Juvenile rheumatoid arthritis as a complex genetic trait

Glass, David N.; Giannini, Edward H.

doi:10.1002/1529-0131(199911)42:11<2261::aid-anr1>3.0.co;2-p

Cited by 179 publications

(102 citation statements)

References 66 publications

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“…The sibling risk ratio for a full sibling of a child with JRA is estimated to be 15 (3). These results are consistent with other autoimmune disorders, such as type 1 diabetes (4).…”

supporting

confidence: 75%

A genome‐wide scan for juvenile rheumatoid arthritis in affected sibpair families provides evidence of linkage

Thompson¹,

Moroldo²,

Guyer³

et al. 2004

Arthritis & Rheumatism

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Methods. Genotype data collected for HLA-DR and 386 microsatellite markers were subjected to multipoint nonparametric linkage analysis. Following analysis of the entire set of families, additional analyses were performed after a priori stratification by disease onset type, age at onset, disease course, and selected HLA-DRB1 alleles. Conclusion. These data support the hypothesis that multiple genes, including at least 1 in the HLA region, influence susceptibility to JRA. These findings for JRA are consistent with findings for other autoimmune diseases and support the notion that common genetic regions contribute to an autoimmune phenotype.Collectively, the varied conditions that constitute juvenile rheumatoid arthritis (JRA) represent the most common chronic rheumatic inflammatory conditions of childhood. Current estimates indicate that as many as 50,000 children in the US have been diagnosed with some form of JRA (1). The diagnosis of JRA is complicated by the heterogeneous nature of the clinical phenotypes and has broadly been defined by the American College of Rheumatology (ACR) (2) based on systemic involvement (fevers, rash, and involvement of other organ systems besides the musculoskeletal system) and mode of disease onset (pauciarticular [Յ4 joints] versus polyarticular [Ն5 joints]).Evidence suggests that JRA is a complex genetic disorder that is influenced by multiple genetic and environmental factors. The sibling risk ratio for a full sibling of a child with JRA is estimated to be 15 (3). These results are consistent with other autoimmune disorders, such as type 1 diabetes (4).

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“…The sibling risk ratio for a full sibling of a child with JRA is estimated to be 15 (3). These results are consistent with other autoimmune disorders, such as type 1 diabetes (4).…”

supporting

confidence: 75%

A genome‐wide scan for juvenile rheumatoid arthritis in affected sibpair families provides evidence of linkage

Thompson¹,

Moroldo²,

Guyer³

et al. 2004

Arthritis & Rheumatism

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“…Multiple factors may affect the onset and persistence of musculoskeletal pain in JIA, including biological influences such as genetic (16), anatomical (16) and disease-related factors (17), psychosocial factors (eg, coping and cognitive health beliefs) (18)(19)(20) and environmental/social cultural context such as parental history of pain (21,22). However, the precise mechanisms through which these factors influence pain are not fully understood (23).…”

Section: Predictors Of Pain In Jiamentioning

confidence: 99%

Assessment and Management of Pain in Juvenile Idiopathic Arthritis

et al. 2014

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“…The pathogenesis is not known, but an antigen-driven autoimmune process is proposed, in which auto-reactive T cells play a central role in joint inflammation and destruction. 8,9 Both susceptibility to and severity of this disease are largely genetically determined, 10,11 and the genes responsible are mostly unknown. The only genetic factors that have been firmly shown to contribute to JRA are genes within the HLA complex.…”

mentioning

confidence: 99%

Genetic association between juvenile rheumatoid arthritis and polymorphism in the SH2D2A gene

et al. 2004

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T-cell-specific adapter protein (TSAd) involved in the negative control of T-cell activation is encoded by the SH2D2A gene. Our recent studies indicate that homozygosity for short (ie GA 13 and GA 16 ) alleles of the SH2D2A gene promoter is associated with development of multiple sclerosis. To study whether the same SH2D2A promoter polymorphism also contributes to the genetic susceptibility to develop juvenile rheumatoid arthritis (JRA), we examined 210 JRA patients and 558 healthy unrelated controls from Norway. The frequency of the short allele GA 13 was increased among the JRA patients compared to control (0.098 vs 0.05; P n ¼ 8 ¼ 0.042). There was a significant increased frequency of HLA-DRB1*08-positive patients carrying two copies of 'short' alleles GA 13 and/or GA 16 compared to healthy controls (16% vs 6%; P n ¼ 4 ¼ 0.016). Our data indicate that the 'short' alleles of the SH2D2A promoter could contribute to the genetic susceptibility to JRA.

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Juvenile rheumatoid arthritis as a complex genetic trait

Cited by 179 publications

References 66 publications

A genome‐wide scan for juvenile rheumatoid arthritis in affected sibpair families provides evidence of linkage

A genome‐wide scan for juvenile rheumatoid arthritis in affected sibpair families provides evidence of linkage

Assessment and Management of Pain in Juvenile Idiopathic Arthritis

Genetic association between juvenile rheumatoid arthritis and polymorphism in the SH2D2A gene

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