{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T06:27:34Z","timestamp":1791354454326,"version":"4.3.1"},"reference-count":53,"publisher":"National Academy of Sciences","issue":"26","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,6,25]]},"abstract":"<jats:p>\n                    IFN-\u03b3 is a major cytokine that is critical for host resistance to a broad range of intracellular pathogens. Production of IFN-\u03b3 by natural killer and T cells is initiated by the recognition of pathogens by Toll-like receptors (TLRs). In an experimental model of toxoplasmosis, we have identified the presence of a nonlymphoid source of IFN-\u03b3 that was particularly evident in the absence of TLR-mediated recognition of\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    . Genetically altered mice lacking all lymphoid cells due to deficiencies in Recombination Activating Gene 2 and IL-2R\u03b3\n                    <jats:sub>c<\/jats:sub>\n                    genes also produced IFN-\u03b3 in response to the protozoan parasite. Flow-cytometry and morphological examinations of non-NK\/non-T IFN-\u03b3\n                    <jats:sup>+<\/jats:sup>\n                    cells identified neutrophils as the cell type capable of producing IFN-\u03b3. Selective elimination of neutrophils in TLR11\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice infected with the parasite resulted in acute susceptibility similar to that observed in IFN-\u03b3\u2013deficient mice. Similarly,\n                    <jats:italic>Salmonella typhimurium<\/jats:italic>\n                    infection of TLR-deficient mice induces the appearance of IFN-\u03b3\n                    <jats:sup>+<\/jats:sup>\n                    neutrophils. Thus, neutrophils are a crucial source for IFN-\u03b3 that is required for TLR-independent host protection against intracellular pathogens.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1307868110","type":"journal-article","created":{"date-parts":[[2013,6,11]],"date-time":"2013-06-11T00:02:47Z","timestamp":1370908967000},"page":"10711-10716","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":127,"title":["TLR-independent neutrophil-derived IFN-\u03b3 is important for host resistance to intracellular pathogens"],"prefix":"10.1073","volume":"110","author":[{"given":"Carolyn R.","family":"Sturge","sequence":"first","affiliation":[{"name":"Departments of aImmunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alicia","family":"Benson","sequence":"additional","affiliation":[{"name":"Departments of aImmunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Megan","family":"Raetz","sequence":"additional","affiliation":[{"name":"Departments of aImmunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cara L.","family":"Wilhelm","sequence":"additional","affiliation":[{"name":"Departments of aImmunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Mirpuri","sequence":"additional","affiliation":[{"name":"Departments of aImmunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen S.","family":"Vitetta","sequence":"additional","affiliation":[{"name":"Departments of aImmunology and"},{"name":"Microbiology, and"},{"name":"Cancer Immunobiology Center, University of Texas Southwestern Medical School, Dallas, TX 75390"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix","family":"Yarovinsky","sequence":"additional","affiliation":[{"name":"Departments of aImmunology and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2013,6,10]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri3044"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri2657"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(04)83004-9"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.15.1.749"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri3210"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1270"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.3128869"},{"key":"e_1_3_3_8_2","doi-asserted-by":"crossref","first-page":"4045","DOI":"10.4049\/jimmunol.157.9.4045","article-title":"In the absence of endogenous IFN-gamma, mice develop unimpaired IL-12 responses to Toxoplasma gondii while failing to control acute infection","volume":"157","author":"Scharton-Kersten TM","year":"1996","unstructured":"TM Scharton-Kersten, et al., In the absence of endogenous IFN-gamma, mice develop unimpaired IL-12 responses to Toxoplasma gondii while failing to control acute infection. 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