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@ARTICLE{Rejeski:283136,
      author       = {K. Rejeski and A. Perez and G. Iacoboni and V.
                      Blumenberg$^*$ and V. L. Bücklein$^*$ and S. Völkl and O.
                      Penack and O. Albanyan and S. Stock$^*$ and F. Müller and
                      P. Karschnia and A. Petrera and K. Reid and R. Faramand and
                      M. L. Davila and K. Modi and E. A. Dean and C. Bachmeier and
                      M. von Bergwelt-Baildon$^*$ and F. L. Locke and W. Bethge
                      and L. Bullinger$^*$ and A. Mackensen and P. Barba and M. D.
                      Jain and M. Subklewe$^*$},
      title        = {{S}evere hematotoxicity after {CD}19 {CAR}-{T} therapy is
                      associated with suppressive immune dysregulation and limited
                      {CAR}-{T} expansion.},
      journal      = {Science advances},
      volume       = {9},
      number       = {38},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2023-01923},
      pages        = {eadg3919},
      year         = {2023},
      abstract     = {Prolonged cytopenias after chimeric antigen receptor (CAR)
                      T cell therapy are a significant clinical problem and the
                      underlying pathophysiology remains poorly understood. Here,
                      we investigated how (CAR) T cell expansion dynamics and
                      serum proteomics affect neutrophil recovery phenotypes after
                      CD19-directed CAR T cell therapy. Survival favored patients
                      with 'intermittent' neutrophil recovery (e.g., recurrent
                      neutrophil dips) compared to either 'quick' or 'aplastic'
                      recovery. While intermittent patients displayed increased
                      CAR T cell expansion, aplastic patients exhibited an
                      unfavorable relationship between expansion and tumor burden.
                      Proteomics of patient serum collected at baseline and in the
                      first month after CAR-T therapy revealed higher markers of
                      endothelial dysfunction, inflammatory cytokines, macrophage
                      activation, and T cell suppression in the aplastic phenotype
                      group. Prolonged neutrophil aplasia thus occurs in patients
                      with systemic immune dysregulation at baseline with
                      subsequently impaired CAR-T expansion and myeloid-related
                      inflammatory changes. The association between neutrophil
                      recovery and survival outcomes highlights critical
                      interactions between host hematopoiesis and the immune state
                      stimulated by CAR-T infusion.},
      keywords     = {Humans / Immunotherapy, Adoptive: adverse effects /
                      Receptors, Chimeric Antigen / Adaptor Proteins, Signal
                      Transducing / Antigens, CD19 / Cell Cycle / Receptors,
                      Chimeric Antigen (NLM Chemicals) / Adaptor Proteins, Signal
                      Transducing (NLM Chemicals) / Antigens, CD19 (NLM
                      Chemicals)},
      cin          = {MU01 / BE01},
      ddc          = {500},
      cid          = {I:(DE-He78)MU01-20160331 / I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37738350},
      pmc          = {pmc:PMC10516499},
      doi          = {10.1126/sciadv.adg3919},
      url          = {https://inrepo02.dkfz.de/record/283136},
}