ArticleThe Journal of allergy and clinical immunology2013
Rapid desensitization of mice with anti-FcγRIIb/FcγRIII mAb safely prevents IgG-mediated anaphylaxis.
Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Bioactive compound ginkgolide B alleviates food allergy by regulating mTOR signaling pathway.Frontiers in immunology · 2026Article
- Importance of mast cell histamine secretion in IgG-mediated systemic anaphylaxis.The Journal of allergy and clinical immunology · 2025Article
- Studies on nanoprotein vaccine alleviating symptoms of mice allergic to rFel d 1.Frontiers in immunology · 2025Article
- Platelet signaling in immune landscape: comprehensive mechanism and clinical therapy.Biomarker research · 2024Review
- Lung ILC2s are activated in BALB/c mice born to immunized mothers despite complete protection against respiratory syncytial virus.Frontiers in immunology · 2024Article
- The B Cell Response and Formation of Allergenic and Anti-Allergenic Antibodies in Food Allergy.Biology · 2023Review
- Blocking the inhibitory receptor programmed cell death 1 prevents allergic immune response and anaphylaxis in mice.The Journal of allergy and clinical immunology · 2022Article
- Allergy, Anaphylaxis, and Nonallergic Hypersensitivity: IgE, Mast Cells, and Beyond.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2022Review
- Platelet FcγRIIA-induced serotonin release exacerbates the severity of transfusion-related acute lung injury in mice.Blood advances · 2021Article
- Non-IgE-Mediated Drug Hypersensitivity Reactions.Current allergy and asthma reports · 2021Review
- Transcriptional frameshifts contribute to protein allergenicity.The Journal of clinical investigation · 2020Article
- Anti-FcγRIIB mAb suppresses murine IgG-dependent anaphylaxis by Fc domain targeting of FcγRIII.The Journal of allergy and clinical immunology · 2018Article
- The pathophysiology of anaphylaxis.The Journal of allergy and clinical immunology · 2017Review
- Pathways of immediate hypothermia and leukocyte infiltration in an adjuvant-free mouse model of anaphylaxis.The Journal of allergy and clinical immunology · 2017Article
- Alternative Anaphylactic Routes: The Potential Role of Macrophages.Frontiers in immunology · 2017Review
- IgG subclasses determine pathways of anaphylaxis in mice.The Journal of allergy and clinical immunology · 2017Article
- Human IgE-independent systemic anaphylaxis.The Journal of allergy and clinical immunology · 2016Review
- Molecular and cellular mechanisms of food allergy and food tolerance.The Journal of allergy and clinical immunology · 2016Review
- Decreased expression of CD200R3 on mouse basophils as a novel marker for IgG1-mediated anaphylaxis.Immunity, inflammation and disease · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundStimulatory IgG receptors (FcγRs) on bone marrow-derived cells contribute to the pathogenesis of several autoimmune and inflammatory disorders. Monoclonal antibodies that block FcγRs might suppress these diseases, but they can induce anaphylaxis.
objectiveWe wanted to determine whether a rapid desensitization approach can safely suppress IgG/FcγR-mediated anaphylaxis.
methodsMice were injected with serially increasing doses of 2.4G2, a rat mAb that blocks the inhibitory FcγR, FcγRIIb, and the stimulatory receptor, FcγRIII. Rectal temperature was used to detect the development of anaphylaxis. Passive and active IgG-mediated anaphylaxis were evaluated in mice that had been rapidly desensitized with 2.4G2 or mock-desensitized in mice in which monocyte/macrophages, basophils, or neutrophils had been depleted or desensitized and in mice in which FcγRI, FcγRIII, and/or FcγRIV had been deleted or blocked.
resultsRapid desensitization with 2.4G2 prevented 2.4G2-induced shock and completely suppressed IgG-mediated anaphylaxis. Rapid desensitization of ovalbumin-sensitized mice with 2.4G2 was safer and more effective than rapid desensitization with ovalbumin. 2.4G2 treatment completely blocked FcγRIII and removed most FcγRI and FcγRIV from nucleated peripheral blood cells. Because IgG(2a)-mediated anaphylaxis was partially FcγRI and FcγRIV dependent, the effects of 2.4G2 on FcγRI and FcγRIV were probably crucial for its complete inhibition of IgG(2a)-mediated anaphylaxis. IgG(2a)-mediated anaphylaxis was partially inhibited by depletion or desensitization of monocyte/macrophages, basophils, or neutrophils.
conclusionIgG-mediated anaphylaxis can be induced by ligation of FcγRI, FcγRIII, or FcγRIV on monocycte/macrophages, basophils, or neutrophils and can be safely suppressed by rapid desensitization with anti-FcγRII/RIII mAb. A similar approach may safely suppress other FcγR-dependent immunopathology.
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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.