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| Home > User submitted records > The remission status of AML patients after allo-HCT is associated with a distinct single-cell bone marrow T-cell signature > print |
| 001 | 294790 | ||
| 005 | 20241204090116.0 | ||
| 024 | 7 | _ | |a 10.1182/blood.2023021815 |2 doi |
| 024 | 7 | _ | |a 0006-4971 |2 ISSN |
| 024 | 7 | _ | |a 1528-0020 |2 ISSN |
| 037 | _ | _ | |a DKFZ-2024-02502 |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Mathioudaki, Anna |0 P:(DE-He78)fc0c97c9d01deff15d0a1f0cb8402459 |b 0 |u dkfz |
| 245 | _ | _ | |a The remission status of AML patients after allo-HCT is associated with a distinct single-cell bone marrow T-cell signature |
| 260 | _ | _ | |a Washington, DC |c 2024 |b American Society of Hematology |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1733298930_24286 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Acute myeloid leukemia (AML) is a hematologic malignancy for which allogeneic hematopoietic cell transplantation (allo-HCT) often remains the only curative therapeutic approach. However, incapability of T cells to recognize and eliminate residual leukemia stem cells might lead to an insufficient graft-versus-leukemia (GVL) effect and relapse. Here, we performed single-cell RNA-sequencing (scRNA-seq) on bone marrow (BM) T lymphocytes and CD34+ cells of 6 patients with AML 100 days after allo-HCT to identify T-cell signatures associated with either imminent relapse (REL) or durable complete remission (CR). We observed a higher frequency of cytotoxic CD8+ effector and gamma delta (γδ) T cells in CR vs REL samples. Pseudotime and gene regulatory network analyses revealed that CR CD8+ T cells were more advanced in maturation and had a stronger cytotoxicity signature, whereas REL samples were characterized by inflammatory tumor necrosis factor/NF-κB signaling and an immunosuppressive milieu. We identified ADGRG1/GPR56 as a surface marker enriched in CR CD8+ T cells and confirmed in a CD33-directed chimeric antigen receptor T cell/AML coculture model that GPR56 becomes upregulated on T cells upon antigen encounter and elimination of AML cells. We show that GPR56 continuously increases at the protein level on CD8+ T cells after allo-HCT and confirm faster interferon gamma (IFN-γ) secretion upon re-exposure to matched, but not unmatched, recipient AML cells in the GPR56+ vs GPR56- CD8+ T-cell fraction. Together, our data provide a single-cell reference map of BM-derived T cells after allo-HCT and propose GPR56 expression dynamics as a surrogate for antigen encounter after allo-HCT. |
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| 588 | _ | _ | |a Dataset connected to CrossRef, Journals: inrepo02.dkfz.de |
| 700 | 1 | _ | |a Wang, Xizhe |b 1 |
| 700 | 1 | _ | |a Sedloev, David |b 2 |
| 700 | 1 | _ | |a Huth, Richard |b 3 |
| 700 | 1 | _ | |a Kamal, Aryan |b 4 |
| 700 | 1 | _ | |a Hundemer, Michael |b 5 |
| 700 | 1 | _ | |a Liu, Yi |b 6 |
| 700 | 1 | _ | |a Vasileiou, Spyridoula |b 7 |
| 700 | 1 | _ | |a Lulla, Premal |0 0000-0002-7707-2331 |b 8 |
| 700 | 1 | _ | |a Müller-Tidow, Carsten |b 9 |
| 700 | 1 | _ | |a Dreger, Peter |b 10 |
| 700 | 1 | _ | |a Luft, Thomas |b 11 |
| 700 | 1 | _ | |a Sauer, Tim |b 12 |
| 700 | 1 | _ | |a Schmitt, Michael |b 13 |
| 700 | 1 | _ | |a Zaugg, Judith B. |0 0000-0001-8324-4040 |b 14 |
| 700 | 1 | _ | |a Pabst, Caroline |b 15 |
| 773 | _ | _ | |a 10.1182/blood.2023021815 |g Vol. 143, no. 13, p. 1269 - 1281 |0 PERI:(DE-600)1468538-3 |n 13 |p 1269 - 1281 |t Blood |v 143 |y 2024 |x 0006-4971 |
| 910 | 1 | _ | |a Deutsches Krebsforschungszentrum |0 I:(DE-588b)2036810-0 |k DKFZ |b 0 |6 P:(DE-He78)fc0c97c9d01deff15d0a1f0cb8402459 |
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