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β 2 ‐integrins in different forms of urticaria
Author(s) -
HAAS N.,
IWEN W.,
GRABBE J.,
HAMANN K.,
CZARNETZKI B. M.
Publication year - 1995
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1995.tb02491.x
Subject(s) - medicine , cd11a , integrin , cd18 , cell adhesion molecule , pathological , integrin alpha m , pathology , downregulation and upregulation , immunology , biology , receptor , immune system , biochemistry , gene
Summary As urticarial lesions involve tissue invasion by inflammatory cells, and as β 2 ‐integrins play a central part in adhesion of leucocytes to endothelia, allowing their migration into the tissues, we have explored the distribution and sequential expression of these molecules in tissue sections from different forms of urticaria. Prick test weals (of 10 min duration) to common inhalant allergens showed only a minor increase of CD18, whereas in a case of cold urticaria CD11b and CD18 molecules were increasingly upregulated within the first 30 min after elicitation of the lesions. Skin test sites in delayed pressure urticaria, and urticarial esions (> 6 h duration) of acute and chronic recurrent urticaria also showed marked upregulation of CD11b and CD18, and to a lesser extent of CD11a, but this did not strongly correlate with the intensity of the mixed cellular infiltrate. Non‐lesional skin showed expression of β 2 ‐integrins in chronic urticaria, delayed pressure urticaria, and less so in acute urticaria, suggesting generalized leucocyte activation. This analysis of integrins thus suggests an early and extensive involvement of these molecules in the pathological events associated with the evolution of urticarial lesions.