{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T18:30:26Z","timestamp":1787596226115,"version":"build-2736575974"},"update-to":[{"DOI":"10.1371\/journal.pntd.0013289","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2025,7,22]],"date-time":"2025-07-22T00:00:00Z","timestamp":1753142400000}}],"reference-count":54,"publisher":"Public Library of Science (PLoS)","issue":"7","license":[{"start":{"date-parts":[[2025,7,15]],"date-time":"2025-07-15T00:00:00Z","timestamp":1752537600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81802030 and 22476096"],"award-info":[{"award-number":["81802030 and 22476096"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004608","name":"Natural Science Foundation of Jiangsu Province","doi-asserted-by":"publisher","award":["BK20200088"],"award-info":[{"award-number":["BK20200088"]}],"id":[{"id":"10.13039\/501100004608","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosntds.org"],"crossmark-restriction":false},"short-container-title":["PLoS Negl Trop Dis"],"abstract":"<jats:p>\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    (\n                    <jats:italic>T. gondii<\/jats:italic>\n                    ) is an opportunistic parasite. After infection, macrophages finely regulate the immune response to restrict parasite proliferation. It is well-known that\n                    <jats:italic>N<\/jats:italic>\n                    <jats:sup>6<\/jats:sup>\n                    -methyladenosine (m\n                    <jats:sup>6<\/jats:sup>\n                    A) plays a critical role in fine-tuning gene expression. To investigate whether m\n                    <jats:sup>6<\/jats:sup>\n                    A modification is involved in regulating the anti-infection immune response in human macrophages against\n                    <jats:italic>T. gondii<\/jats:italic>\n                    , this study utilized\n                    <jats:italic>T. gondii<\/jats:italic>\n                    tachyzoites from the RH strain to infect human THP-1 macrophages. qPCR and ELISA results show that\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection mounted the expression of TNF-\u03b1, IL-1\u03b2, and IL-6. Transcriptomic data suggest that the infection of\n                    <jats:italic>T. gondii<\/jats:italic>\n                    induced differential gene expression in pathways associated with TNF signaling and cytokine-cytokine receptor interaction. Meanwhile, expression of m\n                    <jats:sup>6<\/jats:sup>\n                    A regulators were evaluated using qPCR and Western blotting.\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection increased the abundance of m\n                    <jats:sup>6<\/jats:sup>\n                    A demethylase FTO and methyltransferase WTAP. Joint analysis of RNA-seq and m\n                    <jats:sup>6<\/jats:sup>\n                    A-seq data was utilized for enriching differentially expressed genes (DEGs) with significantly altered m\n                    <jats:sup>6<\/jats:sup>\n                    A modifications. Intriguingly, following\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection, the m\n                    <jats:sup>6<\/jats:sup>\n                    A levels of DEGs associated with toxoplasmosis, TNF signaling pathway, and NF-\u03baB signaling pathway were significantly different. The m\n                    <jats:sup>6<\/jats:sup>\n                    A-IP-qPCR assay further confirmed that\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection led to the decrease in the levels of m\n                    <jats:sup>6<\/jats:sup>\n                    A modification in the 3\u2019UTR and 5\u2019UTR regions of\n                    <jats:italic>TNF-\u03b1<\/jats:italic>\n                    mRNA. Knocking-down of FTO retarded the infection induced-decrease in the levels of m\n                    <jats:sup>6<\/jats:sup>\n                    A modification in\n                    <jats:italic>TNF-\u03b1<\/jats:italic>\n                    transcripts, accompanied by dampened immune response and uncontrolled\n                    <jats:italic>T. gondii<\/jats:italic>\n                    proliferation. Furthermore, the YTHDF2 RIP assay indicates that\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection remarkably weakened the binding of YTHDF2 to\n                    <jats:italic>TNF-\u03b1<\/jats:italic>\n                    mRNA, which could mount TNF-\u03b1 expression by inhibiting the degradation of\n                    <jats:italic>TNF-\u03b1<\/jats:italic>\n                    mRNA. Overall, these findings suggest that m\n                    <jats:sup>6<\/jats:sup>\n                    A plays a role in the\n                    <jats:italic>T. gondii<\/jats:italic>\n                    infection-induced immune response in human macrophages, uncovering a new molecular mechanism for the regulation of TNF-\u03b1 expression from an epitranscriptomic aspect.\n                  <\/jats:p>","DOI":"10.1371\/journal.pntd.0013289","type":"journal-article","created":{"date-parts":[[2025,7,15]],"date-time":"2025-07-15T17:39:51Z","timestamp":1752601191000},"page":"e0013289","update-policy":"https:\/\/doi.org\/10.1371\/journal.pntd.corrections_policy","source":"Crossref","is-referenced-by-count":3,"title":["The m6A demethylase FTO regulates TNF-\u03b1 expression in human macrophages following Toxoplasma gondii 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