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@ARTICLE{Busch:125593,
      author       = {R. Busch and K. Murti and J. Liu and A. K. Patra and K.
                      Muhammad and K.-P. Knobeloch and M. Lichtinger and C.
                      Bonifer and S. Wörtge and A. Waisman and K. Reifenberg$^*$
                      and V. Ellenrieder and E. Serfling and A. Avots},
      title        = {{NFAT}c1 releases {BCL}6-dependent repression of {CCR}2
                      agonist expression in peritoneal macrophages from
                      {S}accharomyces cerevisiae infected mice.},
      journal      = {European journal of immunology},
      volume       = {46},
      number       = {3},
      issn         = {0014-2980},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2017-01719},
      pages        = {634 - 646},
      year         = {2016},
      abstract     = {The link between the extensive usage of calcineurin (CN)
                      inhibitors cyclosporin A and tacrolimus (FK506) in
                      transplantation medicine and the increasing rate of
                      opportunistic infections within this segment of patients is
                      alarming. Currently, how peritoneal infections are favored
                      by these drugs, which impair the activity of several
                      signaling pathways including the Ca(++) /CN/NFAT, Ca(++)
                      /CN/cofilin, Ca(++) /CN/BAD, and NF-κB networks, is
                      unknown. Here, we show that Saccharomyces cerevisiae
                      infection of peritoneal resident macrophages triggers the
                      transient nuclear translocation of NFATc1β isoforms,
                      resulting in a coordinated, CN-dependent induction of the
                      Ccl2, Ccl7, and Ccl12 genes, all encoding CCR2 agonists. CN
                      inhibitors block the CCR2-dependent recruitment of
                      inflammatory monocytes (IM) to the peritoneal cavities of S.
                      cerevisiae infected mice. In myeloid cells, NFATc1/β
                      proteins represent the most prominent NFATc1 isoforms.
                      NFATc1/β ablation leads to a decrease of CCR2 chemokines,
                      impaired mobilization of IMs, and delayed clearance of
                      infection. We show that, upon binding to a composite
                      NFAT/BCL6 regulatory element within the Ccl2 promoter,
                      NFATc1/β proteins release the BCL6-dependent repression of
                      Ccl2 gene in macrophages. These findings suggest a novel
                      CN-dependent cross-talk between NFAT and BCL6 transcription
                      factors, which may affect the outcome of opportunistic
                      fungal infections in immunocompromised patients.},
      keywords     = {Calcineurin Inhibitors (NLM Chemicals) / Ccl12 protein,
                      mouse (NLM Chemicals) / Ccl2 protein, mouse (NLM Chemicals)
                      / Ccl7 protein, mouse (NLM Chemicals) / Ccr2 protein, mouse
                      (NLM Chemicals) / Chemokine CCL2 (NLM Chemicals) / Chemokine
                      CCL7 (NLM Chemicals) / Monocyte Chemoattractant Proteins
                      (NLM Chemicals) / NF-kappa B (NLM Chemicals) / NFATC
                      Transcription Factors (NLM Chemicals) / Nfatc1 protein,
                      mouse (NLM Chemicals) / Protein Isoforms (NLM Chemicals) /
                      Proto-Oncogene Proteins c-bcl-6 (NLM Chemicals) / Receptors,
                      CCR2 (NLM Chemicals) / Calcineurin (NLM Chemicals)},
      cin          = {W410},
      ddc          = {610},
      cid          = {I:(DE-He78)W410-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26631626},
      doi          = {10.1002/eji.201545925},
      url          = {https://inrepo02.dkfz.de/record/125593},
}