{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T09:12:50Z","timestamp":1778058770267,"version":"3.51.4"},"reference-count":54,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,1,2]],"date-time":"2014-01-02T00:00:00Z","timestamp":1388620800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:p>The neutralization of toxins is considered essential for protection against lethal infection with <jats:italic><jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>acillus anthracis<\/jats:italic> (<jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content>), a select agent and bioterrorism threat. However, toxin\u2010neutralizing activity alone would not be expected to provide sterile immunity. Therefore, we hypothesized that the development of an adaptive immune response against <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> is required for bacterial clearance. We found that human monocyte\u2010derived dendritic cells (hDCs) kill germinated <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> bacilli, but not nongerminated <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> spores. h<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s produce <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012, and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023, and these cytokines are differentially regulated by germination\u2010proficient versus germination\u2010deficient <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> spores. Moreover, the <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023 response to <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> spores is regulated by <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101<jats:styled-content style=\"fixed-case\">R<\/jats:styled-content>\u2010mediated signaling. h<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s infected with germinating <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> spores stimulated autologous <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells to secrete <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 in a contact\u2010dependent and antigen\u2010specific manner. The <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell response to <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> spores was not recapitulated by h<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s infected with germination\u2010deficient <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content> spores, implying that the germination of spores into replicating bacilli triggers the proinflammatory cytokine response in h<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s. Our results provide primary evidence that h<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s can generate a <jats:styled-content style=\"fixed-case\">BA<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h17 response, and help elucidate the mechanisms involved. These novel findings suggest that the <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201023\/<jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h17 axis is involved in the immune response to anthrax in humans.<\/jats:p>","DOI":"10.1002\/eji.201343784","type":"journal-article","created":{"date-parts":[[2013,12,5]],"date-time":"2013-12-05T09:46:53Z","timestamp":1386236813000},"page":"752-762","source":"Crossref","is-referenced-by-count":17,"title":["The <scp>IL<\/scp>\u201023\/<scp>T<\/scp>h17 axis is involved in the adaptive immune response to <i><scp>B<\/scp>acillus anthracis<\/i> in humans"],"prefix":"10.1002","volume":"44","author":[{"given":"Kristina M.","family":"Harris","sequence":"first","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Girish","family":"Ramachandran","sequence":"additional","affiliation":[{"name":"Center for Vaccine Development University of Maryland School of Medicine  Baltimore MD USA"},{"name":"Department of Medicine, University of Maryland School of Medicine  Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Subhendu","family":"Basu","sequence":"additional","affiliation":[{"name":"Center for Vaccine Development University of Maryland School of Medicine  Baltimore MD USA"},{"name":"Department of Medicine, University of Maryland School of Medicine  Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandra","family":"Rollins","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dean","family":"Mann","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Maryland School of Medicine  Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alan S.","family":"Cross","sequence":"additional","affiliation":[{"name":"Center for Vaccine Development University of Maryland School of Medicine  Baltimore MD USA"},{"name":"Department of Medicine, University of Maryland School of Medicine  Baltimore MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2014,1,2]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature01794"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200838141"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.11.7495-7501.2005"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni1496"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2009.02.007"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1613"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1698"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI28508"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1007\/3-540-37673-9_8"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature07036"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200939498"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20061308"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2008.03.004"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200839102"},{"key":"e_1_2_7_16_1","first-page":"1899","article-title":"Cellular effectors mediating Th17\u2010dependent clearance of pneumococcal colonization in mice","volume":"119","author":"Zhang Z.","year":"2009","journal-title":"J. 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