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@ARTICLE{Xu:169133,
      author       = {S. Xu and O. Chaudhary and P. Rodríguez-Morales and X. Sun
                      and D. Chen and R. Zappasodi and Z. Xu and A. F. M. Pinto
                      and A. Williams and I. Schulze and Y. Farsakoglu and S. K.
                      Varanasi and J. S. Low and W. Tang and H. Wang and B.
                      McDonald and V. Tripple and M. Downes and R. M. Evans and N.
                      A. Abumrad and T. Merghoub and J. D. Wolchok and M. N.
                      Shokhirev and P.-C. Ho and J. L. Witztum and B. Emu and G.
                      Cui$^*$ and S. M. Kaech},
      title        = {{U}ptake of oxidized lipids by the scavenger receptor
                      {CD}36 promotes lipid peroxidation and dysfunction in {CD}8+
                      {T} cells in tumors.},
      journal      = {Immunity},
      volume       = {54},
      number       = {7},
      issn         = {1074-7613},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2021-01275},
      pages        = {1561-1577.e7},
      year         = {2021},
      note         = {2021 Jul 13;54(7):1561-1577.e7},
      abstract     = {A common metabolic alteration in the tumor microenvironment
                      (TME) is lipid accumulation, a feature associated with
                      immune dysfunction. Here, we examined how CD8+ tumor
                      infiltrating lymphocytes (TILs) respond to lipids within the
                      TME. We found elevated concentrations of several classes of
                      lipids in the TME and accumulation of these in CD8+ TILs.
                      Lipid accumulation was associated with increased expression
                      of CD36, a scavenger receptor for oxidized lipids, on CD8+
                      TILs, which also correlated with progressive T cell
                      dysfunction. Cd36-/- T cells retained effector functions in
                      the TME, as compared to WT counterparts. Mechanistically,
                      CD36 promoted uptake of oxidized low-density lipoproteins
                      (OxLDL) into T cells, and this induced lipid peroxidation
                      and downstream activation of p38 kinase. Inhibition of p38
                      restored effector T cell functions in vitro, and
                      resolution of lipid peroxidation by overexpression of
                      glutathione peroxidase 4 restored functionalities in CD8+
                      TILs in vivo. Thus, an oxidized lipid-CD36 axis promotes
                      intratumoral CD8+ T cell dysfunction and serves as a
                      therapeutic avenue for immunotherapies.},
      keywords     = {CD36 (Other) / CD8(+) T cells (Other) / lipid peroxidation
                      (Other) / oxidized lipids (Other) / tumor microenvironment
                      (Other)},
      cin          = {D140 / D192},
      ddc          = {610},
      cid          = {I:(DE-He78)D140-20160331 / I:(DE-He78)D192-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34102100},
      doi          = {10.1016/j.immuni.2021.05.003},
      url          = {https://inrepo02.dkfz.de/record/169133},
}