{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T20:44:45Z","timestamp":1791233085421,"version":"4.1.0"},"reference-count":44,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,4,4]],"date-time":"2014-04-04T00:00:00Z","timestamp":1396569600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Canadian Institutes of Health Research (CIHR)"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:p>The immune mechanisms underlying delayed induction of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010type immunity in the lungs following pulmonary mycobacterial infection remain poorly understood. We have herein investigated the underlying immune mechanisms for such delayed responses and whether a selected innate immune\u2010modulating strategy can accelerate <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010type responses. We have found that, in the early stage of pulmonary infection with attenuated <jats:italic><jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>ycobacterium tuberculosis<\/jats:italic> (<jats:italic><jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>.tb<\/jats:italic> <jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>37<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>a), the levels of infection in the lung continue to increase logarithmically until days 14 and 21 postinfection in <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 mice. The activation of innate immune responses, particularly <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s, in the lung is delayed. This results in a delay in the subsequent downstream immune responses including the migration of antigen\u2010bearing <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s to the draining lymph node (d<jats:styled-content style=\"fixed-case\">LN<\/jats:styled-content>), the <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010cell priming in d<jats:styled-content style=\"fixed-case\">LN<\/jats:styled-content>, and the recruitment of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1 cells to the lung. However, single lung mucosal exposure to the <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content> agonist <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>im<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content> postinfection is able to accelerate protective <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010type immunity via facilitating <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> migration to the lung and draining lymph nodes, enhancing <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> antigen presentation and <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010cell priming. These findings hold implications for the development of immunotherapeutic and vaccination strategies and suggest that enhancement of early innate immune activation is a viable option for improving <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1\u2010type immunity against pulmonary mycobacterial diseases.<\/jats:p>","DOI":"10.1002\/eji.201344300","type":"journal-article","created":{"date-parts":[[2014,2,12]],"date-time":"2014-02-12T12:21:17Z","timestamp":1392207677000},"page":"1375-1386","source":"Crossref","is-referenced-by-count":24,"title":["Restoration of innate immune activation accelerates <scp>T<\/scp>h1\u2010cell priming and protection following pulmonary mycobacterial infection"],"prefix":"10.1002","volume":"44","author":[{"given":"Rocky","family":"Lai","sequence":"first","affiliation":[{"name":"McMaster Immunology Research Centre M. G. DeGroote Institute for Infectious Disease Research, and Department of Pathology and Molecular Medicine McMaster University  Hamilton Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mangalakumari","family":"Jeyanathan","sequence":"additional","affiliation":[{"name":"McMaster Immunology Research Centre M. G. DeGroote Institute for Infectious Disease Research, and Department of Pathology and Molecular Medicine McMaster University  Hamilton Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher R.","family":"Shaler","sequence":"additional","affiliation":[{"name":"McMaster Immunology Research Centre M. G. DeGroote Institute for Infectious Disease Research, and Department of Pathology and Molecular Medicine McMaster University  Hamilton Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniela","family":"Damjanovic","sequence":"additional","affiliation":[{"name":"McMaster Immunology Research Centre M. G. DeGroote Institute for Infectious Disease Research, and Department of Pathology and Molecular Medicine McMaster University  Hamilton Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amandeep","family":"Khera","sequence":"additional","affiliation":[{"name":"McMaster Immunology Research Centre M. G. DeGroote Institute for Infectious Disease Research, and Department of Pathology and Molecular Medicine McMaster University  Hamilton Ontario Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carly","family":"Horvath","sequence":"additional","affiliation":[{"name":"McMaster Immunology Research Centre M. G. 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