{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:06:28Z","timestamp":1774123588767,"version":"3.50.1"},"reference-count":48,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2008,8,1]],"date-time":"2008-08-01T00:00:00Z","timestamp":1217548800000},"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":[[2008,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Pulmonary complications of hematopoietic stem cell transplantation include infections and graft-versus-host diseases, such as idiopathic pneumonia syndrome (IPS). Conflicting data exist regarding the role of the interferon (IFN)-\u03b3\u2013producing Th1 CD4+ T-cell subset and IL-17A in IPS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To determine the role of IFN-\u03b3 and IL-17A in the establishment of pulmonary graft-versus-host disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A semiallogeneic murine model based on C57BL\/6 \u00d7 BALB\/c as recipients with transplantation of BALB\/c RAG2\u2212\/\u2212 bone marrow and transfer of different genetic knockout T cells (T-bet\u2212\/\u2212, IFN-\u03b3\u2212\/\u2212, IFN-\u03b3R\u2212\/\u2212) on a BALB\/c background. Lung tissue was examined for parenchymal changes and infiltrating cells by histology and fluorescence-activated cell sorter analysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>After transfer of semiallogeneic bone marrow together with donor CD4+ T cells lacking IFN-\u03b3 or T-bet\u2014a T-box transcription factor controlling Th1 commitment\u2014we found severe inflammation in the lungs, but no enhancement in other organs. In contrast, wild-type donor CD4+ T cells mediated minimal inflammation only, and donor CD8+ T cells were not required for IPS development. Mechanistically, the absence of IFN-\u03b3 or IFN-\u03b3 signaling in pulmonary parenchymal cells promoted expansion of IL-17A\u2013producing CD4+ T cells and local IL-17A release. In vivo depletion of IL-17A reduced disease severity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>One mechanism of IFN-\u03b3 protection against IPS is negative regulation of the expansion of pathogenic IL-17A\u2013producing CD4+ T cells through interaction with the IFN-\u03b3 receptor on the pulmonary parenchymal cell population.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.200711-1648oc","type":"journal-article","created":{"date-parts":[[2008,5,29]],"date-time":"2008-05-29T21:36:25Z","timestamp":1212096985000},"page":"379-388","source":"Crossref","is-referenced-by-count":53,"title":["Interferon-\u03b3 Regulates Idiopathic Pneumonia Syndrome, a Th17+CD4+ T-Cell\u2013mediated Graft-versus-Host Disease"],"prefix":"10.1093","volume":"178","author":[{"given":"Nora","family":"Mauermann","sequence":"first","affiliation":[{"name":"Experimental Critical Care 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