Human IgE-independent systemic anaphylaxis
| Autor: | Fred D. Finkelman, Richard T. Strait, Marat Khodoun |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Platelet-activating factor biology business.industry Immunology Degranulation Basophil Mast cell Immunoglobulin E medicine.disease 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Antigen chemistry biology.protein Immunology and Allergy Medicine Anaphylatoxin business Anaphylaxis 030215 immunology |
| Zdroj: | Journal of Allergy and Clinical Immunology. 137:1674-1680 |
| ISSN: | 0091-6749 |
| DOI: | 10.1016/j.jaci.2016.02.015 |
| Popis: | Anaphylaxis is a rapidly developing, life-threatening, generalized or systemic allergic reaction that is classically elicited by antigen crosslinking of antigen-specific IgE bound to the high-affinity IgE receptor FceRI on mast cells and basophils. This initiates signals that induce cellular degranulation with release and secretion of vasoactive mediators, enzymes, and cytokines. However, IgE-independent mechanisms of anaphylaxis have been clearly demonstrated in experimental animals. These include IgG-dependent anaphylaxis, which involves the triggering of mediator release by IgG/antigen complex crosslinking of FcγRs on macrophages, basophils, and neutrophils; anaphylaxis mediated by binding of the complement-derived peptides C3a and C5a to their receptors on mast cells, basophils, and other myeloid cells; and direct activation of mast cells by drugs that interact with receptors on these cells. Here we review the mechanisms involved in these IgE-independent forms of anaphylaxis and the clinical evidence for their human relevance. We conclude that this evidence supports the existence of all 3 IgE-independent mechanisms as important causes of human disease, although practical and ethical considerations preclude their demonstration to the degree of certainty possible with animal models. Furthermore, we cite evidence that different clinical situations can suggest different mechanisms as having a primal role in anaphylaxis and that IgE-dependent and distinct IgE-independent mechanisms can act together to increase anaphylaxis severity. As specific agents become available that can interfere with mechanisms involved in the different types of anaphylaxis, recognition of specific types of anaphylaxis is likely to become important for optimal prophylaxis and therapy. |
| Databáze: | OpenAIRE |
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