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Updated: Feb 21, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
Published on: October 12, 2012
Chronic spontaneous urticaria and the extrinsic coagulation system
Yuhki Yanase1, Shunsuke Takahagi1, Michihiro Hide1
1Department of Dermatology, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan.
Chronic spontaneous urticaria (CSU) involves blood coagulation activation. Vascular cells expressing tissue factor (TF) may trigger this pathway, offering new treatment targets for CSU.
Area of Science:
- Dermatology
- Hematology
- Immunology
Background:
- Chronic spontaneous urticaria (CSU) is a prevalent skin condition causing recurrent edema and itch.
- The role of blood coagulation in CSU pathogenesis is increasingly recognized, yet its initiating trigger remains elusive.
Purpose of the Study:
- To review the current understanding of CSU pathogenesis, focusing on the link between extrinsic coagulation reactions and disease mechanisms.
- To explore the potential role of tissue factor (TF) and its regulatory pathways in CSU.
Main Methods:
- Literature review of recent studies on CSU pathogenesis and coagulation.
- Analysis of the proposed mechanisms involving TF expression on endothelial cells and eosinophils.
- Examination of synergistic effects of Toll-like receptors and histamine H1 receptors on TF expression.
Main Results:
- Vascular endothelial cells and eosinophils are identified as potential TF-expressing cells that activate the extrinsic coagulation pathway in CSU.
- TF expression on endothelial cells is significantly enhanced by Toll-like receptor and histamine H1 receptor activation.
- Activated coagulation factors may lead to plasma extravasation, mast cell degranulation, and wheal formation in CSU.
Conclusions:
- The extrinsic coagulation cascade, initiated by TF-expressing cells, plays a significant role in CSU pathogenesis.
- Targeting molecules within this coagulation cascade presents a promising strategy for developing novel and effective CSU treatments.
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