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Residual signaling pathways that maintain survival of CLL cells might be targeted to improve ibrutinib\u2019s therapeutic activity, but the nature of these pathways is unclear. Ongoing activation of IFN receptors in patients on ibrutinib was suggested by the presence of type I and II IFN in blood together with the cycling behavior of IFN-stimulated gene (ISG) products when IFN signaling was blocked intermittently with the JAK inhibitor ruxolitinib. IFN signaling in CLL cells from human patients was not prevented by ibrutinib in vitro or in vivo, but ISG expression was significantly attenuated in vitro. ISGs such as CXCL10 that require concomitant activation of NF-\u03baB were decreased when this pathway was inhibited by ibrutinib. Other ISGs, exemplified by LAG3, were decreased as a result of inhibited protein translation. Effects of IFN on survival remained intact as type I and II IFN\u2013protected CLL cells from ibrutinib in vitro, which could be prevented by ruxolitinib and IFNR blocking Abs. These observations suggest that IFNs may help CLL cells persist and specific targeting of IFN signaling might deepen clinical responses of patients on ibrutinib.<\/jats:p>","DOI":"10.4049\/jimmunol.2000478","type":"journal-article","created":{"date-parts":[[2020,10,16]],"date-time":"2020-10-16T19:25:18Z","timestamp":1602876318000},"page":"2629-2639","source":"Crossref","is-referenced-by-count":11,"title":["Effect of Ibrutinib on the IFN Response of Chronic Lymphocytic Leukemia Cells"],"prefix":"10.1093","volume":"205","author":[{"given":"Meihui","family":"Xia","sequence":"first","affiliation":[{"name":"Biology Platform, Sunnybrook Research Institute , Toronto, Ontario M4N 3M5 ,","place":["Canada"]},{"name":"Department of Gynecology and Obstetrics, First Hospital, Jilin University , 130021 Changchun, Jilin ,","place":["China"]},{"name":"Department of Human Anatomy, College of Basic Medical Sciences, Jilin University , 130021 Changchun, Jilin 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