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Allergic Reactions02:06

Allergic Reactions

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Overview
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Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

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Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin,...
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Hypersensitivity Reactions: Immune-Complex Reactions01:19

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Hypersensitivities01:30

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Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
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Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing...
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Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial...
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Related Experiment Video

Updated: Mar 21, 2026

Humanized Mediator Release Assay as a Read-Out for Allergen Potency
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Human IgE-independent systemic anaphylaxis.

Fred D Finkelman1, Marat V Khodoun2, Richard Strait3

  • 1Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio; Department of Medicine, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio; Division of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio.

The Journal of Allergy and Clinical Immunology
|May 1, 2016
PubMed
Summary
This summary is machine-generated.

Anaphylaxis can be triggered by mechanisms beyond IgE antibodies. Research suggests IgG antibodies, complement factors, and direct mast cell activation are important in human anaphylaxis.

Keywords:
AnaphylatoxinFcγRFcεRIgEIgGbasophilcomplementmast cellmouse

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Area of Science:

  • Immunology
  • Allergy
  • Pathophysiology

Background:

  • Anaphylaxis is a severe allergic reaction typically involving immunoglobulin E (IgE).
  • IgE triggers mast cells and basophils to release mediators causing anaphylaxis.
  • However, IgE-independent pathways are known in animal models.

Purpose of the Study:

  • To review IgE-independent anaphylaxis mechanisms.
  • To assess clinical evidence for these mechanisms in humans.
  • To discuss the implications for anaphylaxis diagnosis and treatment.

Main Methods:

  • Literature review of experimental and clinical studies.
  • Analysis of evidence for IgG-dependent, complement-mediated, and direct mast cell activation pathways.
  • Evaluation of human relevance and clinical data.

Main Results:

  • IgG-dependent anaphylaxis involves IgG/antigen complexes and FcγRs.
  • Complement anaphylaxis is mediated by C3a and C5a binding to their receptors.
  • Direct mast cell activation occurs with certain drugs.
  • Evidence supports all three IgE-independent mechanisms in human disease.

Conclusions:

  • IgE-independent anaphylaxis mechanisms are relevant in humans.
  • Clinical situations may indicate specific underlying pathways.
  • Combined IgE-dependent and independent mechanisms can worsen severity.
  • Recognizing specific anaphylaxis types is crucial for targeted therapy.