Artigo Revisado por pares

Anti-integrin (LFA-1, VLA-4, and Mac-1) antibody treatment and acute cardiac graft rejection in the rat

1996; Springer Science+Business Media; Volume: 9; Issue: 4 Linguagem: Inglês

10.1007/bf00335706

ISSN

1432-2277

Autores

Lorna Paul, A. Davidoff, Hallgrímur Benediktsson, Thomas B. Issekutz,

Tópico(s)

Monoclonal and Polyclonal Antibodies Research

Resumo

Transplant InternationalVolume 9, Issue 4 p. 420-425 Anti-integrin (LFA-1, VLA-4, and Mac-1) antibody treatment and acute cardiac graft rejection in the rat Leendert C. Paul, Leendert C. Paul Division of Nephrology, University of Toronto at St. Michael's Hospital, 30 Bond Street, Toronto, Ontario, M5B 1W8, Canada, Fax: +14168673701 Department of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, CanadaSearch for more papers by this authorAllen Davidoff, Allen Davidoff Department of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, CanadaSearch for more papers by this authorHallgrimur Benediktsson, Hallgrimur Benediktsson Department of Histopathology, Foothills Hospital, 1403 29th Street NW, Calgary, Alberta, T2N 2T9, Canada L. C. Paul T. Issekutz Multi-Organ Transplant Research Group, Max Bell Research Centre, Toronto Hospital Research Institute, 101 College Street, Toronto, Ontario, M5G 1L7, CanadaSearch for more papers by this authorThomas Issekutz, Thomas Issekutz Division of Nephrology, University of Toronto at St. Michael's Hospital, 30 Bond Street, Toronto, Ontario, M5B 1W8, Canada, Fax: +14168673701Search for more papers by this author Leendert C. Paul, Leendert C. Paul Division of Nephrology, University of Toronto at St. Michael's Hospital, 30 Bond Street, Toronto, Ontario, M5B 1W8, Canada, Fax: +14168673701 Department of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, CanadaSearch for more papers by this authorAllen Davidoff, Allen Davidoff Department of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, T2N 4N1, CanadaSearch for more papers by this authorHallgrimur Benediktsson, Hallgrimur Benediktsson Department of Histopathology, Foothills Hospital, 1403 29th Street NW, Calgary, Alberta, T2N 2T9, Canada L. C. Paul T. Issekutz Multi-Organ Transplant Research Group, Max Bell Research Centre, Toronto Hospital Research Institute, 101 College Street, Toronto, Ontario, M5G 1L7, CanadaSearch for more papers by this authorThomas Issekutz, Thomas Issekutz Division of Nephrology, University of Toronto at St. Michael's Hospital, 30 Bond Street, Toronto, Ontario, M5B 1W8, Canada, Fax: +14168673701Search for more papers by this author First published: July 1996 https://doi.org/10.1111/j.1432-2277.1996.tb00902.xCitations: 12AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Abstract Cell adhesion molecules mediate interactions with other cells and extracellular matrix, control cell infiltration in sites of inflammation, and regulate cell activation. Previous studies have shown that treatment of rat cardiac transplant recipients with a combination of antibodies against the T-cell integrins LFA-1 and VLA-4 gave a modest prolongation of graft survival. Current experiments were designed to examine the effect of blocking Mac-1, an im portant monocyte adhesion receptor and mediator of monocyte migration, together with anti-LFA-1 and anti-VLA-4 antibodies on cardiac graft survival and on the graft rejection pattern. The anti-Mac-1, CDllb-specific antibody OX-42 did not affect graft survival time al though it did decrease the graft in filtration by rounded, ED-2-positive macrophages. 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