ArticleThe Journal of clinical investigation2024
Complement C3 and marginal zone B cells promote IgG-mediated enhancement of RBC alloimmunization in mice.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 7 citations in OpenAlex.
- A biomimetic cryoprotectant preserves extracellular vesicles bioactivity for intravenous administration and potentiates wound healing.Journal of nanobiotechnology · 2026Article
- Analysis of Erythrocyte Membrane Alloantigens.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Suppression of RBC alloimmunization and regulation of CD4Transfusion · 2026Article
- Murine Models of Transfusion-Induced Red Blood Cell Alloimmunization.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Use of Microbial Microarrays to Define Antibody Specificity.Methods in molecular biology (Clifton, N.J.) · 2026Article
- IgG2b enhances alloantibodies to stored red blood cells.Transfusion · 2025Article
- A spleen is required for antibody mediated immune enhancement but not for RBC clearance or antigen-modulation in mice.Transfusion · 2025Article
- CD47 regulates antigen modulation and red blood cell clearance following an incompatible transfusion.Frontiers in immunology · 2025Article
- Harnessing the potential of red blood cells in immunotherapy.Human immunology · 2024Review
- ABO blood groups and galectins: Implications in transfusion medicine and innate immunity.Seminars in immunologyReview
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Administration of anti-RhD immunoglobulin (Ig) to decrease maternal alloimmunization (antibody-mediated immune suppression [AMIS]) was a landmark clinical development. However, IgG has potent immune-stimulatory effects in other settings (antibody-mediated immune enhancement [AMIE]). The dominant thinking has been that IgG causes AMIS for antigens on RBCs but AMIE for soluble antigens. However, we have recently reported that IgG against RBC antigens can cause either AMIS or AMIE as a function of an IgG subclass. Recent advances in mechanistic understanding have demonstrated that RBC alloimmunization requires the IFN-α/-β receptor (IFNAR) and is inhibited by the complement C3 protein. Here, we demonstrate the opposite for AMIE of an RBC alloantigen (IFNAR is not required and C3 enhances). RBC clearance, C3 deposition, and antigen modulation all preceded AMIE, and both CD4+ T cells and marginal zone B cells were required. We detected no significant increase in antigen-specific germinal center B cells, consistent with other studies of RBC alloimmunization that show extrafollicular-like responses. To the best of our knowledge, these findings provide the first evidence of an RBC alloimmunization pathway which is IFNAR independent and C3 dependent, thus further advancing our understanding of RBCs as an immunogen and AMIE as a phenomenon.
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