{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T04:50:34Z","timestamp":1792731034970,"version":"4.5.0"},"reference-count":38,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The obligate intracellular parasite\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma gondii<\/jats:named-content>\n                    is able to infect nearly all nucleated cell types of warm-blooded animals. This is achieved through the injection of hundreds of parasite effectors into the host cell cytosol, allowing the parasite to establish a vacuolar niche for growth, replication, and persistence. Here we show that\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n                    infection actives an inflammasome response in mice and rats, an innate immune sensing system designed to survey the host cytosol for foreign components leading to inflammation and cell death. Oral infection with\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n                    triggers an inflammasome response that is protective to the host, limiting parasite load and dissemination.\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n                    infection is sufficient to generate an inflammasome response in germfree animals. Interleukin 1\u03b2 (IL-1\u03b2) secretion by macrophage requires the effector caspases 1 and 11, the adapter ASC, and NLRP1, the sensor previously described to initiate the inflammasome response to\n                    <jats:named-content content-type=\"genus-species\">Bacillus anthracis<\/jats:named-content>\n                    lethal factor. The allele of NLRP1b derived from 129 mice is sufficient to enhance the B6 bone marrow-derived macrophage (BMDM) inflammasome response to\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n                    independent of the lethal factor proteolysis site. Moreover, N-terminal processing of NLRP1b, the only mechanism of activation known to date, is not observed in response to\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n                    infection. Cumulatively, these data indicate that NLRP1 is an innate immune sensor for\n                    <jats:named-content content-type=\"genus-species\">Toxoplasma<\/jats:named-content>\n                    infection, activated via a novel mechanism that corresponds to a host-protective innate immune response to the parasite.\n                  <\/jats:p>","DOI":"10.1128\/iai.01170-13","type":"journal-article","created":{"date-parts":[[2013,11,12]],"date-time":"2013-11-12T00:09:02Z","timestamp":1384214942000},"page":"460-468","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":245,"title":["NLRP1 Is an Inflammasome Sensor for Toxoplasma gondii"],"prefix":"10.1128","volume":"82","author":[{"given":"Sarah E.","family":"Ewald","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph","family":"Chavarria-Smith","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C.","family":"Boothroyd","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Stanford School of Medicine, Stanford, California, 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