{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T09:02:11Z","timestamp":1790413331697,"version":"4.1.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2006,8,1]],"date-time":"2006-08-01T00:00:00Z","timestamp":1154390400000},"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":[[2006,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The fungus, Histoplasma capsulatum, produces a persistent infection. Reactivation histoplasmosis is largely a result of impaired immunity, but the perturbations associated with escape of the fungus from host defenses remain ill-defined. We analyzed a murine model of reactivation to elucidate the host defects that permit reactivation. C57BL\/6 mice were infected intranasally and, 42 days later, they were depleted of CD4+ and CD8+ cells. Elimination of these cells, but not either alone, produced a persistent infection over several weeks. Neutralization of IFN-\u03b3, TNF-\u03b1, or both did not induce reactivation. Endogenous IL-10 exacerbated reactivation. Depletion of T cells in B cell\u2212\/\u2212 mice induced a markedly higher burden in organs when compared with wild type. However, the infection remained persistent. Elimination of CD4+ cells alone or neutralization of cytokines increased the fungal load. The persistent infection was not dependent on \u03b3\u03b4 T cells or NK cells. Elimination of Thy-1.2+ cells in mice given mAb to CD4 and CD8 transformed reactivation into a progressive, lethal infection in B cell\u2212\/\u2212 and wild-type mice, but the tempo of progression was accelerated in the former. The data reveal the complex control by the host to prevent reactivation of this fungus.<\/jats:p>","DOI":"10.4049\/jimmunol.177.3.1763","type":"journal-article","created":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T16:59:02Z","timestamp":1398358742000},"page":"1763-1771","source":"Crossref","is-referenced-by-count":31,"title":["B Cells and CD4\u2212CD8\u2212 T Cells Are Key Regulators of the Severity of Reactivation Histoplasmosis"],"prefix":"10.1093","volume":"177","author":[{"given":"Holly L","family":"Allen","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Veterans Affairs Hospital, University of Cincinnati College of Medicine , Cincinnati, OH 45267"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"George S","family":"Deepe","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Veterans Affairs Hospital, University of Cincinnati College of Medicine , Cincinnati, OH 45267"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,8,1]]},"reference":[{"key":"2025032807093256700_R1","first-page":"3012","volume-title":"Principles and Practices of Infectious Diseases","year":"2004"},{"key":"2025032807093256700_R2","first-page":"1163","volume-title":"N. 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