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Although T<\/jats:styled-content>\u2010cell activation and type II IFN<\/jats:styled-content>\u2010\u03b3 are required for P<\/jats:styled-content>lasmodium berghei<\/jats:italic> ANKA<\/jats:styled-content> (P<\/jats:styled-content>b<\/jats:italic>A<\/jats:styled-content>)\u2010induced murine experimental cerebral malaria (ECM<\/jats:styled-content>), the role of type I IFN<\/jats:styled-content>\u2010\u03b1\/\u03b2 in ECM<\/jats:styled-content> development remains unclear. Here, we address the role of the IFN<\/jats:styled-content>\u2010\u03b1\/\u03b2 pathway in ECM<\/jats:styled-content> devel\u2010opment in response to hepatic or blood\u2010stage P<\/jats:styled-content>b<\/jats:italic>A<\/jats:styled-content> infection, using mice deficient for types I or II IFN<\/jats:styled-content> receptors. While IFN<\/jats:styled-content>\u2010\u03b3R<\/jats:styled-content>1\u2212\/\u2212<\/jats:sup> mice were fully resistant, IFNAR<\/jats:styled-content>1\u2212\/\u2212<\/jats:sup> mice showed delayed and partial protection to ECM<\/jats:styled-content> after P<\/jats:styled-content>b<\/jats:italic>A<\/jats:styled-content> infection. ECM<\/jats:styled-content> resistance in IFN<\/jats:styled-content>\u2010\u03b3R<\/jats:styled-content>1\u2212\/\u2212<\/jats:sup> mice correlated with unaltered cerebral microcirculation and absence of ischemia, while WT<\/jats:styled-content> and IFNAR<\/jats:styled-content>1\u2212\/\u2212<\/jats:sup> mice developed distinct microvascular pathologies. ECM<\/jats:styled-content> resistance appeared to be independent of parasitemia. Instead, key mediators of ECM<\/jats:styled-content> were attenuated in the absence of IFNAR<\/jats:styled-content>1, including P<\/jats:styled-content>b<\/jats:italic>A<\/jats:styled-content>\u2010induced brain sequestration of CXCR<\/jats:styled-content>3+<\/jats:sup>\u2010activated CD<\/jats:styled-content>8+<\/jats:sup> T<\/jats:styled-content> cells. This was associated with reduced expression of G<\/jats:styled-content>ranzyme B<\/jats:styled-content>, IFN<\/jats:styled-content>\u2010\u03b3, IL<\/jats:styled-content>\u201012R<\/jats:styled-content>\u03b22, and T<\/jats:styled-content>\u2010cell\u2010attracting chemokines CXCL<\/jats:styled-content>9 and CXCL<\/jats:styled-content>10 in IFNAR<\/jats:styled-content>1\u2212\/\u2212<\/jats:sup> mice, more so in the absence of IFN<\/jats:styled-content>\u2010\u03b3R<\/jats:styled-content>1. Therefore, the type I IFN<\/jats:styled-content>\u2010\u03b1\/\u03b2 receptor pathway contributes to brain T<\/jats:styled-content>\u2010cell responses and microvascular pathology, although it is not as essential as IFN<\/jats:styled-content>\u2010\u03b3 for the development of cerebral malaria upon hepatic or blood\u2010stage P<\/jats:styled-content>b<\/jats:italic>A<\/jats:styled-content> infection.<\/jats:p>","DOI":"10.1002\/eji.201343327","type":"journal-article","created":{"date-parts":[[2013,6,18]],"date-time":"2013-06-18T15:09:38Z","timestamp":1371568178000},"page":"2683-2695","source":"Crossref","is-referenced-by-count":42,"title":["Type I interferons contribute to experimental cerebral malaria development in response to sporozoite or blood\u2010stage P<\/scp>lasmodium berghei<\/i>ANKA<\/scp>"],"prefix":"10.1002","volume":"43","author":[{"given":"Jennifer","family":"Palomo","sequence":"first","affiliation":[{"name":"CNRS, UMR7355 Orl\u00e9ans France"},{"name":"Experimental and 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