{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T02:15:37Z","timestamp":1788315337377,"version":"build-2803163510"},"reference-count":82,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2015,12,1]],"date-time":"2015-12-01T00:00:00Z","timestamp":1448928000000},"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":[[2015,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Although acquired bone marrow failure (BMF) is considered a T cell\u2013mediated autoimmune disease, few studies have considered contributing roles of innate immune deviations following otherwise innocuous infections as a cause underlying the immune defects that lead to BMF. Type I IFN signaling plays an important role in protecting hematopoiesis during systemic stress responses to the opportunistic fungal pathogen Pneumocystis. During Pneumocystis lung infection, mice deficient in both lymphocytes and type I IFN receptor (IFrag\u2212\/\u2212) develop rapidly progressing BMF associated with accelerated hematopoietic cell apoptosis. However, the communication pathway eliciting the induction of BMF in response to this strictly pulmonary infection has been unclear. We developed a conditional-null allele of Ifnar1 and used tissue-specific induction of the IFrag\u2212\/\u2212 state and found that, following Pneumocystis lung infection, type I IFNs act not only in the lung to prevent systemic immune deviations, but also within the progenitor compartment of the bone marrow to protect hematopoiesis. In addition, transfer of sterile-filtered serum from Pneumocystis-infected mice as well as i.p. injection of Pneumocystis into uninfected IFrag\u2212\/\u2212 mice induced BMF. Although specific cytokine deviations contribute to induction of BMF, immune-suppressive treatment of infected IFrag\u2212\/\u2212 mice ameliorated its progression but did not prevent loss of hematopoietic progenitor functions. This suggested that additional, noncytokine factors also target and impair progenitor functions; and interestingly, fungal \u03b2-glucans were also detected in serum. In conclusion, our data demonstrate that type 1 IFN signaling protects hematopoiesis within the bone marrow compartment from the damaging effects of proinflammatory cytokines elicited by Pneumocystis in the lung and possibly at extrapulmonary sites via circulating fungal components.<\/jats:p>","DOI":"10.4049\/jimmunol.1501553","type":"journal-article","created":{"date-parts":[[2015,10,30]],"date-time":"2015-10-30T22:28:06Z","timestamp":1446244086000},"page":"5347-5357","source":"Crossref","is-referenced-by-count":64,"title":["Type I IFNs Act upon Hematopoietic Progenitors To Protect and Maintain Hematopoiesis during\n                    <i>Pneumocystis<\/i>\n                    Lung Infection in Mice"],"prefix":"10.1093","volume":"195","author":[{"given":"Justin R","family":"Prigge","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University , Bozeman, MT 59718"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teri R","family":"Hoyt","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University , Bozeman, MT 59718"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erin","family":"Dobrinen","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University , Bozeman, MT 59718"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mario R","family":"Capecchi","sequence":"additional","affiliation":[{"name":"Howard Hughes Medical Institute, University of Utah , Salt Lake City, UT 84112"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward E","family":"Schmidt","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University , Bozeman, MT 59718"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Meissner","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Montana State University , Bozeman, MT 59718"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2015,12,1]]},"reference":[{"key":"2025030704251151800_r1","doi-asserted-by":"crossref","first-page":"27","DOI":"10.4049\/jimmunol.1302061","article-title":"Infection-induced changes in hematopoiesis","volume":"192","author":"Glatman Zaretsky","year":"2014","journal-title":"J. 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