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@ARTICLE{LlaCid:303421,
      author       = {L. Llaó-Cid$^*$ and J. Wong$^*$ and I. Fernandez Botana
                      and Y. Paul and M. Wierz$^*$ and L.-M. Pilger$^*$ and A.
                      Floerchinger$^*$ and C. L. Tan$^*$ and S. Gonder and G.
                      Pagano and M. Chazotte and K. Bestak and C. Schifflers$^*$
                      and M. Iskar$^*$ and T. Roider and F. Czernilofsky and P.-M.
                      Bruch and J. P. Mallm and A. Cosma and D. E. Campton and E.
                      Gerhard-Hartmann and A. Rosenwald and D. Colomer and E.
                      Campo and D. Schapiro and E. Green$^*$ and S. Dietrich and
                      P. Lichter$^*$ and E. Moussay and J. Paggetti and M.
                      Zapatka$^*$ and M. Seiffert$^*$},
      title        = {{I}ntegrative multi-omics reveals a regulatory and
                      exhausted {T}-cell landscape in {CLL} and identifies
                      galectin-9 as an immunotherapy target.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01646},
      pages        = {7271},
      year         = {2025},
      note         = {#EA:B060#LA:B060#},
      abstract     = {T-cell exhaustion contributes to immunotherapy failure in
                      chronic lymphocytic leukemia (CLL). Here, we analyze T cells
                      from CLL patients' blood, bone marrow, and lymph nodes, as
                      well as from a CLL mouse model, using single-cell RNA
                      sequencing, mass cytometry, and tissue imaging. T cells in
                      CLL lymph nodes show the most distinct profiles, with
                      accumulation of regulatory T cells and CD8+ T cells in
                      various exhaustion states, including precursor (TPEX) and
                      terminally exhausted (TEX) cells. Integration of T-cell
                      receptor sequencing data and use of the predicTCR classifier
                      suggest an enrichment of CLL-reactive T cells in lymph
                      nodes. Interactome studies reveal potential immunotherapy
                      targets, notably galectin-9, a TIM3 ligand. Inhibiting
                      galectin-9 in mice reduces disease progression and TIM3+ T
                      cells. Galectin-9 expression also correlates with worse
                      survival in CLL and other cancers, suggesting its role in
                      immune evasion and potential as a therapeutic target.},
      keywords     = {Galectins: metabolism / Galectins: genetics / Galectins:
                      antagonists $\&$ inhibitors / Galectins: immunology /
                      Leukemia, Lymphocytic, Chronic, B-Cell: immunology /
                      Leukemia, Lymphocytic, Chronic, B-Cell: therapy / Leukemia,
                      Lymphocytic, Chronic, B-Cell: genetics / Leukemia,
                      Lymphocytic, Chronic, B-Cell: pathology / Humans / Animals /
                      Mice / Hepatitis A Virus Cellular Receptor 2: metabolism /
                      Immunotherapy: methods / T-Lymphocytes, Regulatory:
                      immunology / T-Lymphocytes, Regulatory: metabolism / Lymph
                      Nodes: immunology / Lymph Nodes: pathology / CD8-Positive
                      T-Lymphocytes: immunology / CD8-Positive T-Lymphocytes:
                      metabolism / Female / Male / Disease Models, Animal /
                      Multiomics / Galectins (NLM Chemicals) / LGALS9 protein,
                      human (NLM Chemicals) / Hepatitis A Virus Cellular Receptor
                      2 (NLM Chemicals) / galectin 9, mouse (NLM Chemicals) /
                      HAVCR2 protein, human (NLM Chemicals)},
      cin          = {B060 / D170},
      ddc          = {500},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)D170-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40775219},
      doi          = {10.1038/s41467-025-61822-x},
      url          = {https://inrepo02.dkfz.de/record/303421},
}