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@ARTICLE{Xydia:167532,
      author       = {M. Xydia$^*$ and R. Rahbari and E. Ruggiero$^*$ and I.
                      Macaulay and M. Tarabichi and R. Lohmayer and S.
                      Wilkening$^*$ and T. Michels and D. Brown and S. Vanuytven
                      and S. Mastitskaya and S. Laidlaw and N. Grabe and M.
                      Pritsch$^*$ and R. Fronza$^*$ and K. Hexel$^*$ and S.
                      Schmitt$^*$ and M. Müller-Steinhardt and N. Halama and C.
                      Domschke and M. Schmidt$^*$ and C. von Kalle$^*$ and F.
                      Schütz and T. Voet and P. Beckhove},
      title        = {{C}ommon clonal origin of conventional {T} cells and
                      induced regulatory {T} cells in breast cancer patients.},
      journal      = {Nature Communications},
      volume       = {12},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2021-00397},
      pages        = {1119},
      year         = {2021},
      note         = {#EA:D015#LA:D015#},
      abstract     = {Regulatory CD4+ T cells (Treg) prevent tumor clearance by
                      conventional T cells (Tconv) comprising a major obstacle of
                      cancer immune-surveillance. Hitherto, the mechanisms of Treg
                      repertoire formation in human cancers remain largely
                      unclear. Here, we analyze Treg clonal origin in breast
                      cancer patients using T-Cell Receptor and single-cell
                      transcriptome sequencing. While Treg in peripheral blood and
                      breast tumors are clonally distinct, Tconv clones, including
                      tumor-antigen reactive effectors (Teff), are detected in
                      both compartments. Tumor-infiltrating CD4+ cells accumulate
                      into distinct transcriptome clusters, including early
                      activated Tconv, uncommitted Teff, Th1 Teff, suppressive
                      Treg and pro-tumorigenic Treg. Trajectory analysis suggests
                      early activated Tconv differentiation either into Th1 Teff
                      or into suppressive and pro-tumorigenic Treg. Importantly,
                      Tconv, activated Tconv and Treg share highly-expanded clones
                      contributing up to $65\%$ of intratumoral Treg. Here we show
                      that Treg in human breast cancer may considerably stem from
                      antigen-experienced Tconv converting into secondary induced
                      Treg through intratumoral activation.},
      cin          = {D015 / W220},
      ddc          = {500},
      cid          = {I:(DE-He78)D015-20160331 / I:(DE-He78)W220-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33602930},
      doi          = {10.1038/s41467-021-21297-y},
      url          = {https://inrepo02.dkfz.de/record/167532},
}