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Type: Journal article
Title: Macrophage migration inhibitory factor induces macrophage recruitment via CC chemokine ligand 2
Author: Gregory, J.
Morand, E.
McKeown, S.
Ralph, J.
Hall, P.
Yang, Y.
McColl, S.
Hickey, M.
Citation: Journal of Immunology, 2006; 177(11):8072-8079
Publisher: Amer Assoc Immunologists
Issue Date: 2006
ISSN: 0022-1767
Statement of
Julia L. Gregory, Eric F. Morand, Sonja J. McKeown, Jennifer A. Ralph, Pamela Hall, Yuan H. Yang, Shaun R. McColl and Michael J. Hickey
Abstract: Macrophage migration inhibitory factor (MIF) was originally identified for its ability to inhibit the random migration of macrophages in vitro. MIF is now recognized as an important mediator in a range of inflammatory disorders. We recently observed that the absence of MIF is associated with a reduction in leukocyte-endothelial cell interactions induced by a range of inflammatory mediators, suggesting that one mechanism whereby MIF acts during inflammatory responses is by promoting leukocyte recruitment. However, it is unknown whether MIF is capable of inducing leukocyte recruitment independently of additional inflammatory stimuli. In this study, we report that MIF is capable of inducing leukocyte adhesion and transmigration in postcapillary venules in vivo. Moreover, leukocytes recruited in response to MIF were predominantly CD68+ cells of the monocyte/macrophage lineage. Abs against the monocyte-selective chemokine CCL2 (JE/MCP-1) and its receptor CCR2, but not CCL3 and CXCL2, significantly inhibited MIF-induced monocyte adhesion and transmigration. CCL2–/– mice displayed a similar reduction in MIF-induced recruitment indicating a critical role of CCL2 in the MIF-induced response. This hypothesis was supported by findings that MIF induced CCL2 release from primary microvascular endothelial cells. These data demonstrate a previously unrecognized function of this pleiotropic cytokine: induction of monocyte migration into tissues. This function may be critical to the ability of MIF to promote diseases such as atherosclerosis and rheumatoid arthritis, in which macrophages are key participants.
Keywords: Macrophages
Endothelial Cells
Mice, Inbred C57BL
RNA, Messenger
Antigens, CD
Antigens, Differentiation, Myelomonocytic
Macrophage Migration-Inhibitory Factors
Reverse Transcriptase Polymerase Chain Reaction
Cell Adhesion
Chemotaxis, Leukocyte
Chemokine CCL2
Rights: Copyright © 2006 by The American Association of Immunologists, Inc.
DOI: 10.4049/jimmunol.177.11.8072
Published version:
Appears in Collections:Aurora harvest
Molecular and Biomedical Science publications

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