2010
DOI: 10.3109/0886022x.2010.516857
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Effect ofIL-6C-572G polymorphism on idiopathic membranous nephropathy risk in a han chinese population

Abstract: Membranous glomerulonephritis (MGN) is viewed as an immune-mediated glomerular disease, with immunologic expression occurring in genetically susceptible persons. The cytokine interleukin-6 (IL-6) gene polymorphism is known to impair intracellular signaling pathways following adaptive immune response. Our study gauged the effects of IL-6 C-572G (rs1800796) single nucleotide polymorphism (SNP) on MGN among Taiwan's Han Chinese population, as analyzed in 265 controls and 106 MGN patients. Genotyping for IL-6 C-57… Show more

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Cited by 23 publications
(12 citation statements)
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“…High levels of LPS activate the NF-κB pathway and lead to the production of pro-inflammatory cytokines(TNF-α, IL-6, and IL-1) 41 . In agreement with this observation, higher abundance of Escherichia-Shigella and Bacteroides increases the circulating levels of pro-inflammatory cytokines such as TNF-α and IL-6, and genetic polymorphisms in these cytokines are associated with the onset/occurrence of MN 42,43 . Actinomyces has been identified to be abundant in patients with rheumatoid arthritis 44 and ulcerative colitis 45 .…”
Section: Investigation Of the Relationships Between Clinical Parametesupporting
confidence: 69%
“…High levels of LPS activate the NF-κB pathway and lead to the production of pro-inflammatory cytokines(TNF-α, IL-6, and IL-1) 41 . In agreement with this observation, higher abundance of Escherichia-Shigella and Bacteroides increases the circulating levels of pro-inflammatory cytokines such as TNF-α and IL-6, and genetic polymorphisms in these cytokines are associated with the onset/occurrence of MN 42,43 . Actinomyces has been identified to be abundant in patients with rheumatoid arthritis 44 and ulcerative colitis 45 .…”
Section: Investigation Of the Relationships Between Clinical Parametesupporting
confidence: 69%
“…31 Supporting this notion, air pollution increases the circulating levels of inflammation mediators such as TNF-a, IL-6, and plasminogen activator inhibitor-1, 21,32,33 and genetic polymorphisms in these cytokines are associated with the development of MN. [34][35][36][37][38] It would also be interesting to test the existence of any interactions between PM 2.5 exposure and the genetic polymorphisms implicated in MN. 39 There were limitations in our study.…”
Section: Discussionmentioning
confidence: 99%
“…It has been hypothesized that cytokines generated in the airways in response to air pollution can spill over into the circulation, influencing autoimmune responses and distant events [89]. Air pollution increases the circulating levels of inflammation mediators, such as TNF-α, IL-6, and plasminogen activator inhibitor-1 [88, 90], and genetic polymorphisms in these cytokines are associated with the development of MN [91-95]. …”
Section: Environmental Studies Of Pmnmentioning
confidence: 99%