{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T07:13:16Z","timestamp":1791529996379,"version":"4.3.4"},"reference-count":52,"publisher":"National Academy of Sciences","issue":"1","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,1,2]]},"abstract":"<jats:p>\n                    Parasitic helminths are a major cause of chronic human disease, affecting more than 3 billion people worldwide. Host protection against most parasitic helminths relies upon Type 2 cytokine production, but the mechanisms that regulate interleukin (IL) 4 and 13 production from CD4\n                    <jats:sup>+<\/jats:sup>\n                    T helper 2 cells (T\n                    <jats:sub>H<\/jats:sub>\n                    2) and innate lymphoid type 2 cells (ILC2s) remain incompletely understood. The epithelial cell-derived cytokines IL-25 and IL-33 promote Type 2 responses, but the extent of functional redundancy between these cytokines is unclear and whether Type 2 memory relies upon either IL-25 or IL-33 is unknown. Herein, we demonstrate a pivotal role for IL-33 in driving primary and anamnestic immunity against the rodent hookworm\n                    <jats:italic>Nippostrongylus brasiliensis<\/jats:italic>\n                    . IL-33\u2013deficient mice have a selective defect in ILC2\u2013derived IL-13 during both primary and secondary challenge infections but generate stronger canonical CD4\n                    <jats:sup>+<\/jats:sup>\n                    T helper 2 cells responses (IL-4, IgE, mast cells, and basophils) than WT controls. Lack of IL-13 production in IL-33\u2013deficient mice impairs resistin-like molecule beta (RELM\u03b2) expression and eosinophil recruitment, which are two mechanisms that eliminate\n                    <jats:italic>N. brasiliensis<\/jats:italic>\n                    parasites from infected hosts. Thus, IL-33 is requisite for IL-13 but not IL-4\u2013driven Type 2 responses during hookworm infection.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1206587110","type":"journal-article","created":{"date-parts":[[2012,12,18]],"date-time":"2012-12-18T00:24:36Z","timestamp":1355790276000},"page":"282-287","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":207,"title":["IL-33 drives biphasic IL-13 production for noncanonical Type 2 immunity against hookworms"],"prefix":"10.1073","volume":"110","author":[{"given":"Li-Yin","family":"Hung","sequence":"first","affiliation":[{"name":"Division of Experimental Medicine, University of California, San Francisco, CA 94110;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian P.","family":"Lewkowich","sequence":"additional","affiliation":[{"name":"Division of Immunobiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, OH 45229; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucas A.","family":"Dawson","sequence":"additional","affiliation":[{"name":"Division of Immunobiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, OH 45229; 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