FcγRIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease

Botto, Marina; Theodoridis, Efstathios; Thompson, E. M.; Beynon, Huw; Briggs, David; Isenberg, David; Walport, Mark J.; Davies, Kevin

doi:10.1046/j.1365-2249.1996.33740.x

Cited by 109 publications

(98 citation statements)

References 15 publications

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“…Fc␥RIIA genotype analysis was performed using polymerase chain reaction (PCR)-allelespecific oligonucleotide hybridization (8,13,17,18), PCRrestriction fragment length polymorphism (12,19), sequencespecific primer-PCR (20,21), or amplification-refractory mutation screening-PCR (22). Databases were assembled and assessed at the coordinating center (Department of Hygeine and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece).…”

Section: Methodsmentioning

confidence: 99%

Role of the Fcγ receptor IIA polymorphism in the antiphospholipid syndrome: An international meta‐analysis

Karassa¹,

Bijl²,

Davies³

et al. 2003

Arthritis & Rheumatism

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Objective. To assess the impact of the Fc␥RIIA-R/ H131 polymorphism on the risk for antiphospholipid syndrome (APS), both primary and secondary to systemic lupus erythematosus (SLE).Methods. This international meta-analysis combined data from 9 research teams. Fc␥RIIA-R/H131 genotypes were determined in 481 APS cases (206 with primary APS), 1,420 SLE controls, and 1,655 diseasefree controls. Data were combined using fixed-effects and random-effects models.Results. Compared with disease-free controls, the RR genotype was enriched in the entire group of APS cases (odds ratio [OR] 1.65, 95% confidence interval [95% CI] 1.28-2.14); this was driven mostly by patients with secondary APS (OR 1.95, 95% CI 1.45-2.63). The excess of RR homozygotes but not heterozygotes among APS patients suggested a recessive mode of inheritance, rather than the additive model seen for SLE susceptibility, where RR conferred greatest risk, and RH intermediate risk, for SLE. This probably reflected the additional influence of another opposing genetic effect of HH homozygosity on APS predisposition (OR 0.72 for RH versus HH, 95% CI 0.55-0.96). Among SLE patients, those with APS were more frequently HH homozygotes than heterozygotes (OR 0.56 for RH versus HH, 95% CI 0.39-0.81). HH homozygosity also tended to predominate in primary APS compared with secondary APS (OR 0.50 for RR versus HH, 95% CI 0.25-0.99 by fixed-effects model). There was no significant betweenstudy heterogeneity for any of these effects.Conclusion. The Fc␥RIIA-R/H131 polymorphism is an important determinant of predisposition to APS, with different influences on SLE and APS susceptibility per se.

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Section: Methodsmentioning

confidence: 99%

Role of the Fcγ receptor IIA polymorphism in the antiphospholipid syndrome: An international meta‐analysis

Karassa¹,

Bijl²,

Davies³

et al. 2003

Arthritis & Rheumatism

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“…Other studies, however, did not find an association within their respective European populations. [78][79][80] These differences may be attributable to genetic variances among different ethnic groups. Fc␥RIIA does appear to play an important role in some SLE populations, while playing a smaller (maybe even undetectable) role in others.…”

Section: Fc␥ Receptorsmentioning

confidence: 99%

The genetics of systemic lupus erythematosus: putting the pieces together

2002

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“…The Fc␥ receptors are active in an immune complex clearance and have been considered candidate genes for the disease since the formation and deposition of immune complexes are characteristic of SLE. Low-affinity variants of both Fc␥ receptor IIA and IIIA have been shown to be associated with SLE, and in particular in patients with nephritis [50][51][52][53][54][55][56].…”

Section: Studies Of Candidate Genesmentioning

confidence: 99%

The Genetics of Systemic Lupus Erythematosus

Lindqvist

Alarcón‐Riquelme

1999

Scand J Immunol

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Lindqvist AKB, Alarcón-Riquelme ME. The Genetics of Systemic Lupus Erythematosus. Scand J Immunol 1999;50:562-571. There is considerable evidence that the development of systemic lupus erythematosus (SLE) has a strong genetic basis. For more than 20 years, much effort has been made to understand the genetics of SLE. Association studies in humans suggest the existence of genetic effects by the alleles encoded in the HLA, deficiencies in the complement genes and the low-affinity variants of Fc␥-receptors. In mouse models of SLE at least 13 loci have been identified, including the MHC, linked to lupus-related phenotypes such as nephritis and production of autoantibodies. Recently, linkage studies have been performed in human SLE; one investigating a candidate region based on synteny to a murine susceptibility locus and four genome-wide linkage studies in various populations. Linkage was demonstrated to several chromosomal regions, some of which are syntenic to murine lupus susceptibility loci. Interestingly, many of the identified chromosomal regions co-localise with loci implicated in other autoimmune diseases.

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FcγRIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease

Cited by 109 publications

References 15 publications

Role of the Fcγ receptor IIA polymorphism in the antiphospholipid syndrome: An international meta‐analysis

Role of the Fcγ receptor IIA polymorphism in the antiphospholipid syndrome: An international meta‐analysis

The genetics of systemic lupus erythematosus: putting the pieces together

The Genetics of Systemic Lupus Erythematosus

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