10.6084/M9.FIGSHARE.15112213.V3
Ran Wei
Ran
Wei
Xin Li
Xin
Li
Xiaocen Wang
Xiaocen
Wang
Nan Zhang
Nan
Zhang
Yuru Wang
Yuru
Wang
Xichen Zhang
Xichen
Zhang
Pengtao Gong
Pengtao
Gong
Jianhua Li
Jianhua
Li
<i>Trypanosoma evansi</i> evades host innate immunity by releasing extracellular vesicles to activate TLR2-AKT signaling pathway
<p>Surra, one of the most important animal diseases with economic consequences in Asia and South America, is caused by <i>Trypanosoma evansi</i>. However, the mechanism of immune evasion by <i>T. evansi</i> has not been extensively studied. In the present study, <i>T. evansi</i> extracellular vesicles (TeEVs) were characterized and the role of TeEVs in <i>T. evansi</i> infection were examined. The results showed that <i>T. evansi</i> and TeEVs could activate TLR2-AKT pathway to inhibit the secretions of IL-12p40, IL-6, and TNF-α in mouse BMDMs. TLR2<sup>−/-</sup> mice and mice with a blocked AKT pathway were more resistant to <i>T. evansi</i> 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 <i>in vitro</i>. TeEVs and KMP-11 could inhibit the productions of IL-12p40 and IFN-γ, promote <i>T. evansi</i> proliferation and shorten the survival time of infected mice <i>in vivo</i>. In conclusion, <i>T. evansi</i> 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 <i>T. evansi</i> infection.</p> <p>Extracellular vesicles (EVs) secreted by <i>Trypanosoma evansi</i> (<i>T. evansi</i>) 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 <i>T.</i> infection via AKT pathway.</p>
Medicine
Microbiology
Cell Biology
Pharmacology
Science Policy
Immunology
Infectious Diseases
Plant Biology
Taylor & Francis
2021
2021-12-27
2024-03-21
Journal contribution
5732292 Bytes
10.6084/m9.figshare.15112213
10.1080/21505594.2021.1959495
CC BY 4.0