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ABSTRACTSurra, one of the most important animal diseases with economic consequences in Asia and South America, is caused by Trypanosoma evansi. However, the mechanism of immune evasion by T. evansihas not been extensively studied. In the present study, T. evansiextracellular vesicles (TeEVs) were characterized and the role of TeEVs in T. evansiinfection were examined. The results showed that T. evansiand TeEVs could activate TLR2-AKT pathway to inhibit the secretions of IL-12p40, IL-6, and TNF-α in mouse BMDMs. TLR2−/-mice and mice with a blocked AKT pathway were more resistant to T. evansiinfection than wild type (WT) mice, with a significantly lower infection rate, longer survival time and less parasite load, as well as an increased secretion level of IL-12p40 and IFN-γ. Kinetoplastid membrane protein-11 (KMP-11) of TeEVs could activate AKT pathway and inhibit the productions of IL-12p40, TNF-α, and IL-6 in vitro. TeEVs and KMP-11 could inhibit the productions of IL-12p40 and IFN-γ, promote T. evansiproliferation and shorten the survival time of infected mice in vivo. In conclusion, T. evansicould escape host immune response through inhibiting the productions of inflammatory cytokines via secreting TeEVs to activate TLR2-AKT pathway. KMP-11 in TeEVs was involved in promoting T. evansiinfection.Extracellular vesicles (EVs) secreted by Trypanosoma evansi(T. evansi) activate the TLR2-AKT signaling pathway to inhibit the production of inflammatory cytokines, thereby escaping the host’s immune response. Kinetoplastid membrane protein-11 (KMP-11) in EVs is related to the promotion of T.evansiinfection via AKT pathway.