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@ARTICLE{Ge:147406,
      author       = {Y. Ge$^*$ and H.-H. Böhm$^*$ and A. Rathinasamy$^*$ and M.
                      Xydia$^*$ and X. Hu$^*$ and M. Pincha$^*$ and L. Umansky$^*$
                      and C. Breyer$^*$ and M. Hillier$^*$ and A. Bonertz$^*$ and
                      A. Sevko$^*$ and C. Domschke and F. Schuetz and H.
                      Frebel$^*$ and S. Dettling and C. C. Herold-Mende and C.
                      Reissfelder and J. Weitz and V. Umansky$^*$ and P. Beckhove},
      title        = {{T}umor-specific regulatory {T} cells from the bone marrow
                      orchestrate antitumor immunity in breast cancer.},
      journal      = {Cancer immunology research},
      volume       = {7},
      number       = {12},
      issn         = {2326-6074},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2019-02523},
      pages        = {1998-2012},
      year         = {2019},
      note         = {7(12):1998-2012},
      abstract     = {Endogenous antitumor effector T cell responses and immune
                      suppressive regulatory T cells (Tregs) critically influence
                      the prognosis of cancer patients, yet many of the mechanisms
                      of how this occurs remain unresolved. Based on an analysis
                      of the function, antigen-specificity and distribution of
                      tumor antigen-reactive T cells and Tregs in breast cancer
                      patients and transgenic mouse tumor models we showed that
                      tumor-specific Tregs were selectively activated in the bone
                      marrow (BM) and egressed into the peripheral blood (PB). The
                      BM was constantly depleted of tumor-specific Tregs and was
                      instead a site of increased induction and activity of
                      tumor-reactive effector/memory T cells. Treg egress from the
                      BM was associated with activation-induced expression of
                      peripheral homing receptors such as CCR2. Since breast
                      cancer tissues express the CCR2 ligand CCL2, the activation
                      and egress of tumor antigen-specific Tregs in the BM
                      resulted in the accumulation of Tregs in breast tumor
                      tissue. Such immune-compartmentalization and redistribution
                      of T cell subpopulations between the BM and peripheral
                      tissues was achieved by vaccination with adenoviral vector
                      encoded TRP-2 tumor antigen in a RET transgenic mouse model
                      of spontaneous malignant melanoma. Thus, the BM
                      simultaneously represented a source of tumor-infiltrating
                      Tregs and a site for the induction of endogenous
                      tumor-specific effector T cell responses, suggesting that
                      both antitumor immunity and local immune suppression are
                      orchestrated in the BM.},
      cin          = {D015 / A370},
      ddc          = {610},
      cid          = {I:(DE-He78)D015-20160331 / I:(DE-He78)A370-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31672785},
      doi          = {10.1158/2326-6066.CIR-18-0763},
      url          = {https://inrepo02.dkfz.de/record/147406},
}