Are circulating neutrophils intravascularly activated in patients with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides?
Autor: | Coen A. Stegeman, Jwc Tervaert, Anna Muller Kobold, G Mesander, Cornelis Kallenberg |
---|---|
Přispěvatelé: | Groningen Kidney Center (GKC), Translational Immunology Groningen (TRIGR), Guided Treatment in Optimal Selected Cancer Patients (GUTS) |
Jazyk: | angličtina |
Rok vydání: | 1998 |
Předmět: |
Adult
Male Pathology medicine.medical_specialty neutrophil activation Shwartzman phenomenon Endothelium Neutrophils Immunology Birmingham Vasculitis Activity Score SURFACE EXPRESSION UP-REGULATION DISEASE-ACTIVITY vasculitis SYSTEMIC LUPUS-ERYTHEMATOSUS Antibodies Antineutrophil Cytoplasmic sepsis medicine Humans Immunology and Allergy adhesion molecules Cell adhesion Aged Anti-neutrophil cytoplasmic antibody Aged 80 and over biology Cell adhesion molecule business.industry ANCA flow cytometry LEUKOCYTE INTEGRINS FLOW-CYTOMETRY ADHESION MOLECULE-1 Original Articles Middle Aged medicine.disease medicine.anatomical_structure biology.protein L-SELECTIN Female L-selectin WEGENERS GRANULOMATOSIS AUTOANTIBODIES business Vasculitis Cell Adhesion Molecules Biomarkers Shwartzman Phenomenon |
Zdroj: | Clinical and Experimental Immunology, 114(3), 491-499. Wiley University of Groningen |
ISSN: | 0009-9104 |
Popis: | SUMMARY Vascular injury in vasculitis may be due to activation of circulating neutrophils resulting in their increased adhesiveness to locally activated endothelium (Shwartzman phenomenon). Previously, we demonstrated up-regulation of endothelial intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in biopsies from patients with ANCA-associated vasculitis. In the present study, we investigated the expression of adhesion molecules (CD11b, ICAM-1, VLA-4, l-selectin) and activation markers (CD66b, CD64, CD63) on circulating neutrophils from patients with ANCA-associated vasculitis in comparison with their expression on cells from healthy volunteers and patients with sepsis. We related these findings to parameters of disease activity. Surface marker expression was determined by using a non-activating whole blood flow cytometric assay. The expression of activation markers, but not the expression of adhesion molecules, was increased on neutrophils from patients with active vasculitis. The expression of CD63 and CD66b on neutrophils correlated with disease activity as determined by the Birmingham Vasculitis Activity Score (BVAS). In contrast to patients with active vasculitis, patients with sepsis showed up-regulation of all markers, including adhesion molecules, suggesting that circulating neutrophils are fully activated in sepsis. We conclude that in ANCA-associated vasculitis, circulating neutrophils are not fully activated, since they do not express increased levels of adhesion molecules as sepsis or in the Shwartzman reaction. These findings are compatible with the concept that in vivo vascular damage in ANCA-associated vasculitides does not occur due to a Shwarzman-like reaction but only after ANCA-induced neutrophil activation at the endothelial cell surface. |
Databáze: | OpenAIRE |
Externí odkaz: |