ArticleBlood advances2019
Potentiation of complement regulator factor H protects human endothelial cells from complement attack in aHUS sera.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Reducing sialylation in melanoma increases classical pathway-mediated complement activation.iScience · 2026Article
- Factor H-related 2 levels dictate FHR dimer composition.Scientific reports · 2025Article
- Decreased complement 4 and interleukin-10 as biomarkers in aqueous humour for non-exudative age-related macular degeneration: a case control study.Journal of translational medicine · 2025Article
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Praziquantel and factor H recruitment differentially affect the susceptibility ofFrontiers in immunology · 2024Article
- The contribution of the alternative pathway in complement activation on cell surfaces depends on the strength of classical pathway initiation.Clinical & translational immunology · 2023Article
- Modeling complement activation on human glomerular microvascular endothelial cells.Frontiers in immunology · 2023Article
- Low Levels of Factor H Family Proteins During Meningococcal Disease Indicate Systemic Processes Rather Than Specific Depletion byFrontiers in immunology · 2022Article
- Halting targeted and collateral damage to red blood cells by the complement system.Seminars in immunopathology · 2021Review
- Common haplotypes at the CFH locus and low-frequency variants in CFHR2 and CFHR5 associate with systemic FHR concentrations and age-related macular degeneration.American journal of human genetics · 2021Article
- A Family Affair: Addressing the Challenges of Factor H and the Related Proteins.Frontiers in immunology · 2021Review
- Therapeutic Lessons to be Learned From the Role of Complement Regulators as Double-Edged Sword in Health and Disease.Frontiers in immunology · 2020Review
- Tuning the Functionality by Splicing: Factor H and Its Alternative Splice Variant FHL-1 Share a Gene but Not All Functions.Frontiers in immunology · 2020Review
- Combining SPR with atomic-force microscopy enables single-molecule insights into activation and suppression of the complement cascade.The Journal of biological chemistry · 2019Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the gene encoding for complement regulator factor H (FH) severely disrupt its normal function to protect human cells from unwanted complement activation, resulting in diseases such as atypical hemolytic uremic syndrome (aHUS). aHUS presents with severe hemolytic anemia, thrombocytopenia, and renal disease, leading to end-stage renal failure. Treatment of severe complement-mediated disease, such as aHUS, by inhibiting the terminal complement pathway, has proven to be successful but at the same time fails to preserve the protective role of complement against pathogens. To improve complement regulation on human cells without interfering with antimicrobial activity, we identified an anti-FH monoclonal antibody (mAb) that induced increased FH-mediated protection of primary human endothelial cells from complement, while preserving the complement-mediated killing of bacteria. Moreover, this FH-activating mAb restored complement regulation in sera from aHUS patients carrying various heterozygous mutations in FH known to impair FH function and dysregulate complement activation. Our data suggest that FH normally circulates in a less active conformation and can become more active, allowing enhanced complement regulation on human cells. Antibody-mediated potentiation of FH may serve as a highly effective approach to inhibit unwanted complement activation on human cells in a wide range of hematological diseases while preserving the protective role of complement against pathogens.
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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.