytokine that has been implicated in the pathogenesis of autoimmune and infectious diseases. Recent association studies have found that the TNF‐ α −857T allele was associated with several disorders. Here we demonstrate, with reporter genes under the control of the two allelic TNF‐ α promoters, that the minor allele −857T is a much stronger transcriptional activator than the major allele −857C in RAW264.7 cell line in response to lipopolysaccharide stimulation. However, the result was not consistent in HeLa cell line. Furthermore, for the quantitative analysis of TNF‐ α synthesis between the −857C/C genotype from healthy subjects and the −857C/T genotype from AS patients, the quantitative reverse transcription‐polymerase chain reaction and enzyme‐linked immunosorbent assay were performed separately. There was no significant difference between the two groups at the level of mRNA and protein. These results show that this polymorphism may have a direct effect on TNF‐ α regulation in a tissue‐specific manner, and apart from the polymorphism at −857 in the TNF‐ α promoter, there may be other factors affecting the expression of TNF‐ α .