{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T16:54:13Z","timestamp":1793379253919,"version":"4.5.0"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2019,11,1]],"date-time":"2019-11-01T00:00:00Z","timestamp":1572566400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Bacterial, parasitic, and viral infections are well-known causes of lymphoid tissue disorganization, although the factors, both host and\/or pathogen derived, that mediate these changes are largely unknown. Ehrlichia muris infection in mice causes a loss of germinal center (GC) B cells that is accompanied by the generation of extrafollicular T-bet+ CD11c+ plasmablasts and IgM memory B cells. We addressed a possible role for TNF-\u03b1 in this process because this cytokine has been shown to regulate GC development. Ablation of TNF-\u03b1 during infection resulted in an 8-fold expansion of GL7+ CD38lo CD95+ GC B cells, and a 2.5- and 5-fold expansion of CD138+ plasmablasts and T-bet+ memory cells, respectively. These changes were accompanied by a reduction in splenomegaly, more organized T and B cell zones, and an improved response to Ag challenge. CXCL13, the ligand for CXCR5, was detected at 6-fold higher levels following infection but was much reduced following TNF-\u03b1 ablation, suggesting that CXCL13 dysregulation also contributes to loss of lymphoid tissue organization. T follicular helper cells, which also underwent expansion in infected TNF-\u03b1\u00ad\u2013deficient mice, may also have contributed to the expansion of T-bet+ B cells, as the latter are known to require T cell help. Our findings contrast with previously described roles for TNF-\u03b1 in GCs and reveal how host\u2013pathogen interactions can induce profound changes in cytokine and chemokine production that can alter lymphoid tissue organization, GC B cell development, and extrafollicular T-bet+ B cell generation.<\/jats:p>","DOI":"10.4049\/jimmunol.1900484","type":"journal-article","created":{"date-parts":[[2019,9,30]],"date-time":"2019-09-30T19:19:48Z","timestamp":1569871188000},"page":"2415-2424","source":"Crossref","is-referenced-by-count":73,"title":["TNF-\u03b1 Contributes to Lymphoid Tissue Disorganization and Germinal Center B Cell Suppression during Intracellular Bacterial Infection"],"prefix":"10.1093","volume":"203","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5126-2209","authenticated-orcid":false,"given":"Maria","family":"Popescu","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Upstate Medical University, State University of New York , Syracuse, NY 13210"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Berenice","family":"Cabrera-Martinez","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Upstate Medical University, State University of New York , Syracuse, NY 13210"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7051-4299","authenticated-orcid":false,"given":"Gary M","family":"Winslow","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Upstate Medical University, State University of New York , Syracuse, NY 13210"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,11,1]]},"reference":[{"key":"2025030417543871500_r1","doi-asserted-by":"crossref","first-page":"764","DOI":"10.1038\/nri2414","article-title":"Form follows function: lymphoid tissue microarchitecture in antimicrobial immune defence","volume":"8","author":"Junt","year":"2008","journal-title":"Nat. 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