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It has been demonstrated that\n                      <jats:italic>Toxoplasma gondii<\/jats:italic>\n                      (\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      ) infection during pregnancy can impair dM\u03c6 function, potentially leading to adverse pregnancy outcomes, through downregulation of these inhibitory molecules.\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      rhoptry protein 18 (\n                      <jats:italic>Tg<\/jats:italic>\n                      ROP18), a key virulence factor of\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      , is associated with the incapacitation of the host\u2019s innate and adaptive immune responses to protect the parasite from elimination. However, the role of\n                      <jats:italic>Tg<\/jats:italic>\n                      ROP18 in modulating CD73 expression on dM\u03c6 and the underlying mechanisms remain to be elucidated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Wild-type (WT) and CD73-deficient (CD73\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) pregnant mice were subjected to intraperitoneal injection of\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      RH or RH-\u0394\n                      <jats:italic>rop18<\/jats:italic>\n                      on gestational day (Gd) 8, and subsequently euthanized on Gd 14. Pregnancy outcomes were then evaluated, and the expression levels of CD73, arginase\u00a01 (Arg-1), and interleukin 10 (IL-10) were quantified by flow cytometry. Mononuclear cells isolated from the human aborted decidual tissues were also infected with\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      RH or RH-\u0394\n                      <jats:italic>rop18<\/jats:italic>\n                      for the analysis of CD73 expression with flow cytometry. Additionally, infected human dM\u03c6 were used to assess the expression levels of CD73, Arg-1, IL-10, and their associated signaling molecules by western blot analysis. Furthermore, chromatin immunoprecipitation (ChIP) assays were performed to validate the involved signaling pathways.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Compared with the\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      RH-infected group, milder adverse pregnancy outcomes and attenuated expression levels of CD73 on dM\u03c6 were observed in\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      RH-\u0394\n                      <jats:italic>rop18<\/jats:italic>\n                      -infected pregnant mice and human decidual tissues. Lysine-specific histone demethylase1 (LSD1) and snail family transcriptional repressor 1 (SNAIL1) were found to be involved in the downregulation of CD73 expression on dM\u03c6 following\n                      <jats:italic>T<\/jats:italic>\n                      .\n                      <jats:italic>gondii<\/jats:italic>\n                      infection. Subsequently, reduced expression of CD73 contribute to the downregulation of Arg-1 and IL-10 expression through adenosine A2a receptor (A2AR) \/ protein kinase A (PKA) \/ phosphorylated cAMP-response element binding protein (p-CREB) \/ CCAAT enhancer binding protein B (C\/EBP\u03b2) pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Tg<\/jats:italic>\n                      ROP18 can significantly reduce CD73 expression on dM\u03c6 through LSD1\/SNAIL1 pathway, subsequently leading to the decreased expression levels of Arg-1 and IL-10 via adenosine\/A2AR\/PKA\/p-CREB\/C\/EBP\u03b2 pathway, which ultimately contributes to maternal\u2013fetal tolerance dysfunction of dM\u03c6.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical Abstract<\/jats:title>\n                  <\/jats:sec>","DOI":"10.1186\/s13071-025-06713-2","type":"journal-article","created":{"date-parts":[[2025,2,24]],"date-time":"2025-02-24T11:30:29Z","timestamp":1740396629000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Toxoplasma gondii ROP18 induces maternal\u2013fetal dysfunction by downregulating CD73 expression on decidual macrophages"],"prefix":"10.1186","volume":"18","author":[{"given":"Jingjing","family":"Guo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Wei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuai","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junwei","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruohan","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Han","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aiqun","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuzhu","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuemei","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,2,24]]},"reference":[{"key":"6713_CR1","doi-asserted-by":"publisher","first-page":"125","DOI":"10.1016\/B978-0-444-53490-3.00008-X","volume":"114","author":"SK Halonen","year":"2013","unstructured":"Halonen SK, Weiss LM. 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Chem Biol Interact. 2023;382:110543.","journal-title":"Chem Biol Interact"}],"container-title":["Parasites &amp; Vectors"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1186\/s13071-025-06713-2.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/article\/10.1186\/s13071-025-06713-2\/fulltext.html","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1186\/s13071-025-06713-2.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,2,24]],"date-time":"2025-02-24T11:30:32Z","timestamp":1740396632000},"score":1,"resource":{"primary":{"URL":"https:\/\/parasitesandvectors.biomedcentral.com\/articles\/10.1186\/s13071-025-06713-2"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,2,24]]},"references-count":43,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2025,12]]}},"alternative-id":["6713"],"URL":"https:\/\/doi.org\/10.1186\/s13071-025-06713-2","relation":{},"ISSN":["1756-3305"],"issn-type":[{"value":"1756-3305","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,2,24]]},"assertion":[{"value":"4 December 2024","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"4 February 2025","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"24 February 2025","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"This study was based on the Declaration of Helsinki and subsequent amendments, and was approved by the Ethics Committee Binzhou Medical University Committee (approval no.: 2017-016-01). The experimental samples were obtained from female patients who were diagnosed as having a normal early pregnancy without complications by a specialized obstetrician-gynecologist, were not treated with medication, and had a history of toxoplasmosis infection. Patients voluntarily chose to terminate their pregnancies. All participants signed an informed consent form, and the collection was performed with the consent of the participants. Animal experiments were licensed by the Association of Laboratory Animals of Binzhou Medical University (license no. 2017-009-09) and were conducted in strict accordance with the Care and Use Guidelines.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"The authors declare no competing interests.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"72"}}