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@ARTICLE{Tsui:281515,
      author       = {Tsui, Carlson and Heyden, Leonie and Wen, Lifen and Gago da
                      Graça, Catarina and Potemkin, Nikita and Frolov, Aleksej
                      and Rawlinson, Daniel and Qin, Lei and Wimmer, Verena C and
                      Hadian-Jazi, Marjan and Malko, Darya and Su, Chun-Hsi and
                      Li, Sining and Wilson, Kayla R and Horvatic, Helena and
                      Wijesinghe, Sharanya K and Moreira, Marcela L and Dryburgh,
                      Lachlan and Schienstock, Dominik and Rausch, Lisa and
                      Utzschneider, Daniel T and Halin, Cornelia and Mueller,
                      Scott N and Beyer, Marc D and Bedoui, Sammy and Abdullah,
                      Zeinab and Schröder, Jan and Kallies, Axel},
      title        = {{L}ymph nodes fuel {KLF}2-dependent effector {CD}8+ {T}
                      cell differentiation during chronic infection and checkpoint
                      blockade.},
      journal      = {Nature immunology},
      volume       = {26},
      number       = {10},
      issn         = {1529-2908},
      address      = {London},
      publisher    = {Springer Nature Limited},
      reportid     = {DZNE-2025-01134},
      pages        = {1752 - 1765},
      year         = {2025},
      abstract     = {Exhausted CD8+ T (TEX) cell responses are maintained by
                      precursors of exhausted T (TPEX) cells that possess high
                      self-renewal and developmental potential. TPEX cells also
                      drive the proliferative burst of effector T cells upon
                      therapeutic immune checkpoint blockade (ICB). However, the
                      spatial context and signals that regulate their
                      differentiation and function are not well defined. Here we
                      identify developmental and functional compartmentalization
                      of TPEX and TEX cells across secondary lymphoid organs
                      during chronic infection. We show that stem-like CD62L+ TPEX
                      and effector-like CX3CR1+ TEX cells constitute a distinct
                      developmental lineage that is promoted by the lymph node
                      (LN) microenvironment and dependent on the transcription
                      factor KLF2. LNs act as a niche in which migratory dendritic
                      cells provide antigen and costimulatory signals to maintain
                      the proliferative fitness of CD62L+ TPEX cells and
                      generation of CX3CR1+ TEX cells. Moreover, LNs exclusively
                      drive the proliferative burst and systemic dissemination of
                      CX3CR1+ TEX cells during ICB. Thus, our findings identify a
                      unique role for LNs in the maintenance of T cell
                      differentiation and function during systemic chronic
                      infection and ICB therapy.},
      keywords     = {Animals / Lymph Nodes: immunology / Cell Differentiation:
                      immunology / CD8-Positive T-Lymphocytes: immunology / Mice /
                      Kruppel-Like Transcription Factors: metabolism /
                      Kruppel-Like Transcription Factors: genetics / Kruppel-Like
                      Transcription Factors: immunology / Mice, Inbred C57BL /
                      Immune Checkpoint Inhibitors: pharmacology / CX3C Chemokine
                      Receptor 1: metabolism / Lymphocytic Choriomeningitis:
                      immunology / Lymphocytic choriomeningitis virus: immunology
                      / Persistent Infection: immunology / Dendritic Cells:
                      immunology / Mice, Knockout / Lymphocyte Activation:
                      immunology / Mice, Transgenic / Kruppel-Like Transcription
                      Factors (NLM Chemicals) / Klf2 protein, mouse (NLM
                      Chemicals) / Immune Checkpoint Inhibitors (NLM Chemicals) /
                      CX3C Chemokine Receptor 1 (NLM Chemicals) / Cx3cr1 protein,
                      mouse (NLM Chemicals)},
      cin          = {AG Beyer / AG Schultze},
      ddc          = {610},
      cid          = {I:(DE-2719)1013035 / I:(DE-2719)1013038},
      pnm          = {351 - Brain Function (POF4-351) / 354 - Disease Prevention
                      and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-354},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40954251},
      doi          = {10.1038/s41590-025-02276-7},
      url          = {https://pub.dzne.de/record/281515},
}