Genomic organization of classical human low-affinity Fcγ receptor genes

Su, Kaihong; Wu, Jianming; Edberg, Jeffrey C.; McKenzie, Steven E.; Kimberly, Robert P.

doi:10.1038/sj.gene.6363879

Cited by 68 publications

(69 citation statements)

References 47 publications

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“…Perhaps these results reflect some linkage disequilibrium between the FcgRIIIA and FcgRIIC genes, as they are in close proximity to one other in the genome. 35 36 and RF can stimulate cytokine release from these cells. 37 More recently, the synovial tissue expression of IL-15 was observed.…”

Section: Fccriiia Allelic Polymorphisms In Ramentioning

confidence: 99%

FcγR expression on NK cells influences disease severity in rheumatoid arthritis

et al. 2004

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Section: Fccriiia Allelic Polymorphisms In Ramentioning

confidence: 99%

FcγR expression on NK cells influences disease severity in rheumatoid arthritis

et al. 2004

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“…1). This low-affinity receptor family comprises three class II genes (FCGR2A, FCGR2B, FCGR2C) and two class III genes (FCGR3A, FCGR3B) [24]. Functionally, the gene products, FcgRs, mediate immune responses by binding specifically to the Fc portion of immunoglobulin G molecules.…”

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confidence: 99%

Copy number variation in the human genome and its implication in autoimmunity

Schaschl

Aitman

2009

Clinical and Experimental Immunology

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SummaryThe causes of autoimmune disease remain poorly defined. However, it is known that genetic factors contribute to disease susceptibility. Hitherto, studies have focused upon single nucleotide polymorphisms as both tools for mapping and as probable causal variants. Recent studies, using genome-wide analytical techniques, have revealed that, in the genome, segments of DNA ranging in size from kilobases to megabases can vary in copy number. These changes of DNA copy number represent an important element of genomic polymorphism in humans and in other species and may therefore make a substantial contribution to phenotypic variation and population differentiation. Furthermore, copy number variation (CNV) in genomic regions harbouring dosage-sensitive genes may cause or predispose to a variety of human genetic diseases. Several recent studies have reported an association between CNV and autoimmunity in humans such as systemic lupus, psoriasis, Crohn's disease, rheumatoid arthritis and type 1 diabetes. The use of novel analytical techniques facilitates the study of complex human genomic structures such as CNV, and allows new susceptibility loci for autoimmunity to be found that are not readily mappable by single nucleotide polymorphism-based association analyses alone.

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“…Other than collagen, OPN is the major extracellular matrix protein in bone, and it has been shown to act as an activator in osteoclasts (1). OPN also works as a Th1 cytokine (2,3). Rheumatoid arthritis (RA) is a typical bone resorption inflammatory disease, the pathogenesis of which is thought to stem from Th1 hyperactivation (4).…”

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confidence: 99%

“…However, considering the limitations in studies using knockout mice and previous reports on OPN as a cytokine and a factor in osteoclast activation (1,2,9) 3B (1,3). Linkage of the chromosomal region encompassing FCGR loci with systemic lupus erythematosus (SLE) has been observed (4)(5)(6), and numerous studies have demonstrated association of 1 or more of the FCGR alleles with SLE (1).…”

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confidence: 99%