evades host innate immunity by releasing extracellular vesicles to activate TLR2-AKT signaling pathway.

Surra, one of the most important animal diseases with economic consequences in Asia and South America, is caused by . However, the mechanism of immune evasion by has not been extensively studied. In the present study, extracellular vesicles (TeEVs) were characterized and the role of TeEVs in infection were examined. The results showed that and 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 infection 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 . TeEVs and KMP-11 could inhibit the productions of IL-12p40 and IFN-γ, promote proliferation and shorten the survival time of infected mice . In conclusion, could 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 infection.Extracellular vesicles (EVs) secreted by () 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 infection via AKT pathway.