ArticlePLoS genetics2011
Association of genetic variants in complement factor H and factor H-related genes with systemic lupus erythematosus susceptibility.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 2 of them syntheses that pooled it.
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Who cites it
110 citing papers in PubMed, 2 syntheses or guidelines pooled it, 225 citations in OpenAlex.
- Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens.Nature genetics · 2014Pooled it
- Genome-wide and gene-centric analyses of circulating myeloperoxidase levels in the charge and care consortia.Human molecular genetics · 2013Pooled it
- Interaction of miR-181b andBioMed research international · 2020Trial
- A plausibly causal functional lupus-associated risk variant in the STAT1-STAT4 locus.Human molecular genetics · 2018Trial
- Extended haplotypes at the complement factor H gene locus are associated with liver transplant rejection.Hepatology communications · 2026Article
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- Genetic Insights into Circulating Complement Proteins in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Potential Inflammatory Subgroup.International journal of molecular sciences · 2026Article
- A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.Frontiers in immunology · 2026Review
- Complement proteins associated with circulatory and glomerular IgA-containing immune complexes in patients with IgA nephropathy.Scientific reports · 2025Article
- Evaluation of Serum Complement Components in Pediatric IgA Vasculitis: A Case-Control Study.Children (Basel, Switzerland) · 2025Article
- Systemic lupus erythematosus as the paradigm for understanding the complex immune relationships and therapeutic opportunities for targeting complement in autoimmune diseases.Immunobiology · 2025Review
- The Complement System.Advances in experimental medicine and biology · 2025Review
- Functional and structural characterization of mouse Factor H-related B protein unveils a novel dimerization domain shared by FHR-B and FH.Frontiers in immunology · 2025Article
- A case of non-lupus full-house nephropathy diagnosed by kidney biopsy but observed IgA nephropathy on second biopsy.CEN case reports · 2024Article
- Exploration of potential novel drug targets for diabetic retinopathy by plasma proteome screening.Scientific reports · 2024Article
- The complement factor H-related protein-5 (CFHR5) exacerbates pathological bone formation in ankylosing spondylitis.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Direct enhancement of viral neutralising antibody potency by the complement system: a largely forgotten phenomenon.Cellular and molecular life sciences : CMLS · 2024Review
- Atypical Hemolytic Uremic Syndrome: A Nationwide Colombian Pediatric Series.Global pediatric health · 2024Article
- Factor H-related protein 1 in systemic lupus erythematosus.Frontiers in immunology · 2024Article
- The impact of early pregnancy metabolic disorders on pregnancy outcome and the specific mechanism.European journal of medical research · 2023Review
50 more citing papers are in PubMed but not listed here.
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Authors and funding
57 authors at 19 institutions in 9 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE), a complex polygenic autoimmune disease, is associated with increased complement activation. Variants of genes encoding complement regulator factor H (CFH) and five CFH-related proteins (CFHR1-CFHR5) within the chromosome 1q32 locus linked to SLE, have been associated with multiple human diseases and may contribute to dysregulated complement activation predisposing to SLE. We assessed 60 SNPs covering the CFH-CFHRs region for association with SLE in 15,864 case-control subjects derived from four ethnic groups. Significant allelic associations with SLE were detected in European Americans (EA) and African Americans (AA), which could be attributed to an intronic CFH SNP (rs6677604, in intron 11, P(meta) = 6.6×10(-8), OR = 1.18) and an intergenic SNP between CFHR1 and CFHR4 (rs16840639, P(meta) = 2.9×10(-7), OR = 1.17) rather than to previously identified disease-associated CFH exonic SNPs, including I62V, Y402H, A474A, and D936E. In addition, allelic association of rs6677604 with SLE was subsequently confirmed in Asians (AS). Haplotype analysis revealed that the underlying causal variant, tagged by rs6677604 and rs16840639, was localized to a ~146 kb block extending from intron 9 of CFH to downstream of CFHR1. Within this block, the deletion of CFHR3 and CFHR1 (CFHR3-1Δ), a likely causal variant measured using multiplex ligation-dependent probe amplification, was tagged by rs6677604 in EA and AS and rs16840639 in AA, respectively. Deduced from genotypic associations of tag SNPs in EA, AA, and AS, homozygous deletion of CFHR3-1Δ (P(meta) = 3.2×10(-7), OR = 1.47) conferred a higher risk of SLE than heterozygous deletion (P(meta) = 3.5×10(-4), OR = 1.14). These results suggested that the CFHR3-1Δ deletion within the SLE-associated block, but not the previously described exonic SNPs of CFH, might contribute to the development of SLE in EA, AA, and AS, providing new insights into the role of complement regulators in the pathogenesis of SLE.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.