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@ARTICLE{Sektioglu:119361,
      author       = {I. M. Sektioglu$^*$ and R. Carretero$^*$ and N. Bulbuc$^*$
                      and T. Bald and T. Tüting and A. Y. Rudensky and G.
                      Hämmerling$^*$},
      title        = {{B}asophils {P}romote {T}umor {R}ejection via {C}hemotaxis
                      and {I}nfiltration of {CD}8+ {T} {C}ells.},
      journal      = {Cancer research},
      volume       = {77},
      number       = {2},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-00116},
      pages        = {291 - 302},
      year         = {2017},
      abstract     = {Elevated numbers of regulatory T cells (Treg) in patient
                      tumors are known to inhibit efficient antitumor T-cell
                      responses. To study the mechanisms controlling tumor
                      rejection, we assessed different mouse models for Treg
                      depletion. In Foxp3DTR knock-in mice, about $99\%$ Treg
                      depletion was achieved, resulting in complete rejection of
                      transplanted HCmel12 melanomas in a CD8(+) T-cell-dependent
                      way. In contrast, about $90\%$ Treg depletion obtained in
                      BAC transgenic Foxp3.LuciDTR4 mice failed to induce complete
                      rejection of HCmel12 melanomas, demonstrating that residual
                      Tregs were able to control CD8(+) T-cell responses against
                      the tumor. Ninety-nine percent of Treg depletion provoked
                      drastic changes in the tumor microenvironment, such as
                      strong infiltration of CD8(+) T cells and basophils.
                      Intratumoral basophils enhanced CD8(+) T-cell infiltration
                      via production of chemokines CCL3 and CCL4; antibody-based
                      blocking of these chemokines inhibited CD8(+) T-cell
                      infiltration. Therapeutic induction of basophilia by
                      IL3/anti-IL3 antibody complexes, combined with transfer of
                      CD8(+) T cells, resulted in enhanced T-cell infiltration and
                      tumor rejection. Our study identifies a critical role
                      basophils play in tumor rejection and that this role can be
                      exploited for therapeutic intervention. Cancer Res; 77(2);
                      291-302. ©2016 AACR.},
      cin          = {G181 / D121 / D030},
      ddc          = {610},
      cid          = {I:(DE-He78)G181-20160331 / I:(DE-He78)D121-20160331 /
                      I:(DE-He78)D030-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27879269},
      doi          = {10.1158/0008-5472.CAN-16-0993},
      url          = {https://inrepo02.dkfz.de/record/119361},
}