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@ARTICLE{Haderk:125347,
      author       = {F. Haderk$^*$ and R. Schulz$^*$ and M. Iskar$^*$ and L. L.
                      Cid$^*$ and T. Worst$^*$ and K. V. Willmund$^*$ and A.
                      Schulz$^*$ and U. Warnken$^*$ and J. Seiler$^*$ and A.
                      Benner$^*$ and M. Nessling$^*$ and T. Zenz$^*$ and M. Göbel
                      and J. Dürig and S. Diederichs$^*$ and J. Paggetti and E.
                      Moussay and S. Stilgenbauer and M. Zapatka$^*$ and P.
                      Lichter$^*$ and M. Seiffert},
      title        = {{T}umor-derived exosomes modulate {PD}-{L}1 expression in
                      monocytes.},
      journal      = {Science immunology},
      volume       = {2},
      number       = {13},
      issn         = {2470-9468},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DKFZ-2017-01480},
      pages        = {eaah5509 -},
      year         = {2017},
      note         = {Science Immunology (Sci. Immunol.) = 2470-9468 (import from
                      CrossRef, PubMed, )},
      abstract     = {In chronic lymphocytic leukemia (CLL), monocytes and
                      macrophages are skewed toward protumorigenic phenotypes,
                      including the release of tumor-supportive cytokines and the
                      expression of immunosuppressive molecules such as programmed
                      cell death 1 ligand 1 (PD-L1). To understand the mechanism
                      driving protumorigenic skewing in CLL, we evaluated the role
                      of tumor cell-derived exosomes in the cross-talk with
                      monocytes. We carried out RNA sequencing and proteome
                      analyses of CLL-derived exosomes and identified noncoding Y
                      RNA hY4 as a highly abundant RNA species that is enriched in
                      exosomes from plasma of CLL patients compared with healthy
                      donor samples. Transfer of CLL-derived exosomes or hY4 alone
                      to monocytes resulted in key CLL-associated phenotypes,
                      including the release of cytokines, such as C-C motif
                      chemokine ligand 2 (CCL2), CCL4, and interleukin-6, and the
                      expression of PD-L1. These responses were abolished in
                      Toll-like receptor 7 (TLR7)-deficient monocytes, suggesting
                      exosomal hY4 as a driver of TLR7 signaling. Pharmacologic
                      inhibition of endosomal TLR signaling resulted in a
                      substantially reduced activation of monocytes in vitro and
                      attenuated CLL development in vivo. Our results indicate
                      that exosome-mediated transfer of noncoding RNAs to
                      monocytes contributes to cancer-related inflammation and
                      concurrent immune escape via PD-L1 expression.},
      cin          = {B060 / B110 / C060 / B150 / W230 / G100 / L601 / B100 /
                      G250},
      ddc          = {610},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)B110-20160331 /
                      I:(DE-He78)C060-20160331 / I:(DE-He78)B150-20160331 /
                      I:(DE-He78)W230-20160331 / I:(DE-He78)G100-20160331 /
                      I:(DE-He78)L601-20160331 / I:(DE-He78)B100-20160331 /
                      I:(DE-He78)G250-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28754746},
      doi          = {10.1126/sciimmunol.aah5509},
      url          = {https://inrepo02.dkfz.de/record/125347},
}