The interleukin-4 −34TT and −590TT genotype is correlated with increased expression and protein production in aggressive periodontitis

Gonzáles, José R.; Gröger, Sabine; Haley, Gabriela; Bödeker, Rolf‐Hasso; Meyle, Joerg

doi:10.1016/j.molimm.2009.10.025

Cited by 16 publications

(17 citation statements)

References 17 publications

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“…In our study, we speculate that the effect of this IL‐4 SNP is due to altered IL‐4 transcription and expression as we found that the C to T switch at position ‐590 was associated with increased serum IL‐4 level and the TT, TC, and CC gene variants were associated with high, intermediate, and low IL‐4 production in our patients. These findings confirm and extend previous studies suggesting that IL‐4 promoters harboring ‐590 T allele plays a unique role in the activation of IL‐4 transcription, and that the homozygous individuals of IL‐4‐590 TT had increased IL‐4 production. Gonzales et al stated that SNPs in the IL4 gene promoter could be functional, as demonstrated by increased IL4 concentration and STAT6 mRNA, as well as IL‐4 protein levels, in CD4+ cells of individuals with −34TT and −590TT genotypes.…”

Section: Discussionsupporting

confidence: 91%

“…These findings confirm and extend previous studies suggesting that IL‐4 promoters harboring ‐590 T allele plays a unique role in the activation of IL‐4 transcription, and that the homozygous individuals of IL‐4‐590 TT had increased IL‐4 production. Gonzales et al stated that SNPs in the IL4 gene promoter could be functional, as demonstrated by increased IL4 concentration and STAT6 mRNA, as well as IL‐4 protein levels, in CD4+ cells of individuals with −34TT and −590TT genotypes.…”

Section: Discussionsupporting

confidence: 91%

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Interleukin‐4 ‐590C/T gene polymorphism in Egyptian children with acute lower respiratory infection: A multicenter study

Emam

Shehab

Allah

et al. 2019

Pediatric Pulmonology

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Background Acute lower respiratory infection (ALRI) is the leading cause of child mortality, especially in the developing world. Polymorphisms in the interleukin 4 (IL‐4) gene have been linked to a variety of human diseases. Objectives To investigate whether the IL‐4 ‐590C/T (rs2243250) polymorphism could be a genetic marker for susceptibility to ALRIs in young Egyptian children. Methods This was a multicenter study conducted on 480 children diagnosed with pneumonia or bronchiolitis, and 480 well‐matched healthy control children. Using PCR‐RFLP analysis, we genotyped a ‐590C/T (rs2243250) single nucleotide polymorphism of the IL‐4 gene promoter, meanwhile the serum IL‐4concentration was measured by ELISA. Results The frequency of the IL‐4 ‐590 T/T genotype and T allele were overrepresented in patients with ALRIs in comparison to the control group (OR = 2.0; [95% confidence interval [CI]: 1.38‐2.96]; for the T/T genotype) and (OR: 1.3; [95%CI: 1.07‐1.56]; for the T allele; P < 0.01). The IL‐4 ‐590 T/T genotype was associated with significantly higher mean serum IL‐4 concentration (58.7 ± 13.4 pg/mL) compared to the C/T genotype (47.6 ± 11 pg/mL) and the C/C genotype (34.8 ± 9.6 pg/mL); P < 0.01. Conclusion The IL‐4 −590C/T (rs2243250) polymorphism may contribute to susceptibility to ALRIs in young Egyptian children.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 91%

Interleukin‐4 ‐590C/T gene polymorphism in Egyptian children with acute lower respiratory infection: A multicenter study

Emam

Shehab

Allah

et al. 2019

Pediatric Pulmonology

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“…Although many of these actually proposed mechanisms of adaptive immunity for susceptibility to periodontitis remain speculative, recent data have provided evidence that the increased amounts of interleukin‐4 and interleukin‐13 produced by activated CD4 + cells from northern European patients with aggressive periodontitis are genetically regulated by the interleukin‐4 promoter . Higher levels of interleukin‐4 and interleukin‐13 produced by activated T‐helper 2 cells might increase the number of resting B‐cells, induce their homotypic aggregation and promote their proliferation and differentiation . Thus, considering these results and the previous evidence provided by many other authors to support these mechanisms, it would appear that in patients with aggressive periodontitis, variants in the interleukin‐4 and/or interleukin‐13 genes will genetically drive T‐helper 2 differentiation and antagonize the effects of T‐helper 1 cytokines (Fig.…”

