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

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Serval ID
serval:BIB_0C2BD99E7A5D
Type
Article: article from journal or magazin.
Collection
Publications
Title
An essential role for macrophage migration inhibitory factor in the tuberculin delayed-type hypersensitivity reaction.
Journal
The Journal of experimental medicine
Author(s)
Bernhagen J., Bacher M., Calandra T., Metz C.N., Doty S.B., Donnelly T., Bucala R.
ISSN
0022-1007 (Print)
ISSN-L
0022-1007
Publication state
Published
Issued date
01/01/1996
Peer-reviewed
Oui
Volume
183
Number
1
Pages
277-282
Language
english
Notes
Publication types: Journal Article ; Research Support, U.S. Gov't, P.H.S.
Publication Status: ppublish
Abstract
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.
Keywords
Animals, Base Sequence, Female, Hindlimb/immunology, Hindlimb/pathology, Hypersensitivity, Delayed/etiology, Immunohistochemistry, In Situ Hybridization, Macrophage Migration-Inhibitory Factors/isolation & purification, Macrophage Migration-Inhibitory Factors/metabolism, Macrophages/metabolism, Mice, Mice, Inbred BALB C, Molecular Sequence Data, Monocytes/metabolism, RNA, Messenger/analysis, Skin/immunology, Skin/pathology, Tuberculin/immunology
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 14:28
Last modification date
09/08/2024 14:01
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