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In this context, IFN-\u03b3 activates a variety of T. gondii\u2013targeting activities in immune and nonimmune cells but can also contribute to host immune pathology. T. gondii has evolved mechanisms to timely counteract the host IFN-\u03b3 defenses by interfering with the transcription of IFN-\u03b3\u2013stimulated genes. We now have identified TgIST (T. gondii inhibitor of STAT1 transcriptional activity) as a critical molecular switch that is secreted by intracellular parasites and traffics to the host cell nucleus where it inhibits STAT1-dependent proinflammatory gene expression. We show that TgIST not only sequesters STAT1 on dedicated loci but also promotes shaping of a nonpermissive chromatin through its capacity to recruit the nucleosome remodeling deacetylase (NuRD) transcriptional repressor. We found that during mice acute infection, TgIST-deficient parasites are rapidly eliminated by the homing Gr1+ inflammatory monocytes, thus highlighting the protective role of TgIST against IFN-\u03b3\u2013mediated killing. By uncovering TgIST functions, this study brings novel evidence on how T. gondii has devised a molecular weapon of choice to take control over a ubiquitous immune gene expression mechanism in metazoans, as a way to promote long-term parasitism.<\/jats:p>","DOI":"10.1084\/jem.20160340","type":"journal-article","created":{"date-parts":[[2016,8,8]],"date-time":"2016-08-08T17:46:30Z","timestamp":1470678390000},"page":"1779-1798","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":219,"title":["<i>Toxoplasma gondii<\/i> TgIST co-opts host chromatin repressors dampening STAT1-dependent gene regulation and IFN-\u03b3\u2013mediated host defenses"],"prefix":"10.1084","volume":"213","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5965-1842","authenticated-orcid":false,"given":"Gabrielle","family":"Gay","sequence":"first","affiliation":[{"name":"Institute for Advanced Biosciences (IAB), Team Host\u2013Pathogen Interactions and Immunity 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