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@ARTICLE{Pfeuffer:298559,
      author       = {L. Pfeuffer and V. Siegert and R. Trozzo and K. Steiger$^*$
                      and R. Rad$^*$ and J. Ruland and M. Buchner},
      title        = {{A}utoimmunity promotes chronic lymphocytic leukemia
                      progression in an indolent disease model.},
      journal      = {Scientific reports},
      volume       = {15},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-00284},
      pages        = {4117},
      year         = {2025},
      abstract     = {Chronic lymphocytic leukemia (CLL) is a heterogeneous B
                      cell malignancy characterized by the accumulation of
                      functionally incompetent B lymphocytes. Despite the
                      availability of highly effective treatments, CLL remains
                      incurable, and the factors contributing to disease
                      progression are not fully understood. Autoimmune
                      complications frequently arise in CLL patients and are
                      associated with poor clinical prognosis. This study
                      investigates the connection between plasma cell-mediated
                      autoimmunity and CLL progression using a mouse model that
                      expresses an active Receptor Activator of NF-κB (RANK) in B
                      cells (RK mice), where autoimmune manifestations coexist
                      with CLL. Transcriptional profiling of RANK-driven leukemic
                      cells revealed a more indolent form of CLL compared to the
                      classical TCL1 model. The discovery of near-identical CDR3
                      regions in both plasma and CLL cells of RK mice suggests a
                      shared progenitor and antigen driving both conditions.
                      Deletion of Blimp-1, which prevents plasma cell
                      differentiation, initially enhanced B1/CLL formation in
                      young mice but nearly halted CLL progression, highlighting
                      the significant influence of autoimmune complications on
                      disease outcomes. This research underscores the intertwined
                      nature of autoimmunity and CLL, suggesting that targeting
                      inflammatory pathways could offer therapeutic potential for
                      managing both conditions.},
      keywords     = {Animals / Leukemia, Lymphocytic, Chronic, B-Cell:
                      immunology / Leukemia, Lymphocytic, Chronic, B-Cell:
                      pathology / Autoimmunity / Mice / Disease Progression /
                      Disease Models, Animal / Humans / B-Lymphocytes: immunology
                      / B-Lymphocytes: metabolism / Plasma Cells: immunology /
                      Plasma Cells: metabolism / Plasma Cells: pathology},
      cin          = {MU01},
      ddc          = {600},
      cid          = {I:(DE-He78)MU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39900937},
      pmc          = {pmc:PMC11791097},
      doi          = {10.1038/s41598-025-86876-1},
      url          = {https://inrepo02.dkfz.de/record/298559},
}