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The Journal of Immunology, 1998, 161: 2383-2390.
Copyright © 1998 by The American Association of Immunologists

Migration Inhibitory Factor Induces Killing of Leishmania major by Macrophages: Dependence on Reactive Nitrogen Intermediates and Endogenous TNF-{alpha}1

Stefan Jüttner*, Jürgen Bernhagen{dagger}, Christine N. Metz{ddagger}, Martin Röllinghoff*, Richard Bucala{ddagger} and André Gessner2,*

* Institute of Clinical Microbiology and Immunology, University of Erlangen-Nürnberg, Erlangen; and {dagger} Laboratory of Biochemistry, Chair for Interfacial Engineering, University of Stuttgart, Stuttgart, Germany; and {ddagger} The Picower Institute for Medical Research, Manhasset, NY 11030

Macrophage migration inhibitory factor (MIF) is a product of activated T cells, anterior pituitary cells, and macrophages. MIF plays an important role in LPS-induced shock and delayed-type hypersensitivity. Furthermore, MIF exhibits a proinflammatory spectrum of action, promoting TNF-{alpha} production by macrophages, and counter-regulates glucocorticoid suppression of cytokine production. Here, we report that purified recombinant MIF activates murine macrophages to kill Leishmania major, with maximal effects at concentrations above 1 µg/ml. This MIF-mediated activation is specific, since it can be blocked completely by anti-MIF mAb. The MIF-mediated activation is dependent on TNF-{alpha} produced endogenously by macrophages, because the administration of anti-TNF-{alpha} antiserum markedly reduced the MIF effect. No MIF-mediated activation was observed in macrophages derived from TNF receptor p55 knockout mice, thus demonstrating the requirement of the smaller TNF receptor molecule for autocrine TNF-{alpha} signaling. A highly specific inhibitor of the inducible nitric oxide synthase (iNOS), L-N6-(1-iminoethyl)lysine, dihydrochloride, also inhibited the action of MIF, suggesting an important role for iNOS in the antiparasitic properties of MIF. In line with this, no MIF-mediated activation was detected analyzing macrophages derived from iNOS-deficient mice. The effect of MIF was blocked completely by the macrophage-deactivating cytokines IL-10, IL-13, and TGF-ß. Finally, the expression of MIF mRNA and protein was up-regulated in lymph nodes of mice during the first week after infection with L. major. MIF therefore represents a cytokine involved not only in the recruitment of proinflammatory cells during infection but also in the complex regulation of the antimicrobial activity of these cells.




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