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@ARTICLE{Frolov:278061,
      author       = {Frolov, Aleksej and Huang, Hao and Schütz, Dagmar and
                      Köhne, Maren Christin and Blank-Stein, Nelli and
                      Osei-Sarpong, Collins and Büttner, Maren and Elmzzahi,
                      Tarek and Khundadze, Mukhran and Zahid, Marina and Reuter,
                      Michael and Becker, Matthias and De Domenico, Elena and
                      Bonaguro, Lorenzo and Kallies, Axel and Morrison, Helen and
                      Hübner, Christian A and Händler, Kristian and Stumm, Ralf
                      and Mass, Elvira and Beyer, Marc D},
      title        = {{M}icroglia and {CD}8+ {T} cell activation precede neuronal
                      loss in a murine model of spastic paraplegia 15.},
      journal      = {Journal of experimental medicine},
      volume       = {222},
      number       = {7},
      issn         = {0022-1007},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DZNE-2025-00556},
      pages        = {e20232357},
      year         = {2025},
      abstract     = {In central nervous system (CNS) diseases characterized by
                      late-onset neurodegeneration, the interplay between innate
                      and adaptive immune responses remains poorly understood.
                      This knowledge gap is exacerbated by the prolonged
                      protracted disease course as it complicates the delineation
                      of brain-resident and infiltrating cells. Here, we conducted
                      comprehensive profiling of innate and adaptive immune cells
                      in a murine model of spastic paraplegia 15 (SPG15), a
                      complicated form of hereditary spastic paraplegia. Using
                      fate-mapping of bone marrow-derived cells, we identified
                      microgliosis accompanied by infiltration and local expansion
                      of T cells in the CNS of Spg15-/- mice. Single-cell analysis
                      revealed an expansion of disease-associated microglia (DAM)
                      and effector CD8+ T cells prior to neuronal loss. Analysis
                      of potential cell-cell communication pathways suggested
                      bidirectional interactions between DAM and effector CD8+ T
                      cells, potentially contributing to disease progression in
                      Spg15-/- mice. In summary, we identified a shift in
                      microglial phenotypes associated with the recruitment and
                      expansion of T cells as a new characteristic of Spg15-driven
                      neuropathology.},
      keywords     = {Animals / CD8-Positive T-Lymphocytes: immunology /
                      CD8-Positive T-Lymphocytes: pathology / Microglia:
                      immunology / Microglia: pathology / Disease Models, Animal /
                      Mice / Neurons: pathology / Neurons: immunology / Mice,
                      Knockout / Lymphocyte Activation: immunology / Spastic
                      Paraplegia, Hereditary: immunology / Spastic Paraplegia,
                      Hereditary: pathology / Mice, Inbred C57BL},
      cin          = {AG Beyer / AG Schultze / AG Bonaguro / AG Becker / PRECISE},
      ddc          = {610},
      cid          = {I:(DE-2719)1013035 / I:(DE-2719)1013038 /
                      I:(DE-2719)1016005 / I:(DE-2719)5000079 /
                      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},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40266307},
      doi          = {10.1084/jem.20232357},
      url          = {https://pub.dzne.de/record/278061},
}