{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:07:43Z","timestamp":1791274063420,"version":"4.1.0"},"reference-count":23,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2001,2,1]],"date-time":"2001-02-01T00:00:00Z","timestamp":980985600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2001,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>To determine the role of endogenous migration-inhibitory factor (MIF) in the development of protective immunity against cutaneous leishmaniasis, we analyzed the course of cutaneous<jats:italic>Leishmania major<\/jats:italic>infection in MIF gene-deficient mice (MIF<jats:sup>\u2212\/\u2212<\/jats:sup>) and wild-type (MIF<jats:sup>+\/+<\/jats:sup>) mice. Following cutaneous<jats:italic>L. major<\/jats:italic>infection, MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice were susceptible to disease and developed significantly larger lesions and greater parasite burdens than MIF<jats:sup>+\/+<\/jats:sup>mice. Interestingly, antigen-stimulated lymph node cells from MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice produced more interleukin-4 (IL-4) and gamma interferon (IFN-\u03b3) than those from MIF<jats:sup>+\/+<\/jats:sup>mice, although the differences were statistically not significant. IFN-\u03b3-activated resting peritoneal macrophages from MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice showed impaired macrophage leishmanicidal activity and produced significantly lower levels of nitric oxide and superoxide in vitro. The macrophages from MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice, however, produced much more IL-6 than macrophages from wild-type mice. These findings demonstrate that endogenous MIF plays an important role in the development of protective immunity against<jats:italic>L. major<\/jats:italic>in vivo. Furthermore, they indicate that the susceptibility of MIF<jats:sup>\u2212\/\u2212<\/jats:sup>mice to<jats:italic>L. major<\/jats:italic>infection is due to impaired macrophage leishmanicidal activity rather than dysregulation of Th1 and Th2 responses.<\/jats:p>","DOI":"10.1128\/iai.69.2.906-911.2001","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T10:01:19Z","timestamp":1027764079000},"page":"906-911","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":98,"title":["Migration-Inhibitory Factor Gene-Deficient Mice Are Susceptible to Cutaneous<i>Leishmania major<\/i>Infection"],"prefix":"10.1128","volume":"69","author":[{"given":"Abhay R.","family":"Satoskar","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Masschusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcelo","family":"Bozza","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Masschusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miriam","family":"Rodriguez Sosa","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Masschusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guoshing","family":"Lin","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Masschusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John R.","family":"David","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Masschusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.112.18.2993"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.15.7849"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/365756a0"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.189.2.341"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.179.6.1895"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(82)90118-X"},{"key":"e_1_3_2_8_2","doi-asserted-by":"crossref","first-page":"3682","DOI":"10.4049\/jimmunol.151.7.3682","article-title":"IL-6 down-modulates the cytokine-enhanced antileishmanial activity in human macrophages","volume":"151","author":"Hatzigeorgiou D. 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