2007
DOI: 10.1371/journal.pmed.0040278
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Abstract: BackgroundRheumatoid arthritis (RA) is a chronic autoimmune disorder affecting ∼1% of the population. The disease results from the interplay between an individual's genetic background and unknown environmental triggers. Although human leukocyte antigens (HLAs) account for ∼30% of the heritable risk, the identities of non-HLA genes explaining the remainder of the genetic component are largely unknown. Based on functional data in mice, we hypothesized that the immune-related genes complement component 5 (C5) and… Show more

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Cited by 240 publications
(233 citation statements)
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“…For the patients from the outpatient clinic, only the RF status was obtained. Patients' characteristics have been described previously (19). As healthy controls, 866 subjects were randomly selected from the Immunogenetics and Transplantation Immunology section of Leiden University Medical Center.…”
Section: Methodsmentioning
confidence: 99%
“…For the patients from the outpatient clinic, only the RF status was obtained. Patients' characteristics have been described previously (19). As healthy controls, 866 subjects were randomly selected from the Immunogenetics and Transplantation Immunology section of Leiden University Medical Center.…”
Section: Methodsmentioning
confidence: 99%
“…Complement activation products such as sC5b-9, Bb, C3a, and C1 inhibitorC1s and C1q-C4 complexes have been shown to be increased in synovial fluid (18)(19)(20)(21)(22), and complement depositions in synovial tissue from RA patients can be visualized by immunohistochemistry (23). Recent genetic association studies have indicated that complement (C5 in one previous study [24]) may be involved in the pathogenesis of human RA. Collectively, the presence of activated complement fragments in synovial fluid, consumption of complement in synovial fluid, and the deposition of complement fragments in the synovium indicate that complement activation does occur in the synovial space and provide evidence of local complement activation in RA.…”
mentioning
confidence: 99%
“…[1][2][3][4] Interestingly, several of these T1D susceptibility loci are shared with other immune-mediated diseases, namely PTPN22, CTLA4, IL2RA, IL2, IL7R and SH2B3 (see Table 1 for full gene names). 1,5,6 Therefore, we sought to test newly identified rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), multiple sclerosis, ankylosing spondylitis (AS) and Crohn's disease (CD) loci for association in T1D [7][8][9][10][11][12][13][14][15][16][17] with the assumption of an increased prior probability of association based on the previous evidence of overlapping risk alleles across autoimmune diseases. 18 We selected single nucleotide polymorphisms (SNPs) for genotyping that had shown a convincing evidence of association with at least one other autoimmune disease from genome-wide association scans published over the past 2 years.…”
mentioning
confidence: 99%
“…18 We selected single nucleotide polymorphisms (SNPs) for genotyping that had shown a convincing evidence of association with at least one other autoimmune disease from genome-wide association scans published over the past 2 years. We genotyped SNPs from the genes: CD58 (rs12044852) which has been associated with multiple sclerosis; 8 STAT3 (rs3816769) which has been associated with CD; 7 IL1A (rs17561) and ERAP1, previously called ARTS1 (rs30187) which have been associated with AS; 15,17 MMEL1-TNFRSF14 (rs3890745), CDK6 (rs42041), the 7q23 gene desert (rs11761231), CCL21 (rs2812378), TRAF1/C5 (rs3761847), KIF5A(rs1678542) and CD40 (rs4810485), which have been associated with RA; 7,12,19 BANK1 (rs10516487), FAM167A previously called C8orf13 (rs13277113) and ITGAM (rs9888739) which have been associated with SLE [9][10][11]20 and STAT4 (rs7574865) and TNFAIP3 (rs6920220 and rs10499194) which have been associated with both RA and SLE 13,14,16,21,22 (See Table 1 for full gene names).…”
mentioning
confidence: 99%