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Here we used MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice to determine the role of endogenous MIF in the regulation of the host immune response against<jats:italic>Trypanosoma cruzi<\/jats:italic>infection. MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice displayed high levels of blood and tissue parasitemia, developed severe heart and skeletal muscle immunopathology, and succumbed to<jats:italic>T. cruzi<\/jats:italic>infection faster than MIF<jats:sup>+\/+<\/jats:sup>mice. The enhanced susceptibility of MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice to<jats:italic>T. cruzi<\/jats:italic>was associated with reduced levels of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin-12 (IL-12), IL-18, gamma interferon (IFN-\u03b3), and IL-1\u03b2, in their sera and reduced production of IL-12, IFN-\u03b3, and IL-4 by spleen cells during the early phase of infection. At all time points, antigen-stimulated splenocytes from MIF<jats:sup>+\/+<\/jats:sup>and MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice produced comparable levels of IL-10. MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice also produced significantly less Th1-associated antigen-specific immunoglobulin G2a (IgG2a) throughout the infection, but both groups produced comparable levels of Th2-associated IgG1. Lastly, inflamed hearts from<jats:italic>T. cruzi<\/jats:italic>-infected MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice expressed increased transcripts for IFN-\u03b3, but fewer for IL-12 p35, IL-12 p40, IL-23, and inducible nitric oxide synthase, compared to MIF<jats:sup>+\/+<\/jats:sup>mice. Taken together, our findings show that MIF plays a role in controlling acute<jats:italic>T. cruzi<\/jats:italic>infection.<\/jats:p>","DOI":"10.1128\/iai.01648-05","type":"journal-article","created":{"date-parts":[[2006,5,19]],"date-time":"2006-05-19T23:52:41Z","timestamp":1148082761000},"page":"3170-3179","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":67,"title":["Macrophage Migration Inhibitory Factor Contributes to Host Defense against Acute<i>Trypanosoma cruzi<\/i>Infection"],"prefix":"10.1128","volume":"74","author":[{"given":"Jose\u0301 L.","family":"Reyes","sequence":"first","affiliation":[{"name":"Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Auto\u0301noma de Me\u0301xico (UNAM) Tlalnepantla"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis I.","family":"Terrazas","sequence":"additional","affiliation":[{"name":"Unidad de Biomedicina, Facultad de 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