ArticleJournal of immunology (Baltimore, Md. : 1950)2019
C1s Inhibition by BIVV009 (Sutimlimab) Prevents Complement-Enhanced Activation of Autoimmune Human B Cells In Vitro.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Insights in bone marrow failure syndromes: take home messages from the 3rd ESH-EBMT-EHA-IPIG translational research conference.Bone marrow transplantation · 2025Article
- Successful rituximab treatment in a seronegative rheumatoid arthritis patient with concurrent cold agglutinin syndrome and immune thrombocytopenia.Rheumatology international · 2024Review
- On the horizon: upcoming new agents for the management of ITP.Hematology. American Society of Hematology. Education Program · 2024Review
- Praziquantel and factor H recruitment differentially affect the susceptibility ofFrontiers in immunology · 2024Article
- Novel therapeutics and future directions for refractory immune thrombocytopenia.British journal of haematology · 2023Review
- Sustained hematologic remission after discontinuation of sutimlimab treatment in patients with cold agglutinin disease.Blood advances · 2023Article
- Sutimlimab suppresses SARS-CoV-2 mRNA vaccine-induced hemolytic crisis in a patient with cold agglutinin disease.Journal of clinical and experimental hematopathology : JCEH · 2023Article
- Cold AIHA and the best treatment strategies.Hematology. American Society of Hematology. Education Program · 2022Article
- A Review of the Immunologic Pathways Involved in Bullous Pemphigoid and Novel Therapeutic Targets.Journal of clinical medicine · 2022Review
- Pemphigus and Pemphigoid: From Disease Mechanisms to Druggable Pathways.The Journal of investigative dermatology · 2022Review
- Complement C1s as a diagnostic marker and therapeutic target: Progress and propective.Frontiers in immunology · 2022Review
- Complement System and Alarmin HMGB1 Crosstalk: For Better or Worse.Frontiers in immunology · 2022Review
- Network analysis indicating the pharmacological mechanism of Yunpi-Qufeng-Chushi-prescription in prophylactic treatment of rheumatoid arthritis.BMC complementary medicine and therapies · 2021Article
- Cold Agglutinin Disease.Clinical hematology international · 2020Review
- Immunological Basis of the Endometriosis: The Complement System as a Potential Therapeutic Target.Frontiers in immunology · 2020Review
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The classical pathway of complement (CP) can mediate C3 opsonization of Ags responsible for the costimulation and activation of cognate B lymphocytes. In this manner, the complement system acts as a bridge between the innate and adaptive immune systems critical for establishing a humoral response. However, aberrant complement activation is often observed in autoimmune diseases in which C3 deposition on self-antigens may serve to activate self-reactive B cell clones. In this study, we use BIVV009 (Sutimlimab), a clinical stage, humanized mAb that specifically inhibits the CP-specific serine protease C1s to evaluate the impact of upstream CP antagonism on activation and proliferation of normal and autoimmune human B cells. We report that BIVV009 significantly inhibited complement-mediated activation and proliferation of primary human B cells. Strikingly, CP antagonism suppressed human Ig-induced activation of B cells derived from patients with rheumatoid arthritis. These results suggest that clinical use of CP inhibitors in autoimmune patients may not only block complement-mediated tissue damage, but may also prevent the long-term activation of autoimmune B cells and the production of autoantibodies that contribute to the underlying pathologic condition of these diseases.
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