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In a prior study, we demonstrated that AML relapse in high-risk patients was prevented by post-HCT immunotherapy with Epstein-Barr virus (EBV)-specific donor CD8\n                  <jats:sup>+<\/jats:sup>\n                  T cells engineered to express a high-affinity Wilms Tumor Antigen 1 (WT1)-specific T-cell receptor (TTCR- C4). However, in the present study, infusion of EBV- or Cytomegalovirus (CMV)-specific T\n                  <jats:sub>TCR-C4<\/jats:sub>\n                  did not clearly improve outcomes in fifteen patients with active disease post-HCT. TCRC4-transduced EBV-specific T cells persisted longer post-transfer than CMV-specific T cells. Persisting T\n                  <jats:sub>TCR-C4<\/jats:sub>\n                  skewed towards dysfunctional natural killer-like terminal differentiation, distinct from the dominant exhaustion programs reported for T-cell therapies targeting solid tumors. In one patient with active AML post-HCT, a sustained T\n                  <jats:sub>TCR-C4<\/jats:sub>\n                  effector-memory profile correlated with long-term T\n                  <jats:sub>TCR-C4<\/jats:sub>\n                  persistence and disease control. These findings reveal complex mechanisms underlying AML-induced T-cell dysfunction, informing future therapeutic strategies for addressing post-HCT relapse.\n                <\/jats:p>","DOI":"10.1101\/2024.12.13.24318504","type":"posted-content","created":{"date-parts":[[2024,12,18]],"date-time":"2024-12-18T18:26:22Z","timestamp":1734546382000},"source":"Crossref","is-referenced-by-count":0,"title":["Acute Myeloid Leukemia Skews Therapeutic WT1-specific CD8 TCR-T Cells Towards an NK-like Phenotype that Compromises Function and Persistence"],"prefix":"10.64898","author":[{"given":"Francesco","family":"Mazziotta","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lauren E.","family":"Martin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel 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