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@ARTICLE{Li:293326,
      author       = {Z.-J. Li and B. He and A. Domenichini and J. Satiaputra and
                      K. H. Wood and D. D. Lakhiani and A. A. Bashaw and L. M.
                      Nilsson and J. Li and E. R. Bastow and A. Johansson-Percival
                      and E. Denisenko and A. R. Forrest and S. Sakaram and R.
                      Carretero$^*$ and G. J. Hämmerling$^*$ and J. A. Nilsson
                      and G. Y. Lee and R. Ganss},
      title        = {{P}ericyte phenotype switching alleviates immunosuppression
                      and sensitizes vascularized tumors to immunotherapy in
                      preclinical models.},
      journal      = {The journal of clinical investigation},
      volume       = {134},
      number       = {18},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2024-01876},
      pages        = {e179860},
      year         = {2024},
      abstract     = {T cell-based immunotherapies are a promising therapeutic
                      approach for multiple malignancies, but their efficacy is
                      limited by tumor hypoxia arising from dysfunctional blood
                      vessels. Here, we report that cell-intrinsic properties of a
                      single vascular component, namely the pericyte, contribute
                      to the control of tumor oxygenation, macrophage
                      polarization, vessel inflammation, and T cell infiltration.
                      Switching pericyte phenotype from a synthetic to a
                      differentiated state reverses immune suppression and
                      sensitizes tumors to adoptive T cell therapy, leading to
                      regression of melanoma in mice. In melanoma patients,
                      improved survival is correlated with enhanced pericyte
                      maturity. Importantly, pericyte plasticity is regulated by
                      signaling pathways converging on Rho kinase activity, with
                      pericyte maturity being inducible by selective low-dose
                      therapeutics that suppress pericyte MEK, AKT, or notch
                      signaling. We also show that low-dose targeted anticancer
                      therapy can durably change the tumor microenvironment
                      without inducing adaptive resistance, creating a highly
                      translatable pathway for redosing anticancer targeted
                      therapies in combination with immunotherapy to improve
                      outcome.},
      keywords     = {Animals / Pericytes: immunology / Pericytes: metabolism /
                      Pericytes: pathology / Mice / Humans / Tumor
                      Microenvironment: immunology / Tumor Microenvironment: drug
                      effects / Immunotherapy / Melanoma, Experimental: immunology
                      / Melanoma, Experimental: therapy / Melanoma, Experimental:
                      pathology / Phenotype / Melanoma: immunology / Melanoma:
                      therapy / Melanoma: pathology / Melanoma: drug therapy /
                      Cell Line, Tumor / Immune Tolerance: drug effects / Cancer
                      immunotherapy (Other) / Mouse models (Other) / Oncology
                      (Other) / Pericytes (Other) / Therapeutics (Other)},
      cin          = {D220 / D470},
      ddc          = {610},
      cid          = {I:(DE-He78)D220-20160331 / I:(DE-He78)D470-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39286984},
      doi          = {10.1172/JCI179860},
      url          = {https://inrepo02.dkfz.de/record/293326},
}