{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T07:52:55Z","timestamp":1793087575188,"version":"4.5.0"},"reference-count":43,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2014,4,1]],"date-time":"2014-04-01T00:00:00Z","timestamp":1396310400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Rapidly after infection, live\n            <jats:named-content content-type=\"genus-species\">Borrelia burgdorferi<\/jats:named-content>\n            , the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust\n            <jats:named-content content-type=\"genus-species\">Borrelia<\/jats:named-content>\n            -specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88- and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19\/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus,\n            <jats:named-content content-type=\"genus-species\">B. burgdorferi<\/jats:named-content>\n            infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust\n            <jats:named-content content-type=\"genus-species\">Borrelia<\/jats:named-content>\n            -specific immunity.\n          <\/jats:p>","DOI":"10.1128\/iai.00969-13","type":"journal-article","created":{"date-parts":[[2014,1,23]],"date-time":"2014-01-23T04:39:04Z","timestamp":1390451944000},"page":"1548-1558","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":44,"title":["MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease"],"prefix":"10.1128","volume":"82","author":[{"given":"Christine J.","family":"Hastey","sequence":"first","affiliation":[{"name":"Center for Comparative Medicine, University of California, Davis, Davis, California, USA"},{"name":"Microbiology Graduate Group, University of California, Davis, Davis, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennine","family":"Ochoa","sequence":"additional","affiliation":[{"name":"Center for Comparative Medicine, University of California, Davis, Davis, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kimberley J.","family":"Olsen","sequence":"additional","affiliation":[{"name":"Center for Comparative Medicine, University of California, Davis, Davis, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen W.","family":"Barthold","sequence":"additional","affiliation":[{"name":"Center for Comparative Medicine, University of California, Davis, Davis, California, USA"},{"name":"Microbiology Graduate Group, University of California, Davis, Davis, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Baumgarth","sequence":"additional","affiliation":[{"name":"Center for Comparative Medicine, University of California, Davis, Davis, California, USA"},{"name":"Microbiology Graduate Group, University of California, Davis, Davis, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198908313210906"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM200107123450207"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1002066"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.65.8.3107-3111.1997"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.61.11.4696-4702.1993"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/1521-4141(200112)31:12<3460::AID-IMMU3460>3.0.CO;2-X"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1103735"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2714"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-127-2-199707150-00006"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.65.10.4043-4047.1997"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.23.021704.115628"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)81798-5"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.193.2.207"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm.2036"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.20486"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01642-06"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1005"},{"key":"e_1_3_3_19_2","first-page":"521","article-title":"Isolation and cultivation of Lyme disease spirochetes","volume":"57","author":"Barbour AG","year":"1984","unstructured":"BarbourAG. 1984. 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