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Imatinib, a tyrosine kinase inhibitor of oncogenic BCR-ABL protein expressed by chronic myelogenous leukemia (CML) cells, possesses off-targets including LCK expressed in T cells. We showed that imatinib-treated CML patients in complete molecular remission (CMR) exhibited selective depletion of effector T reg (eT reg) cells and significant increase in effector\/memory CD8+ T cells while non-CMR patients did not. Imatinib at CML-therapeutic concentrations indeed induced apoptosis specifically in eT reg cells and expanded tumor antigen\u2013specific CD8+ T cells in vitro in healthy individuals and melanoma patients, and suppressed colon tumor growth in vivo in mice. Mechanistically, because of FoxP3-dependent much lower expression of LCK and ZAP-70 in T reg cells compared with other T cells, imatinib inhibition of LCK further reduced their TCR signal intensity, rendering them selectively susceptible to signal-deprived apoptotis. Taken together, eT reg cell depletion by imatinib is instrumental in evoking effective immune responses to various cancers.<\/jats:p>","DOI":"10.1084\/jem.20191009","type":"journal-article","created":{"date-parts":[[2019,11,8]],"date-time":"2019-11-08T14:45:21Z","timestamp":1573224321000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":88,"title":["Tyrosine kinase inhibitor imatinib augments tumor immunity by depleting effector regulatory T cells"],"prefix":"10.1084","volume":"217","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1660-9892","authenticated-orcid":true,"given":"Atsushi","family":"Tanaka","sequence":"first","affiliation":[{"name":"Experimental Immunology, Immunology Frontier Research Center, Osaka University, Osaka, Japan 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