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To unravel this mechanism, we investigated the influence of primary infection of mice with nonlethal<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. microti<\/jats:named-content>using different time courses on the outcome of subsequent lethal<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. rodhaini<\/jats:named-content>infection. Simultaneous infections of mice with these parasites resulted in rapid increases in parasitemia, with 100% mortality in BALB\/c mice, as observed with control mice infected with<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. rodhaini<\/jats:named-content>alone. In contrast, mice with acute, resolving, and chronic-phase<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. microti<\/jats:named-content>infections were completely protected against<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. rodhaini<\/jats:named-content>, resulting in low parasitemia and no mortalities. Mice immunized with dead<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. microti<\/jats:named-content>were not protected from<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. rodhaini<\/jats:named-content>infection, although high antibody responses were induced. Interestingly, the protected mice had significantly decreased levels of antibody response, cytokines (including gamma interferon [IFN-\u03b3], interleukin-2 [IL-2], IL-8, IL-10, and IL-12), and nitric oxide levels after infection with<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. rodhaini<\/jats:named-content>. SCID mice and IFN-\u03b3-deficient mice with chronic<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. microti<\/jats:named-content>infections demonstrated protective responses comparable to those of immunocompetent mice. Likewise,<jats:italic>in vivo<\/jats:italic>NK cell depletion did not significantly impair the protective responses. Conversely, macrophage depletion resulted in increased susceptibility to<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. rodhaini<\/jats:named-content>infection associated with changes in their antibody and cytokines profiles, indicating that macrophages contribute to the protection against this challenge infection. We conclude that future development of vaccines against<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Babesia<\/jats:named-content>should include a strategy that enhances the appropriate activation of macrophages.<\/jats:p>","DOI":"10.1128\/iai.05900-11","type":"journal-article","created":{"date-parts":[[2011,11,8]],"date-time":"2011-11-08T08:23:31Z","timestamp":1320740611000},"page":"311-320","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":23,"title":["Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice"],"prefix":"10.1128","volume":"80","author":[{"given":"Yan","family":"Li","sequence":"first","affiliation":[{"name":"National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido, 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