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pubmed-article:16374458pubmed:abstractTextThe chronic inflammatory skin disease psoriasis is characterized by prominent skin infiltration by neutrophils and microabscess formation. The adhesion of leukocytes and subsequent transmigration through the activated endothelium is one prerequisite for the accumulation of these cells in skin. In recent studies, the human Thy-1 (CD90) was characterized as an adhesion molecule on activated endothelial cells (ECs) mediating the adhesion of neutrophils via the interaction with the beta2-integrin Mac-1. Based on these novel findings, we compared the roles of Thy-1 and ICAM-1 in the adhesion of neutrophils from patients with psoriasis to activated ECs. The adhesion of peripheral blood neutrophils of patients suffering from psoriasis to Thy-1-transfected cells as well as to activated, Thy-1-expressing human dermal microvascular ECs (HDMECs) is distinctly increased in comparison to the adhesion of neutrophils from healthy controls. In contrast, adherence of psoriatic neutrophils to ICAM-1 transfectants is, if at all, only slightly enhanced compared to healthy controls. The interaction of healthy as well as psoriatic polymorphonuclear cells to Thy-1 transfectants and HDMECs was significantly inhibited by blocking Thy-1 on ECs or its receptor Mac-1 on neutrophils, indicating the importance of this interaction for the adhesion of neutrophils to activated endothelium. In conclusion, our data indicate that the adhesion of neutrophils to activated ECs mediated by Thy-1/Mac-1 interaction is an important attachment mechanism facilitating their subsequent migration into lesional psoriatic skin.lld:pubmed
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pubmed-article:16374458pubmed:articleTitleIncreased neutrophil adherence in psoriasis: role of the human endothelial cell receptor Thy-1 (CD90).lld:pubmed
pubmed-article:16374458pubmed:affiliationDepartment of Dermatology, Venerology and Allergy, University of Leipzig, Leipzig, Germany.lld:pubmed
pubmed-article:16374458pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16374458pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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