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Here, we investigated the roles of IFN-\u03b3 and IL-17A, key T-cell cytokines significantly elevated in patients with CRS, in the immunopathogenesis of CRS-induced extrapulmonary ALI. CRS was induced in wild-type (WT), IL-17A- and IFN-\u03b3 knockout (KO) human leukocyte antigen-DR3 transgenic mice with 10 \u03bcg of the superantigen, staphylococcal enterotoxin B, given intraperitoneally. Several ALI parameters, including gene expression profiling in the lungs, were studied 4, 24, or 48 hours later. Systemic T-cell activation with staphylococcal enterotoxin B resulted in robust upregulation of several chemokines, S100A8\/A9, matrix metalloproteases, and other molecules implicated in tissue damage, granulocyte as well as agranulocyte adhesion, and diapedesis in the lungs as early as 4 hours, which was accompanied by subsequent neutrophil\/eosinophil lung infiltration and severe ALI in IFN-\u03b3 KO mice. These pathways were significantly underexpressed in IL-17A KO mice, which manifested mildest ALI and intermediate in WT mice. Neutralization of IFN-\u03b3 worsened ALI in WT and IL-17A KO mice, whereas neutralizing IL-17A did not mitigate lung injury in IFN-\u03b3 KO mice, suggesting a dominant protective role for IFN-\u03b3 in ALI and that IL-17A is dispensable. Ruxolitinib, a Janus kinase inhibitor, increased ALI severity in WT mice. Thus, our study identified novel mechanisms of ALI in CRS and its differential modulation by IFN-\u03b3 and IL-17A.<\/jats:p>","DOI":"10.1165\/rcmb.2022-0117oc","type":"journal-article","created":{"date-parts":[[2022,9,20]],"date-time":"2022-09-20T09:39:29Z","timestamp":1663666769000},"page":"75-89","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":17,"title":["IFN-\n                    <b>\u03b3<\/b>\n                    is Protective in Cytokine Release Syndrome-associated Extrapulmonary Acute Lung Injury"],"prefix":"10.1093","volume":"68","author":[{"given":"Ying","family":"Sun","sequence":"first","affiliation":[{"name":"Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Buqu","family":"Hu","sequence":"additional","affiliation":[{"name":"Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gail","family":"Stanley","sequence":"additional","affiliation":[{"name":"Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zachary M.","family":"Harris","sequence":"additional","affiliation":[{"name":"Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samir","family":"Gautam","sequence":"additional","affiliation":[{"name":"Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Homer","sequence":"additional","affiliation":[{"name":"Section of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, and"},{"name":"Department of Pathology, Yale University 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