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A third of the LPMs express the surface receptor VSIG4, but it is unclear whether these cells differ from their VSIG4\u2010negative counterparts and perform dedicated functions. We demonstrate that VSIG4\n                    <jats:sup>+<\/jats:sup>\n                    , but not VSIG4\n                    <jats:sup>\u2212<\/jats:sup>\n                    , LPMs are in the majority derived from embryonal precursors, and their occurrence is largely independent of sex and microbiota but increases with age. Although their transcriptome and surface proteome are indistinguishable from VSIG4\n                    <jats:sup>\u2212<\/jats:sup>\n                    LPMs at steady\u2010state, VSIG4\n                    <jats:sup>+<\/jats:sup>\n                    LPMs are superior in phagocytosing\n                    <jats:italic>S. aureus<\/jats:italic>\n                    bioparticles and colorectal carcinoma (CRC) cells. Anti\u2010VSIG4 nanobody constructs that are ADCC\u2010enabled allowed a selective elimination of the VSIG4\n                    <jats:sup>+<\/jats:sup>\n                    LPM subset without affecting overall LPM abundance. This strategy uncovered a role for VSIG4\n                    <jats:sup>+<\/jats:sup>\n                    LPMs in lowering the first peak of parasitemia in a\n                    <jats:italic>Trypanosoma brucei brucei<\/jats:italic>\n                    infection model and in reducing CRC outgrowth in the peritoneal cavity, a prime metastatic site in CRC patients. Altogether, our data uncover a protective role for VSIG4\n                    <jats:sup>+<\/jats:sup>\n                    LPMs in infectious and oncological diseases in the peritoneal cavity.\n                  <\/jats:p>","DOI":"10.1002\/eji.202551804","type":"journal-article","created":{"date-parts":[[2025,5,15]],"date-time":"2025-05-15T05:42:56Z","timestamp":1747287776000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["VSIG4\u2010Expressing Macrophages Contribute to Antiparasitic and Antimetastatic Responses in the Peritoneal Cavity"],"prefix":"10.1002","volume":"55","author":[{"given":"Els","family":"Lebegge","sequence":"first","affiliation":[{"name":"Laboratory of Cellular and Molecular Immunology Brussels Center for Immunology (BCIM) Vrije Universiteit Brussel  Brussels Belgium"},{"name":"Laboratory of Myeloid Cell Immunology VIB Center for Inflammation Research  Brussels Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daliya","family":"Kancheva","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular and Molecular Immunology Brussels Center for Immunology (BCIM) Vrije Universiteit Brussel  Brussels Belgium"},{"name":"Laboratory of Myeloid Cell Immunology VIB Center for Inflammation Research  Brussels Belgium"},{"name":"Laboratory of Dendritic Cell Biology and Cancer Immunotherapy VIB Center for Inflammation Research  Brussels Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jolien","family":"Van Craenenbroeck","sequence":"additional","affiliation":[{"name":"Laboratory of Cellular and Molecular Immunology Brussels Center for Immunology (BCIM) Vrije Universiteit Brussel  Brussels Belgium"},{"name":"Laboratory of Myeloid Cell Immunology VIB Center for Inflammation Research  Brussels Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sam","family":"Ernst","sequence":"additional","affiliation":[{"name":"Department of GI Surgery Ghent University Hospital  Ghent Belgium"},{"name":"Laboratory of Experimental Surgery Ghent University  Ghent Belgium"},{"name":"Cancer Research Institute Ghent (CRIG) Ghent University  Ghent Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4454-9823","authenticated-orcid":false,"given":"Pauline M. 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