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Titolo:
VCAM-1 IS A CS1 PEPTIDE-INHIBITABLE ADHESION MOLECULE EXPRESSED BY LYMPH-NODE HIGH ENDOTHELIUM
Autore:
MAY MJ; ENTWISTLE G; HUMPHRIES MJ; AGER A;
Indirizzi:
NATL INST MED RES,CELLULAR IMMUNOL LAB,MILL HILL LONDON NW7 1AA ENGLAND NATL INST MED RES,CELLULAR IMMUNOL LAB,MILL HILL LONDON NW7 1AA ENGLAND UNIV MANCHESTER,DEPT BIOCHEM & MOLEC BIOL MANCHESTER M13 9PT LANCS ENGLAND UNIV MANCHESTER,DEPT CELL & STRUCT BIOL MANCHESTER M13 9PT LANCS ENGLAND
Titolo Testata:
Journal of Cell Science
, volume: 106, anno: 1993,
parte:, 1
pagine: 109 - 119
SICI:
0021-9533(1993)106:<109:VIACPA>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
MONONUCLEAR LEUKOCYTE ADHESION; HUMAN-PLASMA FIBRONECTIN; III CONNECTING SEGMENT; HOMING RECEPTORS; BINDING-SITE; STIMULATED ENDOTHELIUM; MONOCLONAL-ANTIBODY; MELANOMA ADHESION; CELL INTERACTIONS; INTEGRIN VLA-4;
Keywords:
VCAM-1; HIGH ENDOTHELIUM; CS1 PEPTIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
M.J. May et al., "VCAM-1 IS A CS1 PEPTIDE-INHIBITABLE ADHESION MOLECULE EXPRESSED BY LYMPH-NODE HIGH ENDOTHELIUM", Journal of Cell Science, 106, 1993, pp. 109-119

Abstract

Previous studies have shown that unactivated lymphocytes bind to CS1 peptide and that the adhesion of these cells to high endothelium is inhibited by CS1 peptide. These results suggest that lymphocyte binding occurs via recognition of the CS1-containing splice variant of fibronectin expressed on the high endothelial surface. We have now extended these studies by determining the role of the CS1 receptor, alpha4beta1 (VLA-4) and the alternative VLA-4 ligand, VCAM-1 in a rat model of lymphocyte-high endothelial cell interaction. Anti-VLA-4 antibody, HP2/1,blocked lymphocyte adhesion to resting and IFN-gamma (interferon-gamma) pretreated cultured high endothelial cells (HEC) in a dose-dependent manner with maximal inhibition of 60%. HP2/1 completely blocked the adhesion of rat lymphocytes to immobilized CS1 peptide and to a recombinant soluble (rs) form of human VCAM-1. Lymphocyte binding to rsVCAM-1 was also completely blocked by CS1 peptide. Anti-rat VCAM-1 monoclonal antibody 5F10 inhibited adhesion to untreated and IFN-gamma-treatedHEC equally and its effect at 50% inhibition was slightly less than that of HP2/1. These findings suggest that a CS1 peptide-inhibitable ligand expressed by high endothelium is VCAM-1. The majority of culturedHEC expressed significant levels of VCAM-1 under basal conditions, asdid HEV in peripheral lymph nodes. VCAM-1 expression by HEC was upregulated by cytokine pretreatment and the effects were ordered: IFN-gamma > TNF-alpha > IL-1beta. The results described here demonstrate that rat peripheral lymph node HEC express VCAM-1, its expression is upregulated by cytokines, in particular IFN-gamma, and it supports the adhesion of unactivated lymphocytes. They also suggest that the VLA-4/VCAM-1 adhesion pathway may operate during the constitutive migration of lymphocytes into lymphoid organs. Although the mechanism of CS1 peptide inhibition was not determined, these results show that VCAM-1 is a CS1peptide-inhibitable ligand and therefore CS1, on its own, cannot be used as a specific indicator of fibronectin activity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 06:45:49