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@ARTICLE{Turco:267546,
      author       = {V. Turco$^*$ and K. Pfleiderer$^*$ and J. Hunger$^*$ and N.
                      K. Horvat and K. Karimian-Jazi and K. Schregel and M.
                      Fischer and G. Brugnara and K. Jähne$^*$ and V. Sturm and
                      Y. Streibel and D. Nguyen$^*$ and S. Altamura and D. A.
                      Agardy$^*$ and S. S. Soni and A. Alsasa and T. Bunse$^*$ and
                      M. Schlesner$^*$ and M. U. Muckenthaler and R. Weissleder
                      and W. Wick$^*$ and S. Heiland and P. Vollmuth and M.
                      Bendszus and C. B. Rodell and M. Breckwoldt$^*$ and M.
                      Platten$^*$},
      title        = {{T} cell-independent eradication of experimental glioma by
                      intravenous {TLR}7/8-agonist-loaded nanoparticles.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00324},
      pages        = {771},
      year         = {2023},
      note         = {#EA:D170#LA:B320#LA:D170#},
      abstract     = {Glioblastoma, the most common and aggressive primary brain
                      tumor type, is considered an immunologically 'cold' tumor
                      with sparse infiltration by adaptive immune cells.
                      Immunosuppressive tumor-associated myeloid cells are drivers
                      of tumor progression. Therefore, targeting and reprogramming
                      intratumoral myeloid cells is an appealing therapeutic
                      strategy. Here, we investigate a β-cyclodextrin
                      nanoparticle (CDNP) formulation encapsulating the Toll-like
                      receptor 7 and 8 (TLR7/8) agonist R848 (CDNP-R848) to
                      reprogram myeloid cells in the glioma microenvironment. We
                      show that intravenous monotherapy with CDNP-R848 induces
                      regression of established syngeneic experimental glioma,
                      resulting in increased survival rates compared with unloaded
                      CDNP controls. Mechanistically, CDNP-R848 treatment reshapes
                      the immunosuppressive tumor microenvironment and
                      orchestrates tumor clearing by pro-inflammatory
                      tumor-associated myeloid cells, independently of T cells and
                      NK cells. Using serial magnetic resonance imaging, we
                      identify a radiomic signature in response to CDNP-R848
                      treatment and ultrasmall superparamagnetic iron oxide
                      (USPIO) imaging reveals that immunosuppressive macrophage
                      recruitment is reduced by CDNP-R848. In conclusion,
                      CDNP-R848 induces tumor regression in experimental glioma by
                      targeting blood-borne macrophages without requiring adaptive
                      immunity.},
      cin          = {D170 / HD01 / W610 / B320},
      ddc          = {500},
      cid          = {I:(DE-He78)D170-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)W610-20160331 / I:(DE-He78)B320-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36774352},
      doi          = {10.1038/s41467-023-36321-6},
      url          = {https://inrepo02.dkfz.de/record/267546},
}