{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T03:36:25Z","timestamp":1793849785240,"version":"4.6.1"},"reference-count":42,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,1,30]],"date-time":"2008-01-30T00:00:00Z","timestamp":1201651200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2008,3]]},"abstract":"<jats:title>SUMMARY<\/jats:title><jats:p> <jats:italic>The caecal\u2010dwelling nematode <\/jats:italic>Trichuris muris<jats:italic> provides a natural model of human whipworm infection. Resistance to <\/jats:italic>T. muris <jats:italic>is dependent on a host Th2 response, and CD4<jats:sup>+<\/jats:sup>Th2 cells migrate to the gut\u2010associated lymphoid tissue (GALT) to elicit parasite expulsion. Thus, CD4<jats:sup>+<\/jats:sup>T cells infiltrate the caecal lamina propria during infection, along with other leucocyte subsets that are not critical for parasite expulsion, such as eosinophils. Trafficking of leucocytes to the GALT has been shown to be dependent on the \u03b1<jats:sub>4<\/jats:sub>\u03b2<jats:sub>7<\/jats:sub>\/MAdCAM\u20101 integrin\u2013addressin interaction. However, where inflammation is present, such as during <\/jats:italic>T. muris <jats:italic>infection, redundant mechanisms of leucocyte recruitment may also occur in addition to traditional gut\u2010homing interactions. We utilized an anti\u2010integrin\/addressin antibody treatment regime to investigate this redundancy in resistant, <\/jats:italic>T. muris<jats:italic>\u2010infected C57BL\/6 mice. Where only the \u03b1<jats:sub>4<\/jats:sub>\u03b2<jats:sub>7<\/jats:sub>\/MAdCAM\u20101 interaction was blocked, mice remained resistant to <\/jats:italic>T. muris <jats:italic>infection, making a Th2 response and both CD4<jats:sup>+<\/jats:sup>T cells and eosinophils infiltrated the site of infection. However, in the absence of available \u03b1<jats:sub>4<\/jats:sub>\u03b2<jats:sub>7<\/jats:sub> and \u03b1<jats:sub>4<\/jats:sub>\u03b2<jats:sub>1<\/jats:sub>, mice became chronically infected with <\/jats:italic>T. muris <jats:italic>and mounted a more Th1\u2010biased immune response. Interestingly, CD4<jats:sup>+<\/jats:sup>T cells, but not eosinophils, were able to infiltrate the caecum, showing different levels of redundancy between leucocyte subsets during infection.<\/jats:italic><\/jats:p>","DOI":"10.1111\/j.1365-3024.2007.01017.x","type":"journal-article","created":{"date-parts":[[2008,1,30]],"date-time":"2008-01-30T15:22:36Z","timestamp":1201706556000},"page":"163-170","source":"Crossref","is-referenced-by-count":17,"title":["Mechanisms of leucocyte recruitment to the inflamed large intestine: redundancy in integrin and addressin usage"],"prefix":"10.1111","volume":"30","author":[{"given":"L. V.","family":"BELL","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K. 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