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Blocking B7 after <jats:italic>Trichuris muris<\/jats:italic> inoculation inhibits resistance and IL\u20104 elevations, instead resulting in an IFN\u2010\u03b3\u2010dominant response associated with susceptibility. However, blocking IFN\u2010\u03b3 under these conditions restores IL\u201013\u2010dependent resistance. In this study, we examined the mechanism of IL\u201013 up\u2010regulation and associated protection during this <jats:italic>in vivo<\/jats:italic> immune response. CD4<jats:sup>+<\/jats:sup> T cells and DX5<jats:sup>+<\/jats:sup>TCR<jats:sup>\u2013<\/jats:sup> cells were identified as the major producers of IL\u201013, and the DX5<jats:sup>+<\/jats:sup>TCR<jats:sup>\u2013<\/jats:sup> cells were phenotyped as NK cells, since they expressed CD11b, IL\u20102R\u03b2 and Ly49C but not c\u2010kit or Fc\u03f5RI. NK cell\u2010derived IL\u201013 elevations were T cell\u2010dependent, as CD4<jats:sup>+<\/jats:sup> T cell depletion blocked IL\u201013 production by mesenteric lymph node cells and induced susceptibility. IL\u201013 expression was increased independently of IL\u201012; however, blocking IL\u201018 function inhibited IL\u201013 production and increased susceptibility. These results indicate that CD4<jats:sup>+<\/jats:sup> T cells and NK cells are the major sources of IL\u201013 during the <jats:italic>in vivo<\/jats:italic> Th1 response induced by B7 blockade and that under these conditions, IL\u201018 is specifically required for the <jats:italic>in vivo<\/jats:italic> up\u2010regulation of IL\u201013 production and associated host protection.<\/jats:p>","DOI":"10.1002\/eji.200535668","type":"journal-article","created":{"date-parts":[[2006,3,28]],"date-time":"2006-03-28T10:46:34Z","timestamp":1143542794000},"page":"1187-1198","source":"Crossref","is-referenced-by-count":11,"title":["IL\u201018 stimulates IL\u201013\u2010mediated IFN\u2010\u03b3\u2010sensitive host resistance <i>in vivo<\/i>"],"prefix":"10.1002","volume":"36","author":[{"given":"Qian","family":"Liu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhugong","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeannette","family":"Whitmire","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Farhang","family":"Alem","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hossein","family":"Hamed","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Pesce","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"suffix":"Jr.","given":"Joseph\u2004F.","family":"Urban","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William\u2004C.","family":"Gause","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,4,25]]},"reference":[{"key":"e_1_2_7_1_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.21.120601.141142"},{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.0105-2896.2004.00186.x"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4906(03)00101-7"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni712"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.20.083001.084359"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.180.2.693"},{"key":"e_1_2_7_7_2","doi-asserted-by":"crossref","first-page":"4088","DOI":"10.4049\/jimmunol.158.9.4088","article-title":"Effects of blocking B7\u20101 and B7\u20102 interactions during a type 2 in vivo immune response.","volume":"158","author":"Greenwald R.","year":"1997","journal-title":"J. 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