Cerebral malaria is a severe complication of Plasmodium falciparum infection. Although T‐cell activation and type II IFN‐γ are required for Plasmodium berghei ANKA (PbA)‐induced murine experimental cerebral malaria (ECM), the role of type I IFN‐α/β in ECM development remains unclear. Here, we address the role of the IFN‐α/β pathway in ECM devel‐opment in response to hepatic or blood‐stage PbA infection, using mice deficient for types I or II IFN receptors. While IFN‐γR1^−/− mice were fully resistant, IFNAR1^−/− mice showed delayed and partial protection to ECM after PbA infection. ECM resistance in IFN‐γR1^−/− mice correlated with unaltered cerebral microcirculation and absence of ischemia, while WT and IFNAR1^−/− mice developed distinct microvascular pathologies. ECM resistance appeared to be independent of parasitemia. Instead, key mediators of ECM were attenuated in the absence of IFNAR1, including PbA‐induced brain sequestration of CXCR3⁺‐activated CD8⁺ T cells. This was associated with reduced expression of Granzyme B, IFN‐γ, IL‐12Rβ2, and T‐cell‐attracting chemokines CXCL9 and CXCL10 in IFNAR1^−/− mice, more so in the absence of IFN‐γR1. Therefore, the type I IFN‐α/β receptor pathway contributes to brain T‐cell responses and microvascular pathology, although it is not as essential as IFN‐γ for the development of cerebral malaria upon hepatic or blood‐stage PbA infection.