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We found in this study that Tyk2\u2010deficient (\u2013\/\u2013) mice showed increased susceptibility at the early stage after an i.p. infection with <jats:italic>Listeria monocytogenes<\/jats:italic>, accompanied by impaired IFN\u2010\u03b3 production. The numbers of both MHC class\u2004Ib (H2\u2010M3)\u2010 or MHC class\u2004Ia (K<jats:sup>b<\/jats:sup>)\u2010restricted CD8<jats:sup>+<\/jats:sup> T cells producing IFN\u2010\u03b3 and exhibiting cytotoxicity were significantly decreased in Tyk2<jats:sup>\u2013\/\u2013<\/jats:sup> mice after infection with <jats:italic>L.\u2004monocytogenes<\/jats:italic>. Using an adoptive transfer system of OT\u2010I cells expressing OVA<jats:sub>257\u2013264<\/jats:sub>\/K<jats:sup>b<\/jats:sup>\u2010specific TCR into Tyk2<jats:sup>\u2013\/\u2013<\/jats:sup> mice followed by challenge with recombinant <jats:italic>L.\u2004monocytogenes<\/jats:italic> expressing OVA, we found that the defective Tyk2 signaling in the host environment was at least partially responsible for the impaired CD8<jats:sup>+<\/jats:sup> T cytotoxic\u20101 (Tc1) cell responses in Tyk2<jats:sup>\u2013\/\u2013<\/jats:sup> mice following the infection. Adoptive transfer with MHC class\u2004Ib\u2010 or MHC class\u2004Ia\u2010binding peptide\u2010pulsed BM\u2010derived DC from Tyk2<jats:sup>\u2013\/\u2013<\/jats:sup> mice induced lower levels of the Ag\u2010specific CD8<jats:sup>+<\/jats:sup> Tc1 cells producing IFN\u2010\u03b3. These results suggest that Tyk2 signaling is also important for DC function in the induction of MHC class\u2004Ia\u2010 and class\u2004Ib\u2010restricted CD8<jats:sup>+<\/jats:sup> Tc1 cells following <jats:italic>L.\u2004monocytogenes<\/jats:italic> infection.<\/jats:p>","DOI":"10.1002\/eji.200636173","type":"journal-article","created":{"date-parts":[[2006,10,18]],"date-time":"2006-10-18T12:11:15Z","timestamp":1161173475000},"page":"3060-3070","source":"Crossref","is-referenced-by-count":23,"title":["An important role of Tyk2 in APC function of dendritic cells for priming CD8<sup>+<\/sup> T cells producing IFN\u2010\u03b3"],"prefix":"10.1002","volume":"36","author":[{"given":"Keiji","family":"Aizu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiki","family":"Yajima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshiyuki","family":"Arai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuya","family":"Shimoda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuji","family":"Nimura","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasunobu","family":"Yoshikai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,10,30]]},"reference":[{"key":"e_1_2_7_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/32588"},{"key":"e_1_2_7_2_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.20.100301.064828"},{"key":"e_1_2_7_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1127"},{"key":"e_1_2_7_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1112"},{"key":"e_1_2_7_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/79734"},{"key":"e_1_2_7_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/35006097"},{"key":"e_1_2_7_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/79758"},{"key":"e_1_2_7_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni0901-816"},{"key":"e_1_2_7_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/89726"},{"key":"e_1_2_7_10_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.21.120601.141040"},{"key":"e_1_2_7_11_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1246"},{"key":"e_1_2_7_12_2","doi-asserted-by":"crossref","first-page":"211","DOI":"10.1016\/S1074-7613(02)00365-5","article-title":"In vivo depletion of CD11c(+) dendritic cells abrogates priming of CD8(+) T cells by exogenous cell\u2010associated antigens.","volume":"17","author":"Jung S.","year":"2002","journal-title":"Immunity"},{"key":"e_1_2_7_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/377591a0"},{"key":"e_1_2_7_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)00055-8"},{"key":"e_1_2_7_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1074-7613(00)00054-6"},{"key":"e_1_2_7_16_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V99.6.2094"},{"key":"e_1_2_7_17_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200324465"},{"key":"e_1_2_7_18_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri1461"},{"key":"e_1_2_7_19_2","doi-asserted-by":"crossref","first-page":"2511","DOI":"10.4049\/jimmunol.151.5.2511","article-title":"Modulation of perforin and granzyme messenger RNA expression in human natural killer cells.","volume":"151","author":"Salcedo T. 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