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A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-\u03b3 and TNF-\u03b1, is activated without infection. In relation to inflammatory liver injury, we hypothesized that &lt;i&gt;Toxoplasma gondii&lt;\/i&gt; inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1\/IRF-1 mechanism in liver inflammation. This study used IFN-\u03b3 and TNF-\u03b1 as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1\/IRF-1 axis. In stable cells transfected with &lt;i&gt;TgIST&lt;\/i&gt;, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-\u03baB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9\/10\/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3\/8\/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-\u03b3\/TNF-\u03b1 stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.<\/jats:p>","DOI":"10.3347\/phd.23129","type":"journal-article","created":{"date-parts":[[2024,2,29]],"date-time":"2024-02-29T00:37:27Z","timestamp":1709167047000},"page":"30-41","update-policy":"https:\/\/doi.org\/10.3347\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Toxoplasma gondii IST suppresses inflammatory and apoptotic responses by inhibiting STAT1-mediated signaling in IFN-\u03b3\/TNF-\u03b1-stimulated 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