Lack of association between the chemokine receptor 5 polymorphism CCR5delta32 in rheumatoid arthritis and juvenile idiopathic arthritis

Lindner, Ewald; Nordang, Gry B. N.; Melum, Espen; Flatø, Berit; Selvaag, Anne M; Thorsby, E.; Kvien, Tore K; Førre, Ø; Lie, Benedicte A.

doi:10.1186/1471-2350-8-33

Cited by 29 publications

(24 citation statements)

References 23 publications

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“…Contradictory results have been observed. Lindner et al did not show any association (in a Norwegian population) and Scheibel et al found an association (in a Brazilian population) between this polymorphism and JIA (27,28). When we compared the allele frequencies of our study with these two studies, we recognized that the allele frequencies are different in various populations (in Brazilian, Norwegian, and Turkish populations, delta32 allele frequency in JIA, respectively, is 9.4%, 9.7%, and 3%; in control groups, respectively, is 3.8%, 11.4%, and 2%).…”

Section: Discussionmentioning

confidence: 99%

TNF-alpha 863C > A promoter and TNFRII 196T > G exonic variationsmay be risk factors for juvenile idiopathic arthritis

Batar¹,

Özman²,

Barut³

et al. 2017

Turk J Med Sci

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Background/aim: Juvenile idiopathic arthritis (JIA) is a chronic complex autoimmune disease. Genetic and environmental factors increase the risk of JIA. It is accepted that alterations in immune system pathways play an important role in the pathogenesis of JIA. The aim of the study was to investigate the possible association between immune system regulatory gene polymorphisms and JIA in Turkish patients.

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Section: Discussionmentioning

confidence: 99%

TNF-alpha 863C > A promoter and TNFRII 196T > G exonic variationsmay be risk factors for juvenile idiopathic arthritis

Batar¹,

Özman²,

Barut³

et al. 2017

Turk J Med Sci

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“…These authors also performed a meta-analysis of three studies including .2000 patients and confirmed the protective effect of the polymorphism. One of the studies included in this meta-analysis, however, failed to independently show an association of D32 with JIA (Lindner et al, 2007). Another recent small study showed no correlation of the D32 polymorphism with either the incidence of RA or SLE or disease severity in these patients (Martens et al, 2010).…”

Section: Ccr5mentioning

confidence: 99%

CC Chemokine Receptors and Chronic Inflammation—Therapeutic Opportunities and Pharmacological Challenges

2013

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“…23 A protective effect of CCR5-D32 has also been reported for inflammatory diseases such as rheumatoid arthritis 24 although conflicting results exist. 25 A correlation between the CCR5-D32 and copy number variation within the CCL3L1 gene has been found to enhance HIV/AIDS susceptibility, 26 as well as increase the risk of developing systemic lupus erythematosus. 27 Our results did not support rs333 as the primary causal polymorphism within the CCR1/CCR3/CCR2 gene region.…”

Section: Discussionmentioning

confidence: 99%

Four novel coeliac disease regions replicated in an association study of a Swedish–Norwegian family cohort

et al. 2009

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Recent genome-wide association studies have identified 1q31 (RGS1), 2q11-12 (IL18RAP), 3p21 (CCR1/CCR3/CCR2), 3q25-26 (IL12A/SCHIP1), 3q28 (LPP), 4q27 (IL2/IL21), 6q25 (TAGAP) and 12q24 (SH2B3) as susceptibility regions for coeliac disease (CD). We have earlier replicated association with the IL2/IL21 region. This study aimed at replicating the remaining regions in a family cohort using the transmission disequilibrium test, which is not prone to population stratification as a source of false-positive results. Nine single nucleotide polymorphisms (SNPs) within these regions were genotyped in 325 SwedishNorwegian CD families. We found significant associations with the same alleles in the regions 1q31 (rs2816316; P nc ¼ 0.0060), 3p21 (rs6441961; P nc ¼ 0.0006), 3q25-26 (rs17810564; P nc ¼ 0.0316 and rs9811792; P nc ¼ 0.0434) and 3q28 (rs1464510; P nc ¼ 0.0037). Borderline, but non-significant, associations were found for rs917997 (IL18RAP), whereas no evidence for association could be obtained for rs13015714 (IL18RAP) or rs1738074 (TAGAP). The lack of replication of the latter SNPs could be because of limited power. rs3184504 (SH2B3) was not analysed because of assay failure. The most significantly associated region, 3p21 (CCR1/CCR3/CCR2), was further analysed by typing of 30 SNPs, with the aim of identifying the causal variant responsible for the initial association. Several SNPs showed association with CD, but none displayed associations stronger than rs6441961, nor did any of them add to the effect initially marked by rs6441961 in a conditional analysis. However, differential effects of rs6441961*C carrying haplotypes were indicated, and we thus cannot exclude the possibility that our inability to obtain evidence for multiple independent effects in the CCR1/CCR3/CCR2 gene region was related to a power issue.

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Lack of association between the chemokine receptor 5 polymorphism CCR5delta32 in rheumatoid arthritis and juvenile idiopathic arthritis

Cited by 29 publications

References 23 publications

TNF-alpha 863C > A promoter and TNFRII 196T > G exonic variationsmay be risk factors for juvenile idiopathic arthritis

TNF-alpha 863C > A promoter and TNFRII 196T > G exonic variationsmay be risk factors for juvenile idiopathic arthritis

CC Chemokine Receptors and Chronic Inflammation—Therapeutic Opportunities and Pharmacological Challenges

Four novel coeliac disease regions replicated in an association study of a Swedish–Norwegian family cohort

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