{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:32:26Z","timestamp":1791307946096,"version":"4.3.1"},"reference-count":73,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,3,11]]},"abstract":"<jats:p>Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasia arising from the oncogenic break point cluster region\/Abelson murine leukemia viral oncogene homolog 1 translocation in hematopoietic stem cells (HSCs), resulting in a leukemia stem cell (LSC). Curing CML depends on the eradication of LSCs. Unfortunately, LSCs are resistant to current treatment strategies. The host\u2019s immune system is thought to contribute to disease control, and several immunotherapy strategies are under investigation. However, the interaction of the immune system with LSCs is poorly defined. In the present study, we use a murine CML model to show that LSCs express major histocompatibility complex (MHC) and co-stimulatory molecules and are recognized and killed by leukemia-specific CD8+ effector CTLs in vitro. In contrast, therapeutic infusions of effector CTLs into CML mice in vivo failed to eradicate LSCs but, paradoxically, increased LSC numbers. LSC proliferation and differentiation was induced by CTL-secreted IFN-\u03b3. Effector CTLs were only able to eliminate LSCs in a situation with minimal leukemia load where CTL-secreted IFN-\u03b3 levels were low. In addition, IFN-\u03b3 increased proliferation and colony formation of CD34+ stem\/progenitor cells from CML patients in vitro. Our study reveals a novel mechanism by which the immune system contributes to leukemia progression and may be important to improve T cell\u2013based immunotherapy against leukemia.<\/jats:p>","DOI":"10.1084\/jem.20121229","type":"journal-article","created":{"date-parts":[[2013,2,12]],"date-time":"2013-02-12T02:58:18Z","timestamp":1360637898000},"page":"605-621","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":78,"title":["Cytotoxic T cells induce proliferation of chronic myeloid leukemia stem cells by secreting interferon-\u03b3"],"prefix":"10.1084","volume":"210","author":[{"given":"Christian","family":"Sch\u00fcrch","sequence":"first","affiliation":[{"name":"Tumor Immunology, Department of Clinical Research 1 , 2 , and 3"},{"name":"Institute of Pathology 1 , 2 , and 3"},{"name":"Department of Medical Oncology, University of Bern, 3010 Bern, Switzerland 1 , 2 , and 3"},{"name":"Tumor Immunology, Department of Clinical Research 1 , 2 , and 3"},{"name":"Institute of Pathology 1 , 2 , and 3"},{"name":"Department of Medical Oncology, University of Bern, 3010 Bern, Switzerland 1 , 2 , and 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carsten","family":"Riether","sequence":"additional","affiliation":[{"name":"Tumor Immunology, Department of Clinical Research 1 , 2 , and 3"},{"name":"Institute of Pathology 1 , 2 , and 3"},{"name":"Department of Medical Oncology, University of Bern, 3010 Bern, Switzerland 1 , 2 , and 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael A.","family":"Amrein","sequence":"additional","affiliation":[{"name":"Tumor Immunology, Department of Clinical Research 1 , 2 , and 3"},{"name":"Institute of Pathology 1 , 2 , and 3"},{"name":"Department of Medical Oncology, University of Bern, 3010 Bern, Switzerland 1 , 2 , and 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrian F.","family":"Ochsenbein","sequence":"additional","affiliation":[{"name":"Tumor Immunology, Department of Clinical Research 1 , 2 , and 3"},{"name":"Institute of Pathology 1 , 2 , and 3"},{"name":"Department of Medical Oncology, University of Bern, 3010 Bern, Switzerland 1 , 2 , and 3"},{"name":"Tumor Immunology, Department of Clinical Research 1 , 2 , and 3"},{"name":"Institute of Pathology 1 , 2 , and 3"},{"name":"Department of Medical Oncology, University of Bern, 3010 Bern, Switzerland 1 , 2 , and 3"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2013,2,11]]},"reference":[{"key":"2023072601300490800_bib1","doi-asserted-by":"publisher","first-page":"1809","DOI":"10.1182\/blood-2006-02-005686","article-title":"Evolving concepts in the management of chronic myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet","volume":"108","author":"Baccarani","year":"2006","journal-title":"Blood."},{"key":"2023072601300490800_bib2","doi-asserted-by":"publisher","first-page":"793","DOI":"10.1038\/nature09135","article-title":"Quiescent haematopoietic stem cells are activated by IFN-gamma in response to chronic infection","volume":"465","author":"Baldridge","year":"2010","journal-title":"Nature."},{"key":"2023072601300490800_bib3","doi-asserted-by":"publisher","first-page":"1109","DOI":"10.1172\/JCI35660","article-title":"Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells","volume":"119","author":"Bellodi","year":"2009","journal-title":"J. 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