Section: Interactions Of T‐ and B‐cell Subsets In Periodontitismentioning

confidence: 67%

T‐ and B‐cell subsets in periodontitis

Gonzáles¹

2015

Periodontology 2000

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A large amount of information is available, in the medical literature, on the molecular and immunological mechanisms in which T- and B-cells are involved in the pathogenesis of inflammatory diseases. This review attempts to describe the most important features of the T-cell subsets and their cytokine networks in periodontitis, including the interaction of pathogens with different cell subsets and their gene-expression profiles. Additionally, the known interactions of T- and B-cell subsets in periodontitis are described. The purpose of this article was to provide an overview of the cell interactions and cytokine networks specifically involved in the pathogenesis of periodontitis, and models and paradigms from recent research in this area are presented. However, the review of the literature also revealed that relatively little is known about the genetic or structural factors that confer cross-reactivity of natural and/or autoreactive antibodies in the immunopathogenesis of periodontitis. Pathogens, in turn, are continuously evolving and creating mechanisms to evade immunological reactions controlled and modulated by T- and B-cells.

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“…Conversely, IL-4 was described as an inhibitor of RANKL expression, but in certain conditions may increase osteoclast activity [32]. While some studies suggest a possible destructive role for IL-4 in both chronic and aggressive periodontitis [33], [34], other studies suggest that this cytokine has a protective role against tissue destruction [35], [36]. Therefore, it is possible to suppose that FAM5C may somehow modulate/interfere in cytokine network in diseased periodontal tissues, and consequently impact disease outcome.…”

Section: Discussionmentioning

confidence: 99%

FAM5C Contributes to Aggressive Periodontitis

et al. 2010

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Aggressive periodontitis is characterized by a rapid and severe periodontal destruction in young systemically healthy subjects. A greater prevalence is reported in Africans and African descendent groups than in Caucasians and Hispanics. We first fine mapped the interval 1q24.2 to 1q31.3 suggested as containing an aggressive periodontitis locus. Three hundred and eighty-nine subjects from 55 pedigrees were studied. Saliva samples were collected from all subjects, and DNA was extracted. Twenty-one single nucleotide polymorphisms were selected and analyzed by standard polymerase chain reaction using TaqMan chemistry. Non-parametric linkage and transmission distortion analyses were performed. Although linkage results were negative, statistically significant association between two markers, rs1935881 and rs1342913, in the FAM5C gene and aggressive periodontitis (p = 0.03) was found. Haplotype analysis showed an association between aggressive periodontitis and the haplotype A-G (rs1935881-rs1342913; p = 0.009). Sequence analysis of FAM5C coding regions did not disclose any mutations, but two variants in conserved intronic regions of FAM5C, rs57694932 and rs10494634, were found. However, these two variants are not associated with aggressive periodontitis. Secondly, we investigated the pattern of FAM5C expression in aggressive periodontitis lesions and its possible correlations with inflammatory/immunological factors and pathogens commonly associated with periodontal diseases. FAM5C mRNA expression was significantly higher in diseased versus healthy sites, and was found to be correlated to the IL-1β, IL-17A, IL-4 and RANKL mRNA levels. No correlations were found between FAM5C levels and the presence and load of red complex periodontopathogens or Aggregatibacter actinomycetemcomitans. This study provides evidence that FAM5C contributes to aggressive periodontitis.

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The interleukin-4 −34TT and −590TT genotype is correlated with increased expression and protein production in aggressive periodontitis

Cited by 16 publications

References 17 publications

Interleukin‐4 ‐590C/T gene polymorphism in Egyptian children with acute lower respiratory infection: A multicenter study

Interleukin‐4 ‐590C/T gene polymorphism in Egyptian children with acute lower respiratory infection: A multicenter study

T‐ and B‐cell subsets in periodontitis

FAM5C Contributes to Aggressive Periodontitis

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