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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Khodoun, Marat V. Kucuk, Zeynep Yesim Strait, Richard T. Krishnamurthy, Durga Janek, Kevin Clay, Corey D. Morris, Suzanne C. Finkelman, Fred D. |
| Description | Author Affiliation: Khodoun MV ( Department of Research, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio) |
| Abstract | BACKGROUND: Stimulatory 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. OBJECTIVE: We wanted to determine whether a rapid desensitization approach can safely suppress IgG/FcγR-mediated anaphylaxis. METHODS: Mice 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. RESULTS: Rapid 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. CONCLUSION: IgG-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. |
| File Format | HTM / HTML |
| ISSN | 00916749 |
| e-ISSN | 10976825 |
| Journal | Journal of Allergy and Clinical Immunology |
| Issue Number | 6 |
| Volume Number | 132 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2013-12-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Immunology Anaphylaxis Prevention & Control Antibodies, Blocking Administration & Dosage Antibodies, Monoclonal Desensitization, Immunologic Hypersensitivity Therapy Receptors, Igg Antagonists & Inhibitors Immunology Animals Adverse Effects Basophils Drug Effects Body Temperature Disease Models, Animal Complications Macrophages Mice Mice, Inbred Balb C Mice, Inbred C57bl Neutrophils Ovalbumin Research Support, U.s. Gov't, Non-p.h.s. |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
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