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Related Experiment Video

Updated: Jul 19, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Chronic urticaria: pathogenesis and treatment.

Allen P Kaplan¹

¹Department of Medicine, Division of Pulmonary and Critical Care Medicine, Allergy and Clinical Immunology, Medical University of South Carolina, Charleston, SC 92425, USA. kaplana@musc.edu

The Journal of Allergy and Clinical Immunology

|September 10, 2004

Summary

Chronic idiopathic urticaria is now classified into autoimmune and idiopathic subtypes. Autoimmune chronic urticaria involves IgG antibodies targeting IgE receptors or IgE, often linked to antithyroid antibodies, and requires specific treatment strategies.

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Area of Science:

Immunology
Dermatology
Allergy

Background:

Chronic idiopathic urticaria (CIU) is reclassified into chronic autoimmune urticaria (CAU) and chronic idiopathic urticaria (CIU).
Approximately 40-50% of CIU patients are now identified with CAU.
Both conditions can present with concomitant angioedema in about 40% of cases.

Purpose of the Study:

To delineate the immunological mechanisms underlying chronic urticaria subtypes.
To identify specific autoantibodies and cellular infiltrates involved in CAU.
To outline therapeutic approaches for severe chronic urticaria.

Main Methods:

Immunological assays to detect IgG antibodies against IgE receptors and IgE.
Histological examination of skin biopsies to analyze cellular infiltrates (CD4+ lymphocytes, monocytes, neutrophils, eosinophils, basophils).
Assessment of complement activation pathways (C5a) and cytokine/chemokine involvement.

Main Results:

CAU is associated with antithyroid antibodies and pathogenic IgG subclasses (IgG1, IgG3, IgG4) targeting the IgE receptor alpha subunit or IgE.
Complement activation via C5a contributes to histamine release.
Histology reveals perivascular infiltrates of T(H)1/T(H)2 lymphocytes, monocytes, and inflammatory cells.

Conclusions:

Chronic urticaria encompasses distinct autoimmune and idiopathic forms with different underlying mechanisms.
Autoantibodies, complement activation, and specific cellular infiltrates are key in CAU pathogenesis.
Treatment strategies should be tailored, with severe cases potentially requiring high-dose antihistamines, H-2 antagonists, leukotriene antagonists, or immunosuppressants like cyclosporine.