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Related Concept Videos

Hypersensitivities01:30

Hypersensitivities

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.
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Allergic Reactions02:06

Allergic Reactions

Overview
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

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 sickness, a systemic...
Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

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 exposure to a...
Asthma I: Introduction01:28

Asthma I: Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction and heightened bronchial responsiveness to a wide range of triggers. The underlying inflammation leads to airway swelling, mucus hypersecretion, and smooth muscle constriction, all of which narrow the airway lumen and impede airflow. Clinically, asthma presents with recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, symptoms that typically vary in intensity and...

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Related Experiment Video

Updated: May 16, 2026

Basophil Activation Test for Allergy Diagnosis
07:22

Basophil Activation Test for Allergy Diagnosis

Published on: May 31, 2021

Endotypes in chronic spontaneous urticaria.

Allen P Kaplan1, Marta Ferrer Puga2, Sabaté-Bresco Marina3

  • 1The Medical University of South Carolina, Department of Medicine, Division of Pulmonary, Critical Care, and Clinical Immunology, Charleston, SC.

The Journal of Allergy and Clinical Immunology
|May 14, 2026
PubMed
Summary
This summary is machine-generated.

Chronic spontaneous urticaria (CSU) pathogenesis is complex. Current evidence suggests the type IIb mechanism, involving IgG antibodies to the IgE receptor and C5a, is more consistently implicated in CSU than the type Ia mechanism. Further research is needed.

Keywords:
Urticariahistamine

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Area of Science:

  • Immunology
  • Dermatology
  • Allergology

Background:

  • Chronic spontaneous urticaria (CSU) pathogenesis is debated, with proposed mechanisms involving mast cell and basophil activation.
  • Two distinct pathogenic pathways, type Ia and type IIb, have been suggested.
  • Type Ia involves IgE antibodies to thyroperoxidase or interleukin 24 (IL24), while type IIb involves IgG antibodies to the IgE receptor and complement activation via C5a.

Purpose of the Study:

  • To critically evaluate the evidence supporting the type Ia pathogenic mechanism in CSU.
  • To assess the role of the type IIb mechanism in CSU pathogenesis.
  • To clarify the contribution of different immunological pathways to CSU.

Main Methods:

  • Review of existing literature on CSU pathogenesis, IgE, and IgG antibodies.
  • Analysis of data regarding patient responses to Omalizumab.
  • Examination of in vitro studies on basophil histamine release.

Main Results:

  • Insufficient reproducible data exists to support type Ia mechanism as pathogenic for CSU.
  • Evidence for thyroid antigen in skin is limited, and IL24's role is unclear.
  • The type IIb mechanism, involving IgG antibodies to the IgE receptor and C5a, accounts for a significant portion of CSU patients.
  • Omalizumab efficacy trials did not show response differences based on IgE levels.

Conclusions:

  • The type Ia mechanism for CSU is not well-supported by current evidence due to conflicting data and lack of reproducibility.
  • The type IIb mechanism, involving IgG antibodies to the IgE receptor and C5a, appears to be a more significant factor in CSU pathogenesis.
  • Further research is required to fully elucidate the complex immunological pathways involved in CSU.