{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T02:39:11Z","timestamp":1774579151859,"version":"3.50.1"},"reference-count":43,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2023,7,6]],"date-time":"2023-07-06T00:00:00Z","timestamp":1688601600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007812","name":"University of Washington","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007812","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Intestinal helminth infection promotes a Type 2 inflammatory response in resistant C57BL\/6 mice that is essential for worm clearance. The study of inbred mouse strains has revealed factors that are critical for parasite resistance and delineated the role of Type 1 versus Type 2 immune responses in worm clearance. In C57BL\/6 mice, basophils are key innate immune cells that promote Type 2 inflammation and are programmed via the Notch signalling pathway during infection with the helminth <jats:italic>Trichuris muris<\/jats:italic>. However, how the host genetic background influences basophil responses and basophil expression of Notch receptors remains unclear. Here we use genetically susceptible inbred AKR\/J mice that have a Type 1\u2010skewed immune response during <jats:italic>T<\/jats:italic>. <jats:italic>muris<\/jats:italic> infection to investigate basophil responses in a susceptible host. Basophil population expansion occurred in AKR\/J mice even in the absence of fulminant Type 2 inflammation during <jats:italic>T<\/jats:italic>. <jats:italic>muris<\/jats:italic> infection. However, basophils in AKR\/J mice did not robustly upregulate expression of the Notch2 receptor in response to infection as occurred in C57BL\/6 mice. Blockade of the Type 1 cytokine interferon\u2010\u03b3 in infected AKR\/J mice was not sufficient to elicit infection\u2010induced basophil expression of the Notch2 receptor. These data suggest that the host genetic background, outside of the Type 1 skew, is important in regulating basophil responses during <jats:italic>T<\/jats:italic>. <jats:italic>muris<\/jats:italic> infection in susceptible AKR\/J mice.<\/jats:p>","DOI":"10.1111\/pim.12999","type":"journal-article","created":{"date-parts":[[2023,7,7]],"date-time":"2023-07-07T03:49:31Z","timestamp":1688701771000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Basophil responses in susceptible <scp>AKR<\/scp> mice upon infection with the intestinal helminth parasite <i>Trichuris muris<\/i>"],"prefix":"10.1111","volume":"45","author":[{"given":"Shuchi","family":"Smita","sequence":"first","affiliation":[{"name":"Department of Immunology University of Washington  Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1903-7570","authenticated-orcid":false,"given":"Lauren M.","family":"Webb","sequence":"additional","affiliation":[{"name":"Department of Immunology University of Washington  Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bridget","family":"Mooney","sequence":"additional","affiliation":[{"name":"Department of Immunology University of Washington  Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simon P.","family":"Fr\u00fch","sequence":"additional","affiliation":[{"name":"Baker Institute for Animal Health and Department of Microbiology and Immunology Cornell University College of Veterinary Medicine  Ithaca New York USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5347-7502","authenticated-orcid":false,"given":"Oyebola O.","family":"Oyesola","sequence":"additional","affiliation":[{"name":"Department of Immunology University of Washington  Seattle Washington USA"},{"name":"Baker Institute for Animal Health and Department of Microbiology and Immunology Cornell University College of Veterinary Medicine  Ithaca New York USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Macy K.","family":"Matheson","sequence":"additional","affiliation":[{"name":"Department of Immunology University of Washington  Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Seth A.","family":"Peng","sequence":"additional","affiliation":[{"name":"Baker Institute for Animal Health and Department of Microbiology and Immunology Cornell University College of Veterinary Medicine  Ithaca New York USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elia D. 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