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@ARTICLE{Heyden:282555,
      author       = {Heyden, Leonie and Rausch, Lisa and Shannon, Michael H and
                      Dryburgh, Lachlan and Moreira, Marcela L and Frolov, Aleksej
                      and Scheffler, Christina M and van Elsas, Marit J and Tong,
                      Junming and Hidajat, Olivia and Wijesinghe, Sharanya K M and
                      Li, Sining and Horvatic, Helena and Huynh-Anh, Nhat Truong
                      and Gago da Graça, Catarina and Tsui, Carlson and Köhne,
                      Maren and Sommer, Daniel and Wunderlich, F Thomas and von
                      Scheidt, Bianca and Park, Simone L and Mackay, Laura K and
                      Utzschneider, Daniel T and Schröder, Jan and Turner,
                      Stephen J and Darcy, Phillip K and Beyer, Marc D and
                      Abdullah, Zeinab and Kallies, Axel},
      title        = {{T}ranscriptional regulator {SATB}1 limits {CD}8+ {T} cell
                      population expansion and effector differentiation in chronic
                      infection and cancer.},
      journal      = {Nature immunology},
      volume       = {26},
      number       = {12},
      issn         = {1529-2908},
      address      = {London},
      publisher    = {Springer Nature Limited},
      reportid     = {DZNE-2025-01318},
      pages        = {2312 - 2327},
      year         = {2025},
      abstract     = {CD8+ T cells are major mediators of antiviral and antitumor
                      immunity. During persistent antigen stimulation as in
                      chronic infection and cancer, however, they differentiate
                      into exhausted T cells that display impaired functionality.
                      Precursors of exhausted T (TPEX) cells exhibit stem-like
                      properties, including high proliferative, self-renewal and
                      developmental potential, and are responsible for long-term
                      CD8+ T cell responses against persistent antigens. Here we
                      identify the chromatin organizer and transcriptional
                      regulator SATB1 as a major regulator of exhausted CD8+ T
                      cell differentiation. SATB1 was specifically expressed in
                      TPEX cells where it limited population expansion and
                      effector differentiation while preserving functionality of
                      CD8+ T cells. SATB1 downregulation was required for TPEX
                      cell-to-effector cell differentiation in chronic infection
                      and contributed to coordinated effector and memory
                      differentiation in acute viral infection. DNA binding of
                      SATB1 regulated gene expression both dependent and
                      independent of chromatin accessibility. Finally, SATB1
                      limited antitumor CD8+ and chimeric antigen receptor T cell
                      immunity. Overall, our results identify SATB1 as a central
                      regulator of precursor fate and effector differentiation of
                      CD8+ T cells both in infection and in cancer.},
      keywords     = {Matrix Attachment Region Binding Proteins: metabolism /
                      Matrix Attachment Region Binding Proteins: genetics / Matrix
                      Attachment Region Binding Proteins: immunology /
                      CD8-Positive T-Lymphocytes: immunology / Animals / Cell
                      Differentiation: immunology / Mice / Immunologic Memory /
                      Mice, Inbred C57BL / Neoplasms: immunology / Humans /
                      Persistent Infection: immunology / Lymphocytic
                      Choriomeningitis: immunology / Mice, Knockout / Cell
                      Proliferation / Lymphocytic choriomeningitis virus:
                      immunology / Matrix Attachment Region Binding Proteins (NLM
                      Chemicals) / Satb1 protein, mouse (NLM Chemicals) / SATB1
                      protein, human (NLM Chemicals)},
      cin          = {AG Beyer / AG Schultze / PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1013035 / I:(DE-2719)1013038 /
                      I:(DE-2719)1013031},
      pnm          = {351 - Brain Function (POF4-351) / 354 - Disease Prevention
                      and Healthy Aging (POF4-354) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-354 /
                      G:(DE-HGF)POF4-352},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41145844},
      doi          = {10.1038/s41590-025-02316-2},
      url          = {https://pub.dzne.de/record/282555},
}