{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T15:49:09Z","timestamp":1780328949051,"version":"3.54.1"},"reference-count":84,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,5,19]],"date-time":"2020-05-19T00:00:00Z","timestamp":1589846400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004359","name":"Vetenskapsr\u00e5det","doi-asserted-by":"publisher","award":["2018\u201302411"],"award-info":[{"award-number":["2018\u201302411"]}],"id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Biology of the Cell"],"published-print":{"date-parts":[[2020,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Toxoplasma gondii<\/jats:italic> is an obligate intracellular protozoan with the ability to infect virtually any type of nucleated cell in warm\u2010blooded vertebrates including humans. <jats:italic>Toxoplasma gondii<\/jats:italic> invades immune cells, which the parasite employs as shuttles for dissemination by a <jats:italic>Trojan horse<\/jats:italic> mechanism. Recent findings are starting to unveil how this parasite orchestrates the subversion of the migratory functions of parasitised mononuclear phagocytes, especially dendritic cells (DCs) and monocytes. Here, we focus on how <jats:italic>T. gondii<\/jats:italic> impacts host cell signalling that regulates leukocyte motility and systemic migration in tissues. Shortly after active parasite invasion, DCs undergo mesenchymal\u2010to\u2010amoeboid transition and adopt a high\u2010speed amoeboid mode of motility. To trigger migratory activation \u2013 termed hypermigratory phenotype \u2013 <jats:italic>T. gondii<\/jats:italic> induces GABAergic signalling, which results in calcium fluxes mediated by voltage\u2010gated calcium channels in parasitised DCs and brain microglia. Additionally, a TIMP\u20101\u2010CD63\u2010ITGB1\u2010FAK signalling axis and signalling via the receptor tyrosine kinase MET promotes sustained hypermigration of parasitised DCs. Recent reports show that the activated signalling pathways converge on the small GTPase Ras to activate the MAPK Erk signalling cascade, a central regulator of cell motility. To date, three <jats:italic>T. gondii<\/jats:italic>\u2010derived putative effector molecules have been linked to hypermigration: Tg14\u20103\u20103, TgWIP and ROP17. Here, we discuss their impact on the hypermigratory phenotype of phagocytes. Altogether, the emerging concept suggests that <jats:italic>T. gondii<\/jats:italic> induces metastasis\u2010like migratory properties in parasitised mononuclear phagocytes to promote infection\u2010related dissemination.<\/jats:p>","DOI":"10.1111\/boc.202000005","type":"journal-article","created":{"date-parts":[[2020,5,2]],"date-time":"2020-05-02T16:24:52Z","timestamp":1588436692000},"page":"239-250","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["The unicellular eukaryotic parasite <i>Toxoplasma gondii<\/i> hijacks the migration machinery of mononuclear phagocytes to promote its dissemination"],"prefix":"10.1111","volume":"112","author":[{"given":"Einar B.","family":"\u00d3lafsson","sequence":"first","affiliation":[{"name":"Department of Molecular Biosciences The Wenner\u2010Gren Institute Stockholm University  Stockholm 10691 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