ArticleClinical immunology (Orlando, Fla.)2016
Uncoupling complement C1s activation from C1q binding in apoptotic cell phagocytosis and immunosuppressive capacity.
Article in Clinical immunology (Orlando, Fla.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Trial
- A Randomized, First-in-Human, Healthy Volunteer Trial of sutimlimab, a Humanized Antibody for the Specific Inhibition of the Classical Complement Pathway.Clinical pharmacology and therapeutics · 2018Trial
- Do microenvironmental changes in degenerative disc disease reflect in systemic circulation? A proteomic investigation.Clinical proteomics · 2025Article
- Immunomodulatory potential of cytokine-licensed human bone marrow-derived mesenchymal stromal cells correlates with potency marker expression profile.Stem cells (Dayton, Ohio) · 2024Article
- Article
- ACK1 and BRK non-receptor tyrosine kinase deficiencies are associated with familial systemic lupus and involved in efferocytosis.medRxiv : the preprint server for health sciences · 2024Article
- Long-term sutimlimab improves quality of life for patients with cold agglutinin disease: CARDINAL 2-year follow-up.Blood advances · 2023Article
- Review
- Sutimlimab for the Treatment of Cold Agglutinin Disease.HemaSphere · 2023Review
- Balancing the View of C1q in Transplantation: Consideration of the Beneficial and Detrimental Aspects.Frontiers in immunology · 2022Article
- Inhibition of the Classical Pathway of Complement Activation Impairs Bacterial Clearance during Enterococcus faecalis Infection.Infection and immunity · 2021Article
- Complement peptide C3a receptor 1 promotes optic nerve degeneration in DBA/2J mice.Journal of neuroinflammation · 2020Article
- Complement-Mediated Events in Alzheimer's Disease: Mechanisms and Potential Therapeutic Targets.Journal of immunology (Baltimore, Md. : 1950) · 2020Review
- Functional and Structural Characterization of a Potent C1q Inhibitor Targeting the Classical Pathway of the Complement System.Frontiers in immunology · 2020Article
- C1s Inhibition by BIVV009 (Sutimlimab) Prevents Complement-Enhanced Activation of Autoimmune Human B Cells In Vitro.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- C1r/C1s deficiency is insufficient to induce murine systemic lupus erythematosus.Genes and immunity · 2019Article
- Article
- Efferocytosis and autoimmune disease.International immunology · 2018Review
- C1q: A fresh look upon an old molecule.Molecular immunology · 2017Review
- TLR7/8 activation in neutrophils impairs immune complex phagocytosis through shedding of FcgRIIA.The Journal of experimental medicine · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Complement activation contributes to inflammation in many diseases, yet it also supports physiologic apoptotic cells (AC) clearance and its downstream immunosuppressive effects. The roles of individual complement components in AC phagocytosis have been difficult to dissect with artificially depleted sera. Using human in vitro systems and the novel antibody complement C1s inhibitor TNT003, we uncoupled the role of the enzymatic activation of the classical pathway from the opsonizing role of C1q in mediating a) the phagocytosis of early and late AC, and b) the immunosuppressive capacity of early AC. We found that C1s inhibition had a small impact on the physiologic clearance of early AC, leaving their immunosuppressive properties entirely unaffected, while mainly inhibiting the phagocytosis of late apoptotic/secondary necrotic cells. Our data suggest that C1s inhibition may represent a valuable therapeutic strategy to control classical pathway activation without causing significant AC accumulation in diseases without defects in AC phagocytosis.
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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.