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Exosomes are tubular vesicles secreted by cells, and function in intercellular communication. It has been reported that the exosomes secreted by <jats:italic>T. gondii-<\/jats:italic>infected immune cells transmit infection signals to the uninfected cells. However, the mechanism and effect of the exosome transmission are still vague. We therefore investigated the function of the exosomes transmitted from DC2.4 cells infected with the <jats:italic>T. gondii<\/jats:italic> RH strain (<jats:italic>Tg<\/jats:italic>-DC-Exo) to the uninfected cells, as well as their roles in anti-infection.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>We conducted exosome isolation and identification with ultracentrifugation, transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blot (WB) analysis. Exosome uptake by recipient cells was identified by PKH67 assay. The signal transmission and the abundance of miR-155-5p were determined using transwell assay and qRT-PCR. For detection of immune responses, cytokine secretion was evaluated. The <jats:italic>T. gondii<\/jats:italic> B1 gene was determined to evaluate tachyzoite proliferation.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>We observed that <jats:italic>Toxoplasma<\/jats:italic> infection upregulated miR-155-5p expression in DC2.4 cell-secreted exosomes, and those exosomes could be ingested by murine macrophage RAW264.7 cells. <jats:italic>Tg<\/jats:italic>-DC-Exo and miR-155-5p stimulated host proinflammatory immune responses including increased production of proinflammatory cytokines IL-6 and TNF-\u03b1, and proinflammatory marker-inducible nitric oxide synthase (iNOS). The NF-\u03baB pathway was activated by downregulation of SOCS1, leading to inhibition of <jats:italic>T. gondii<\/jats:italic> tachyzoite proliferation in RAW264.7 cells.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Our findings provide a novel mechanism for how infected cells transmit infection signals to the uninfected cells through exosome secretion after <jats:italic>T. gondii<\/jats:italic> infection, followed by inflammatory responses and anti-infection reactions, which may help us develop a new strategy for toxoplasmosis prevention, especially in immunocompromised patients.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Graphical Abstract<\/jats:title>\n                \n              <\/jats:sec>","DOI":"10.1186\/s13071-021-05003-x","type":"journal-article","created":{"date-parts":[[2022,1,6]],"date-time":"2022-01-06T00:03:59Z","timestamp":1641427439000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Anti-infection roles of miR-155-5p packaged in exosomes secreted by dendritic cells infected with Toxoplasma gondii"],"prefix":"10.1186","volume":"15","author":[{"given":"Dan","family":"Jiang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuizhen","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liqing","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guantai","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dongliang","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongjuan","family":"Peng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2022,1,6]]},"reference":[{"key":"5003_CR1","doi-asserted-by":"publisher","first-page":"1965","DOI":"10.1016\/S0140-6736(04)16412-X","volume":"363","author":"JG Montoya","year":"2004","unstructured":"Montoya JG, Liesenfeld O. 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