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Examination of SLAMF9 expression and function indicates that SLAMF9 promotes inflammation by specialized subsets of antigen\u2010presenting cells. Within healthy liver and circulating mouse peripheral blood mononuclear cells, SLAMF9 is expressed on CD11b<jats:sup>+<\/jats:sup>, Ly6C<jats:sup>\u2212<\/jats:sup>, CD11c<jats:sup>low<\/jats:sup>, F4\/80<jats:sup>low<\/jats:sup>, MHC\u2010II<jats:sup>+<\/jats:sup>, CX<jats:sub>3<\/jats:sub>CR1<jats:sup>+<\/jats:sup> mononuclear phagocytes as well as plasmacytoid dendritic cells. In addition, SLAMF9 can be found on peritoneal B1 cells and small (F4\/80<jats:sup>low<\/jats:sup>), but not large (F4\/80<jats:sup>high<\/jats:sup>), peritoneal macrophages. Upon systemic challenge with <jats:italic>Salmonella enterica<\/jats:italic> Typhimurium, <jats:italic>Slamf9<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice were impaired in their ability to clear the infection from the liver. In humans, SLAMF9 is up\u2010regulated upon differentiation of monocytes into macrophages, and lipopolysaccharide stimulation of PMA\u2010differentiated, SLAMF9 knockdown THP\u20101 cells showed an essential role of SLAMF9 in production of granulocyte\u2013macrophage colony\u2010stimulating factor, tumour necrosis factor\u2010<jats:italic>\u03b1<\/jats:italic>, and interleukin\u20101<jats:italic>\u03b2<\/jats:italic>. Taken together, these data implicate SLAMF9 in the initiation of inflammation and clearance of bacterial infection.<\/jats:p>","DOI":"10.1111\/imm.13169","type":"journal-article","created":{"date-parts":[[2019,12,27]],"date-time":"2019-12-27T12:57:25Z","timestamp":1577451445000},"page":"393-403","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Signalling lymphocyte activation molecule family member 9 is found on select subsets of antigen\u2010presenting cells and promotes resistance to <i>Salmonella<\/i> infection"],"prefix":"10.1111","volume":"159","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8403-9401","authenticated-orcid":false,"given":"Timothy J.","family":"Wilson","sequence":"first","affiliation":[{"name":"Department of Microbiology Miami University Oxford OH USA"},{"name":"Department of Medicine Cambridge Institute for Medical Research University of Cambridge Cambridge UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon","family":"Clare","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute Hinxton Cambridge UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joseph","family":"Mikulin","sequence":"additional","affiliation":[{"name":"Department of Microbiology Miami University Oxford OH USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher M.","family":"Johnson","sequence":"additional","affiliation":[{"name":"MRC Laboratory of Molecular Biology Cambridge UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katherine","family":"Harcourt","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute Hinxton Cambridge UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul A.","family":"Lyons","sequence":"additional","affiliation":[{"name":"Department of Medicine Cambridge Institute for Medical Research University of Cambridge Cambridge UK"},{"name":"Cambridge Institute for Therapeutic Immunology and Infectious Disease Department of Medicine University of Cambridge Cambridge UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gordon","family":"Dougan","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute Hinxton Cambridge UK"},{"name":"Cambridge Institute for Therapeutic Immunology and Infectious Disease Department of Medicine University of Cambridge Cambridge UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3829-4326","authenticated-orcid":false,"given":"Kenneth G. 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