ArticleBlood advances2018
Recombinant factor VIII Fc fusion protein drives regulatory macrophage polarization.
Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Trial
- Myeloid Cell Function and Cytokine Profiles in Paediatric Haemophilia A: Insights From FVIII and Emicizumab Prophylaxis.Journal of cellular and molecular medicine · 2026Article
- Macrophage fate: to kill or not to kill?Infection and immunity · 2024Review
- Factor VIII moiety of recombinant Factor VIII Fc fusion protein impacts Fc effector function and CD16Frontiers in immunology · 2024Article
- Unveiling Atherosclerotic Plaque Heterogeneity and SPP1Journal of inflammation research · 2024Article
- Rescue immune tolerance induction with a recombinant factor Fc-fused VIII: prospective ReITIrate study of clinical, humoral and cellular immune responses.Therapeutic advances in hematology · 2024Article
- Factor VIII-Fc Activates Natural Killer CellsFrontiers in immunology · 2021Article
- Emerging benefits of Fc fusion technology in the context of recombinant factor VIII replacement therapy.Haemophilia : the official journal of the World Federation of Hemophilia · 2020Review
- Factor VIII Fc Fusion Protein but not FVIII Drives Human Monocyte-Derived Dendritic Cell Activation via FcγRIIa.HemaSphere · 2020Article
- Recombinant Factor VIII Fc Inhibits B Cell Activation via Engagement of the FcγRIIB Receptor.Frontiers in immunology · 2020Article
- Hemophilia A Inhibitor Subjects Show Unique PBMC Gene Expression Profiles That Include Up-Regulated Innate Immune Modulators.Frontiers in immunology · 2020Article
- Fc-Fusion Drugs Have FcγR/C1q Binding and Signaling Properties That May Affect Their Immunogenicity.The AAPS journal · 2019Article
- The Neonatal Fc Receptor (FcRn): A Misnomer?Frontiers in immunology · 2019Review
- Immunomodulation in Primary Immune Thrombocytopenia: A Possible Role of the Fc Fragment of Romiplostim?Frontiers in immunology · 2019Review
- PDL1 Fusion Protein Protects Against Experimental Cerebral Malaria via Repressing Over-Reactive CD8Frontiers in immunology · 2018Article
- Joint Bleeding Tendencies in Adult Patients With Hemophilia: It's Not All Pharmacokinetics.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main complication of replacement therapy with factor in hemophilia A (HemA) is the formation of inhibitors (neutralizing anti-factor VIII [FVIII] antibodies) in ∼30% of severe HemA patients. Because these inhibitors render replacement FVIII treatment essentially ineffective, preventing or eliminating them is of top priority in disease management. The extended half-life recombinant FVIII Fc fusion protein (rFVIIIFc) is an approved therapy for HemA patients. In addition, it has been reported that rFVIIIFc may induce tolerance to FVIII more readily than FVIII alone in HemA patients that have developed inhibitors. Given that the immunoglobulin G1 Fc region has the potential to interact with immune cells expressing Fc receptors (FcRs) and thereby affect the immune response to rFVIII, we investigated how human macrophages, expressing both FcRs and receptors reported to bind FVIII, respond to rFVIIIFc. We show herein that rFVIIIFc, but not rFVIII, uniquely skews macrophages toward an alternatively activated regulatory phenotype. rFVIIIFc initiates signaling events that result in morphological changes, as well as a specific gene expression and metabolic profile that is characteristic of the regulatory type Mox/M2-like macrophages. Further, these changes are dependent on rFVIIIFc-FcR interactions. Our findings elucidate mechanisms of potential immunomodulatory properties of rFVIIIFc.
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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.