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í Lácha*
ibylová||
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* Department of Nephrology, Transplant Unit, Institute for Clinical and Experimental Medicine, Prague 4, Czech Republic;
Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Headington, United Kingdom;
Institute of Anatomy, 1st Faculty of Medicine, Charles University, Prague 2, Czech Republic; and Departments of
Immunology and Gnotobiology, Institute of Microbiology, and
|| Mammalian Development, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague 4, Czech Republic
Correspondence: Petr Mal, Ph.D., Department of Mammalian Development, Institute of Molecular Genetics ASCR, Víde
ská 1083, 142 20 Prague 4, Czech Republic. E-mail: pemal{at}biomed.cas.cz
Cell adhesion molecules and their ligands are essential for regulating
lymphocyte recirculation and leucocyte emigration into an inflamed or
injured tissue. Vascular endothelial selectins as mediators of
leucocyte rolling and intercellular cell adhesion molecule-1 (ICAM-1)
have been found to be up-regulated on activated endothelium during
acute allograft rejection. This study was designed to investigate
whether ICAM-1 or selectin-ligand deficiency, or a combination of both,
affected graft survival during acute cardiac allograft rejection. To
this goal, we performed cardiac transplantation using mice deficient in
genes for ICAM-1 or 
(1,3)fucosyltransferase Fuc-TVII, representing a
model for general absence of selectin-ligand expression, and a newly
developed strain with a double mutation in Fuc-TVII and ICAM-1 alleles.
Transplantation of a heart from ICAM-1 -/- or Fuc-TVII/ICAM-1
double-mutated mice into allogeneic recipients resulted in limited
(2–2.5 days) but nevertheless significant prolongation of the graft
survival (P<0.01 and P<0.01 in log-rank test)
compared with the survival of unmodified hearts. When ICAM-1 -/-
hearts were transplanted into Fuc-TVII -/- recipients, the median
survival time was prolonged by 8 days (P<0.01). These data
indicate that endothelial ICAM-1 is involved in adhesion events during
acute cardiac allograft rejection but reveal that the loss of one
type, selectin/leucocyte ligand or selectin/endothelial ligand
interaction, does not markedly affect graft survival, thereby
suggesting a role for other compensatory adhesion molecule/ligand
interactions.
Key Words: selectin ligand • fucosyltransferase • LFA-1 • ICAM-1 • transplantation • Fuc-TVII
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