{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T18:30:37Z","timestamp":1793644237718,"version":"4.5.1"},"reference-count":116,"publisher":"American Society of Hematology","issue":"26","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,6,27]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Single-cell and spatial multimodal technologies have propelled discoveries of the solid tumor microenvironment (TME) molecular features and their correlation with clinical response and resistance to immunotherapy. Computational tools are incessantly being developed to characterize tumor-infiltrating immune cells and to model tumor immune escape. These advances have led to substantial research into T-cell hypofunctional states in the TME and their reinvigoration with T-cell\u2013targeting approaches, including checkpoint inhibitors (CPIs). Until recently, we lacked a high-dimensional picture of the acute myeloid leukemia (AML) TME, including compositional and functional differences in immune cells between disease onset and postchemotherapy or posttransplantation relapse, and the dynamic interplay between immune cells and AML blasts at various maturation stages. AML subgroups with heightened interferon gamma (IFN-\u03b3) signaling were shown to derive clinical benefit from CD123\u00d7CD3\u2013bispecific\u00a0dual-affinity retargeting molecules and CPIs, while being less likely to respond to standard-of-care cytotoxic chemotherapy. In this review, we first highlight recent progress into deciphering immune effector states in AML (including T-cell exhaustion and senescence), oncogenic signaling mechanisms that could reduce the susceptibility of AML cells to T-cell\u2013mediated killing, and the dichotomous roles of type I and II IFN in antitumor immunity. In the second part, we\u00a0discuss how this knowledge could be translated into\u00a0opportunities to manipulate the AML TME with the aim to overcome resistance to CPIs and other T-cell immunotherapies, building on recent success stories in the solid tumor field, and we provide an outlook for the future.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2023019961","type":"journal-article","created":{"date-parts":[[2023,7,19]],"date-time":"2023-07-19T17:20:02Z","timestamp":1689787202000},"page":"2689-2700","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":75,"title":["Escape from T-cell\u2013targeting immunotherapies in acute myeloid leukemia"],"prefix":"10.1182","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2671-4285","authenticated-orcid":false,"given":"Jayakumar","family":"Vadakekolathu","sequence":"first","affiliation":[{"name":"John van Geest Cancer Research Centre, Nottingham Trent 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