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- Title
Leucocyte/endothelial cell adhesion receptors in muscle biopsies from patients with idiopathic inflammatory myopathies (IIM).
- Authors
Cid, M.-C.; Grau, J.-M.; Casademont, J.; Tobías, E.; Picazo, A.; Coll-Vinent, B.; Esparza, J.; Pedrol, E.; Urbano-Márquez, A.
- Abstract
Interactions between leucocytes and endothelial cells through specific adhesion receptors play an increasingly recognized crucial role in the development of inflammatory infiltrates in chronic inflammatory diseases. In this study we investigated adhesion molecule expression in muscle biopsies from 18 dermatomyositis, six polymyositis, five inclusion-body myositis patients and from eight normal controls. Immunohistochemical detection of leucocyte integrins LFA-1 and VLA-4, their endothelial counter-receptors intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). and the endothelial cell markers CD31 and von Willebrand factor-related antigen (vWFAg) was performed using specific MoAbs and an alkaline phosphatase anti-alkaline phosphatase technique. ICAM-1 expression was up-regulated and VCAM-I induced in muscle capillaries of dermatomyositis samples. In both dermatomyositis and polymyositis, endothelial cells from vessels surrounded by inflammatory infiltrates strongly expressed ICAM-1 and VCAM-I. Infiltrating leucocytes were intensively LFA-I- and VLA-4-positive, These data suggest that leucocyte/endothelial cell interactions mediated by the receptor/ligand pairs LFA-1/ ICAM-1 and VLA-4/VCAM-I actively participate in the development of muscle inflammatory infiltrates in the major inflammatory myopathies. In addition, ICAM-1 and VCAM-1 overexpression by capillary endothelial cells in dermatomyositis supports the hypothesis that capillary activation and/or injury is a major feature in this disease.
- Subjects
ADHESION; CELL communication; MUSCLE diseases; CELLULAR control mechanisms; COHESION; ADSORPTION (Chemistry); CELL adhesion
- Publication
Clinical & Experimental Immunology, 1996, Vol 104, Issue 3, p467
- ISSN
0009-9104
- Publication type
Article