A genetic marker at the OLIG3/TNFAIP3 locus associates with methotrexate continuation in early inflammatory polyarthritis: results from the Norfolk Arthritis Register

Plant, Darren; Farragher, Tracey; Flynn, Edward; Martin, Paul; Eyre, Steve; Bunn, Diane; Worthington, Jane; Symmons, Deborah; Barton, Anne; Thomson, Wendy

doi:10.1038/tpj.2010.80

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…18,[28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43] Several identified SNPs were located in or near genes that might be involved in biological pathway leading to lung function impairment (ie, GALNT13 and PCDH9, respectively). GALNT13 belongs to the GalNAcT family of enzymes, which initiate O-glycosylation of mucins.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide interaction study of gene-by-occupational exposure and effects on FEV1 levels

Jong

Vonk

Timens

et al. 2015

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 99%

Genome-wide interaction study of gene-by-occupational exposure and effects on FEV1 levels

Jong

Vonk

Timens

et al. 2015

Journal of Allergy and Clinical Immunology

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“…No association has been detected with continuation on methotrexate as a monotherapy 9 , response to TNF blockade therapy 10 , or premature mortality 11,12 . However, the markers rs10818488 (r 2 = 0.97 with rs3761847) and rs2900180 have both been correlated with radiological severity 1,13 .…”

mentioning

confidence: 99%

Investigation of Rheumatoid Arthritis Genetic Susceptibility Markers in the Early Rheumatoid Arthritis Study Further Replicates the TRAF1 Association with Radiological Damage

Plant¹,

Fu²,

Flynn³

et al. 2012

J Rheumatol

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Objective.The TRAF1 genetic region conferring susceptibility to rheumatoid arthritis (RA) has been reported to associate with radiological damage. We aimed to test RA genetic susceptibility markers for association with a continuous measure of radiological damage over time using longitudinal modeling techniques.Methods.Sixty-seven RA susceptibility variants were genotyped in 474 patients in the Early Rheumatoid Arthritis Study (ERAS) using Sequenom MassArray technology. Correlation between genetic markers and Larsen score was assessed longitudinally using zero-inflated negative binomial regression to include repeat measurements in the same individual at different timepoints. Genetic markers associated with radiological damage in ERAS were tested using the same modeling techniques on previously published data from the Norfolk Arthritis Register (NOAR).Results.The single marker associated longitudinally with Larsen score in ERAS (p = 0.02) and in NOAR (p = 0.04) was rs2900180 at the TRAF1 locus. Analysis of individual timepoints in ERAS showed that rs2900180 displays its effect primarily on the extent of Larsen score early in the disease course. Combined longitudinal analysis of the 2 cohorts suggests further association of several loci with Larsen score (KIF5A, PTPN22, AFF3, TAGAP) and therefore a significant accumulation of RA severity markers among RA susceptibility markers (p = 0.016).Conclusion.The marker rs2900180 is associated with the extent of radiological damage in the ERAS cohort. This represents the second independent study correlating rs2900180 at the TRAF1 locus with radiological severity in RA. Replication in a large dataset is required to establish the role of other RA susceptibility loci in disease severity.

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“…Interestingly, some SNPs in the A20 locus may protect people from RA, such as rs13207033, which is not associated with RA in isolation but is associated in multivariate models [ 100 ]. In the absence of rs13207033, the combination of rs6920220 and rs5029937 alleles significantly increased the risk of RA [ 101 ]. Rs675520 and rs9376293 were associated with increased joint destruction in ACPA-positive patients but not in APCA-negative patients [ 102 ].…”

Section: Single Nucleotide Polymorphisms (Snps) Of the A20 Gene And Amentioning

confidence: 99%

A20: a master regulator of arthritis

Huang

et al. 2020

Arthritis Res Ther

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A20, also known as TNF-α-induced protein 3 (TNFAIP3), is an anti-inflammatory protein that plays an important part in both immune responses and cell death. Impaired A20 function is associated with several human inflammatory and autoimmune diseases. Although the role of A20 in mediating inflammation has been frequently discussed, its intrinsic link to arthritis awaits further explanation. Here, we review new findings that further demonstrate the molecular mechanisms through which A20 regulates inflammatory arthritis, and we discuss the regulation of A20 by many factors. We conclude by reviewing the latest A20-associated mouse models that have been applied in related research because they reflect the characteristics of arthritis, the study of which will hopefully cast new light on anti-arthritis treatments.

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A genetic marker at the OLIG3/TNFAIP3 locus associates with methotrexate continuation in early inflammatory polyarthritis: results from the Norfolk Arthritis Register

Cited by 14 publications

References 39 publications

Genome-wide interaction study of gene-by-occupational exposure and effects on FEV1 levels

Genome-wide interaction study of gene-by-occupational exposure and effects on FEV1 levels

Investigation of Rheumatoid Arthritis Genetic Susceptibility Markers in the Early Rheumatoid Arthritis Study Further Replicates the TRAF1 Association with Radiological Damage

A20: a master regulator of arthritis

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