An essential role for macrophage migration inhibitory factor in the tuberculin delayed-type hypersensitivity reaction

Détails

ID Serval
serval:BIB_0C2BD99E7A5D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
An essential role for macrophage migration inhibitory factor in the tuberculin delayed-type hypersensitivity reaction
Périodique
Journal of Experimental Medicine
Auteur(s)
Bernhagen  J., Bacher  M., Calandra  T., Metz  C. N., Doty  S. B., Donnelly  T., Bucala  R.
ISSN
0022-1007 (Print)
Statut éditorial
Publié
Date de publication
01/1996
Volume
183
Numéro
1
Pages
277-82
Notes
Journal Article
Research Support, U.S. Gov't, P.H.S. --- Old month value: Jan 1
Résumé
30 years ago, investigations into the molecular basis of the delayed-type hypersensitivity reaction (DTH) provided evidence for the first lymphokine activity: a lymphocyte-derived mediator called macrophage migration inhibitory factor (MIF), which inhibited the random migration of peritoneal macrophages. Despite the long-standing association of MIF with the DTH reaction and the cloning of a human protein with macrophage migration inhibitory activity, the precise role of MIF in this classic cell-mediated immune response has remained undefined. This situation has been further complicated by the fact that two other cytokines, interferon gamma and IL-4, similarly inhibit macrophage migration and by the identification of mitogenic contaminants in some preparations of cloned human MIF. Using recently developed molecular probes for mouse MIF, we have examined the role of this protein in a classical model of DTH, the tuberculin reaction in mice. Both MIF messenger RNA and protein were expressed prominently in DTH lesions, as assessed by reverse transcription polymerase chain reaction, in situ hybridization, and immunostaining with anti-MIF antibody. The predominant cellular origin of MIF appeared to be the monocyte/macrophage, a cell type identified recently to be a major source of MIF release in vivo. The administration of neutralizing anti-MIF antibodies to mice inhibited significantly the development of DTH, thus affirming the central role of MIF in this classic immunological response.
Mots-clé
Animals Base Sequence Female Hindlimb/immunology/pathology Hypersensitivity, Delayed/*etiology Immunohistochemistry In Situ Hybridization Macrophage Migration-Inhibitory Factors/isolation & purification/*metabolism Macrophages/metabolism Mice Mice, Inbred BALB C Molecular Sequence Data Monocytes/metabolism RNA, Messenger/analysis Skin/*immunology/pathology Tuberculin/*immunology
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 13:28
Dernière modification de la notice
20/08/2019 12:33
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