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Beta 2-integrins in different forms of urticaria
1Department of Dermatology, Clinical Immunology and Asthma, Rudolf Virchow Hospital, Free University Berlin, Germany.
The British Journal of Dermatology
|July 1, 1995
Summary
Beta 2-integrins are crucial for leukocyte migration in urticarial lesions. This study reveals their early and widespread involvement in various urticaria types, indicating significant roles in the condition's pathology.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Urticarial lesions involve inflammatory cell infiltration.
- Beta 2-integrins mediate leukocyte adhesion and tissue migration.
Purpose of the Study:
- To investigate the distribution and sequential expression of beta 2-integrins in different forms of urticaria.
- To understand the role of these molecules in urticarial lesion development.
Main Methods:
- Analysis of tissue sections from various urticaria types (cold, delayed pressure, acute, chronic).
- Examination of beta 2-integrin expression (CD11a, CD11b, CD18) via immunohistochemistry.
- Comparison of integrin expression with cellular infiltrate intensity.
Main Results:
- Minor CD18 increase in short-term prick test weals.
- Upregulation of CD11b and CD18 in cold urticaria within 30 minutes.
- Marked upregulation of CD11b, CD18, and CD11a in delayed pressure and established urticarial lesions.
- Non-lesional skin showed beta 2-integrin expression in chronic and delayed pressure urticaria, suggesting generalized leukocyte activation.
Conclusions:
- Beta 2-integrins are extensively and early involved in the pathogenesis of urticarial lesions.
- These molecules play a significant role in the inflammatory processes underlying various urticaria types.