{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T00:06:11Z","timestamp":1791331571819,"version":"4.3.1"},"reference-count":31,"publisher":"Rockefeller University Press","issue":"4","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,4,7]]},"abstract":"<jats:p>Ectopic lymphoid tissue, such as bronchus-associated lymphoid tissue (BALT) in the lung, develops spontaneously at sites of chronic inflammation or during infection. The molecular mechanisms underlying the neogenesis of such tertiary lymphoid tissue are still poorly understood. We show that the type of inflammation-inducing pathogen determines which key factors are required for the formation and maturation of BALT. Thus, a single intranasal administration of the poxvirus modified vaccinia virus Ankara (MVA) is sufficient to induce highly organized BALT with densely packed B cell follicles containing a network of CXCL13-expressing follicular DCs (FDCs), as well as CXCL12-producing follicular stromal cells. In contrast, mice treated with P. aeruginosa (P.a.) develop BALT but B cell follicles lack FDCs while still harboring CXCL12-positive follicular stromal cells. Furthermore, in IL-17\u2013deficient mice, P.a.-induced BALT largely lacks B cells as well as CXCL12-expressing stromal cells, and only loose infiltrates of T cells are present. We show that Toll-like receptor pathways are required for BALT induction by P.a., but not MVA, and provide evidence that IL-17 drives the differentiation of lung stroma toward podoplanin-positive CXCL12-expressing cells that allow follicle formation even in the absence of FDCs. Taken together, our results identify distinct pathogen-dependent induction and maturation pathways for BALT formation.<\/jats:p>","DOI":"10.1084\/jem.20131737","type":"journal-article","created":{"date-parts":[[2014,3,25]],"date-time":"2014-03-25T05:04:24Z","timestamp":1395723864000},"page":"643-651","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":211,"title":["IL-17\u2013induced CXCL12 recruits B cells and induces follicle formation in BALT in the absence of differentiated FDCs"],"prefix":"10.1084","volume":"211","author":[{"given":"Henrike","family":"Fleige","sequence":"first","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarina","family":"Ravens","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georgios Leandros","family":"Moschovakis","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jasmin","family":"B\u00f6lter","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefanie","family":"Willenzon","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerd","family":"Sutter","sequence":"additional","affiliation":[{"name":"Institute for Infectious Diseases and Zoonoses, University of Munich LMU, 80539 Munich, Germany 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susanne","family":"H\u00e4ussler","sequence":"additional","affiliation":[{"name":"Institute of Molecular Bacteriology 3 and 4"},{"name":"Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz-Centre for Infection Research and the Hannover Medical School, 30625 Hannover, Germany 3 and 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich","family":"Kalinke","sequence":"additional","affiliation":[{"name":"Institute of Molecular Bacteriology 3 and 4"},{"name":"Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz-Centre for Infection Research and the Hannover Medical School, 30625 Hannover, Germany 3 and 4"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Immo","family":"Prinz","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Reinhold","family":"F\u00f6rster","sequence":"additional","affiliation":[{"name":"Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany 1"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2014,3,24]]},"reference":[{"key":"2023072602093308000_bib1","doi-asserted-by":"publisher","first-page":"143","DOI":"10.1016\/S1074-7613(00)80596-8","article-title":"Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function","volume":"9","author":"Adachi","year":"1998","journal-title":"Immunity."},{"key":"2023072602093308000_bib2","doi-asserted-by":"publisher","first-page":"627","DOI":"10.1165\/rcmb.2003-0260OC","article-title":"Pseudomonas aeruginosa flagella activate airway epithelial cells through asialoGM1 and toll-like receptor 2 as well as toll-like receptor 5","volume":"30","author":"Adamo","year":"2004","journal-title":"Am. 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