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Different expression of adhesion molecules and tetraspanins of monocytes of patients with atopic eczema
Author(s) -
Jockers J. J.,
Novak N.
Publication year - 2006
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2006.01191.x
Subject(s) - immunology , cell adhesion molecule , medicine , adhesion , monocyte , immunopathology , immunoglobulin e , antibody , chemistry , organic chemistry
Background: Atopic eczema (AE) and psoriasis vulgaris (Pso) represent the most frequent chronic inflammatory skin diseases, which have a high number of characteristics in common but differ in their clinical picture and immunological background. A shared feature of both AE and Pso is a high recruitment of distinct proinflammatory cells from the blood into the skin at the initiation of the disease. A multistep adhesion cascade via different adhesion receptors consisting of ‘tethering’ and ‘rolling’ mediated by selectins, α ‐integrins and β ‐integrins and the ‘arrest’ of the cells is initiated during this process. Aims of the study: To evaluate the expression of adhesion molecules and tetraspanins of monocytes of patients with AE and Pso in comparison with healthy controls. Methods: We analysed the expression of adhesion molecules and tetraspanins on monocytes freshly isolated from the peripheral blood of patients with AE ( n = 40) and Pso ( n = 65) during exacerbation of their disease in comparison with healthy, non‐atopic controls ( n = 50). Results: A high number of similarities between monocytes of patients with AE and patients with Pso, and disease‐related differences in the expression of CD62L, CD62P, CD11a, CD11b, CD11c, CD49b, CD49d, CD49e and CD18 and the tetraspanins CD9, CD53, CD63 and CD151, which were elevated on monocytes of patients with AE could be observed. Conclusion: A distinct expression pattern of adhesion molecules and tetraspanins on monocytes of patients with AE and Pso might influence the recruitment process of inflammatory precursor cells and facilitate new approaches for therapeutic strategies aimed at interrupting the very earliest steps of the fateful recruitment process.