Late administration of monoclonal antibody to leukocyte function-antigen 1 abrogates incipient murine cerebral malaria

Détails

ID Serval
serval:BIB_30D20A9FF531
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Late administration of monoclonal antibody to leukocyte function-antigen 1 abrogates incipient murine cerebral malaria
Périodique
European Journal of Immunology
Auteur(s)
Grau  G. E., Pointaire  P., Piguet  P. F., Vesin  C., Rosen  H., Stamenkovic  I., Takei  F., Vassalli  P.
ISSN
0014-2980 (Print)
Statut éditorial
Publié
Date de publication
1991
Volume
21
Numéro
9
Pages
2265-2267
Notes
PT - Journal Article PT - Research Support, Non-U.S. Gov't
Résumé
We analyzed the role of adhesion molecules in the pathogenesis of experimental cerebral malaria (ECM), since tumor necrosis factor (TNF) plays a major role in this condition and has been shown to up-regulate in vitro expression of cell adhesion molecules (CAM), particularly intercellular CAM-1 (ICAM-1). We found increased expression of ICAM-1 on brain endothelial cells from mice with ECM. Treatment with monoclonal antibodies (mAb) directed against leukocyte function-antigen 1 (LFA-1, the ligand of ICAM-1) on days 6, 8 and 10 almost totally prevented ECM, while decreasing blood TNF levels. To exclude the possibility that the effects of anti-LFA-1 mAb resulted from an even partial inhibition of TNF overproduction, mice with signs of imminent death (hypothermia and neurologic defects) were treated with the anti-LFA-1 mAb, with dramatically protective effect. In contrast, injection of anti-ICAM-1 mAb on day 6 caused rapid death, while it was innocuous in normal mice. An mAb directed against complement receptor type 3 (CR3) was ineffective, as were injections of soluble human ICAM-1. These results suggest that adhesion of LFA-1+ cells to endothelial cells, stimulated by TNF to express high levels of ICAM-1, is critical in the pathogenesis of ECM. Emergency therapy at interfering with cytoadherence could be considered in the treatment of cerebral malaria in man, in which high blood TNF levels are also observed
Mots-clé
Animals/Antibodies,Monoclonal/pharmacology/Brain/metabolism/microbiology/Pathology/Cell Adhesion Molecules/physiology/Disease Models,Animal/Hypothermia/prevention & control/Intercellular Adhesion Molecule-1/Lymphocyte Function-Associated Antigen-1/immunology/Malaria/Male/Mice/Mice,Inbred CBA/Plasmodium berghei/Tumor Necrosis Factor-alpha/biosynthesis/Research
Pubmed
Web of science
Création de la notice
29/01/2008 19:33
Dernière modification de la notice
20/08/2019 14:15
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