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@ARTICLE{Delecluse:301495,
      author       = {S. Delecluse$^*$ and F. Baccianti$^*$ and M. Zala and A.
                      Steffens$^*$ and C. Drenda$^*$ and D. Judt$^*$ and T.
                      Holland-Letz$^*$ and R. Poirey$^*$ and P. Sujobert and H.-J.
                      Delecluse$^*$},
      title        = {{E}pstein-{B}arr virus induces aberrant {B} cell migration
                      and diapedesis via {FAK}-dependent chemotaxis pathways.},
      journal      = {Nature Communications},
      volume       = {16},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01037},
      pages        = {4581},
      year         = {2025},
      note         = {#EA:D400#LA:D400#},
      abstract     = {Infection with the Epstein-Barr virus (EBV) is a major risk
                      factor for the development of cancer and autoimmune
                      disorders. The virus enters the body in the pharynx, but EBV
                      causes disease in distant organs, including the gut and the
                      brain. Here we show, using in vitro culture and mouse
                      infection models, that EBV-infected B cells display features
                      of homing cells. Infected B cells undergo migration
                      following paracrine CCL4 release and CCR1 induction, while
                      CCR1 deficiency inhibits migration and, unexpectedly,
                      proliferation of infected B cells. Furthermore, migrating
                      EBV-infected B cells undergo CCL4-dependent diapedesis,
                      induce ICAM-1 on endothelial cells, and disrupt the
                      integrity of endothelial barriers. Both migration and
                      diapedesis are regulated by FAK, with FAK inhibition
                      blocking growth and survival of EBV-transformed B cells, as
                      well as their spreading to spleen and brain in an animal
                      model in vivo. Moreover, IL-10 secreted by EBV-infected B
                      cells attracts and facilitates diapedesis of EBV-negative
                      CD52highCD11c+ B cells, which have reported autoimmune
                      properties. Our results thus provide mechanistic insight on
                      EBV-induced B cell dysregulation, and also hint curbing
                      migration as a potential target for reducing the
                      pathogenicity of EBV-infected B cells.},
      keywords     = {Animals / B-Lymphocytes: virology / B-Lymphocytes:
                      immunology / B-Lymphocytes: metabolism / Herpesvirus 4,
                      Human: physiology / Herpesvirus 4, Human: immunology / Mice
                      / Humans / Chemotaxis / Epstein-Barr Virus Infections:
                      immunology / Epstein-Barr Virus Infections: virology /
                      Epstein-Barr Virus Infections: pathology / Epstein-Barr
                      Virus Infections: metabolism / Interleukin-10: metabolism /
                      Cell Movement / Mice, Inbred C57BL / Receptors, CCR1:
                      metabolism / Receptors, CCR1: genetics / Intercellular
                      Adhesion Molecule-1: metabolism / Focal Adhesion Kinase 1:
                      metabolism / Endothelial Cells: metabolism / Mice, Knockout
                      / Interleukin-10 (NLM Chemicals) / Receptors, CCR1 (NLM
                      Chemicals) / Intercellular Adhesion Molecule-1 (NLM
                      Chemicals) / Focal Adhesion Kinase 1 (NLM Chemicals) / Ptk2
                      protein, mouse (NLM Chemicals)},
      cin          = {D400 / C060},
      ddc          = {500},
      cid          = {I:(DE-He78)D400-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40389409},
      doi          = {10.1038/s41467-025-59813-z},
      url          = {https://inrepo02.dkfz.de/record/301495},
}