{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T01:35:20Z","timestamp":1791336920438,"version":"4.3.1"},"reference-count":38,"publisher":"National Academy of Sciences","issue":"47","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2010,11,23]]},"abstract":"<jats:p>\n                    The propensity of helminths, such as schistosomes, to immunomodulate the host's immune system is an essential aspect of their survival. Previous research has demonstrated how soluble schistosomal egg antigens (SEA) dampen TLR-signaling during innate immune responses. We show here that the suppressive effect by SEA on TLR signaling is simultaneously coupled to the activation of the Nlrp3 (NLR family, pyrin domain containing 3) inflammasome and thus IL-1\u03b2 production. Therefore, the responsible protein component of SEA contains the second signal that is required to trigger proteolytic pro-IL-1\u03b2 processing. Moreover, the SEA component binds to the Dectin-2\/FcR\u03b3 (Fc receptor \u03b3 chain) complex and activates the Syk kinase signaling pathway to induce reactive oxygen species and potassium efflux. As IL-1\u03b2 has been shown to be an essential orchestrator against several pathogens we studied the in vivo consequences of\n                    <jats:italic>Schistosoma mansoni<\/jats:italic>\n                    infection in mice deficient in the central inflammasome adapter ASC and Nlrp3 molecule. These mice failed to induce local IL-1\u03b2 levels in the liver and showed decreased immunopathology. Interestingly, antigen-specific Th1, Th2, and Th17 responses were down-regulated. Overall, these data imply that component(s) within SEA induce IL-1\u03b2 production and unravel a crucial role of Nlrp3 during\n                    <jats:italic>S.<\/jats:italic>\n                    <jats:italic>mansoni<\/jats:italic>\n                    infection.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1010337107","type":"journal-article","created":{"date-parts":[[2010,11,9]],"date-time":"2010-11-09T02:04:38Z","timestamp":1289268278000},"page":"20459-20464","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":219,"title":["<i>Schistosoma<\/i>\n                    <i>mansoni<\/i>\n                    triggers Dectin-2, which activates the Nlrp3 inflammasome and alters adaptive immune responses"],"prefix":"10.1073","volume":"107","author":[{"given":"Manuel","family":"Ritter","sequence":"first","affiliation":[{"name":"Institute for Microbiology, Immunology and Hygiene, Technische Universit\u00e4t M\u00fcnchen, 81675 Munich, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olaf","family":"Gross","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Kays","sequence":"additional","affiliation":[{"name":"Institute for Microbiology, Immunology and Hygiene, Technische Universit\u00e4t M\u00fcnchen, 81675 Munich, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00fcrgen","family":"Ruland","sequence":"additional","affiliation":[{"name":"Institute of Molecular Immunology, University Hospital rechts der Isar, Technische Universit\u00e4t M\u00fcnchen, 81675 Munich, Germany;"},{"name":"Laboratory of Signaling in the Immune System, Helmholtz-Zentrum M\u00fcnchen-Germany, Research Center for Environmental Health, 85764 Neuherberg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Falk","family":"Nimmerjahn","sequence":"additional","affiliation":[{"name":"Experimental Immunology and Immunotherapy Medical Department 3, University of Erlangen-Nuernberg, 91054 Erlangen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinobu","family":"Saijo","sequence":"additional","affiliation":[{"name":"Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00fcrg","family":"Tschopp","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura E.","family":"Layland","sequence":"additional","affiliation":[{"name":"Institute for Microbiology, Immunology and Hygiene, Technische Universit\u00e4t M\u00fcnchen, 81675 Munich, Germany;"},{"name":"Institute of Medical Microbiology, Immunology and Parasitology, University Clinic Bonn, 53105 Bonn, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clarissa","family":"Prazeres da Costa","sequence":"additional","affiliation":[{"name":"Institute for Microbiology, Immunology and Hygiene, Technische Universit\u00e4t M\u00fcnchen, 81675 Munich, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2010,11,8]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri843"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200526273"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.173.1.159"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/376594a0"},{"key":"e_1_3_3_5_2","doi-asserted-by":"crossref","first-page":"4489","DOI":"10.4049\/jimmunol.163.8.4489","article-title":"TNF is essential for the cell-mediated protective immunity induced by the radiation-attenuated schistosome vaccine","volume":"163","author":"Street M","year":"1999","unstructured":"M Street, et al., TNF is essential for the cell-mediated protective immunity induced by the radiation-attenuated schistosome vaccine. 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