% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{delaRosa:285047,
      author       = {de la Rosa, Clara and Kendirli, Arek and Baygün, Seren and
                      Bauernschmitt, Franz and Thomann, Anna S and Kisioglu, Ilgin
                      and Beckmann, Daniela and Carpentier Solorio, Yves and
                      Pfaffenstaller, Veronika and Tai, Yi-Heng and Mehraein, Niel
                      and Sanchez, Paula and Spieth, Lena and Gerdes, Lisa Ann and
                      Beltran, Eduardo and Dornmair, Klaus and Simons, Mikael and
                      Peters, Anneli and Schmidt-Supprian, Marc and
                      Kerschensteiner, Martin},
      title        = {{I}n vivo {CRISPR} screen reveals regulation of macrophage
                      states in neuroinflammation.},
      journal      = {Nature neuroscience},
      volume       = {29},
      number       = {2},
      issn         = {1097-6256},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DZNE-2026-00171},
      pages        = {493 - 509},
      year         = {2026},
      abstract     = {Here we established an in vivo CRISPR screening pipeline
                      using genetically editable progenitor cells to dissect
                      macrophage regulation in mouse models of multiple sclerosis
                      (MS). Screening over 100 cytokine receptors and signaling
                      molecules identified interferon-γ, tumor necrosis factor,
                      granulocyte-macrophage colony-stimulating factor and
                      transforming growth factor-β as essential regulators of
                      macrophage polarization in vivo. Single-cell transcriptomics
                      confirmed that transferred progenitor cells generate all
                      blood-derived CNS myeloid cell populations, enabling
                      Perturb-seq analysis of cytokine actions in
                      neuroinflammation. Combined with biosensor expression, our
                      approach allows monitoring cytokine effects on myeloid cell
                      migration, debris phagocytosis and oxidative activity in
                      vivo. Comparative transcriptomic analyses revealed conserved
                      neuroinflammatory cytokine signatures across myeloid
                      populations, CNS compartments and species, elucidating
                      cytokine cues shaping myeloid function in the cerebrospinal
                      fluid and parenchyma of individuals with MS. This versatile
                      pipeline thus provides a scalable framework for
                      high-resolution analysis of macrophage states and uncovers
                      the cytokine signals that underlie their regulation in MS
                      and MS models.},
      keywords     = {Animals / Macrophages: metabolism / Mice / Cytokines:
                      metabolism / Cytokines: genetics / Mice, Inbred C57BL /
                      Clustered Regularly Interspaced Short Palindromic Repeats /
                      Multiple Sclerosis: immunology / Multiple Sclerosis:
                      genetics / Humans / Neuroinflammatory Diseases: genetics /
                      CRISPR-Cas Systems / Encephalomyelitis, Autoimmune,
                      Experimental: immunology / Cytokines (NLM Chemicals)},
      cin          = {AG Simons},
      ddc          = {610},
      cid          = {I:(DE-2719)1110008},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41345278},
      pmc          = {pmc:PMC12880918},
      doi          = {10.1038/s41593-025-02151-6},
      url          = {https://pub.dzne.de/record/285047},
}