The CXCR3 chemokine receptor is critical for the protective immune response to <i>Plasmodium</i>parasite infection of the liver.

Abstract No highly efficacious anti-malaria vaccine exists, but whole parasite immunization (WPI)where hosts receive live attenuated Plasmodium parasites that arrest in the liver is only strategy confers complete protection against future infection. Liver-resident memory CD8 T cells (TRM)that express chemokine receptor, CXCR3, are essential for WPI-induced protection. Yet, whether CXCR3-dependent signaling plays a functional role anti-parasite RMimmunity not fully understood. RNA-seq analyses on hepatocytes isolated from Plasmodium-infected mice showed an upregulation of chemokines, CXCL9 and CXCL10. We examined WT CXCR3 −/−mice upon WPI report contrast to animals, exhibit impaired control challenge given 40 days after immunization. Next, we set out enumerate cell recruitment RMnumbers WPI. exhibited reduced numbers early yet by day contained equivalent as compared immunized counterparts. hypothesize while critical activated into liver, other chemokines compensate loss ensuring eventually recruited liver. However, infection despite containing RMnumbers, axis must play unidentified roles. Immune known be asymmetrically positioned Ongoing studies will determine if optimal positioning function RMs