TREM2 governs Kupffer cell activation and explains belr1 genetic resistance to malaria liver stage infection

 Current efforts in malaria therapeutics and vaccine development include strategies aimed at deterring infection at the liver stage, preventing subsequent clinical complications and malaria transmission. To elucidate response mechanisms operating during liver stage infection, we searched for host genetic factors that control parasite expansion in a mouse model of malaria liver stage resistance. Here we report that the cell surface receptor TREM2 is expressed in innate immune cell types residing in the liver and takes part in a mechanism enabling such cells to control the yield of hepatocyte infection. This work highlights the relevance of innate immunity mechanisms in controlling expansion of the malaria parasite in the liver.

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