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@ARTICLE{Heger:278395,
      author       = {L. Heger and L. Hatscher and C. Liang and C. H. K. Lehmann
                      and L. Amon and J. J. Lühr and T. Kaszubowski and R.
                      Nzirorera and N. Schaft and J. Dörrie and P. Irrgang and M.
                      Tenbusch and M. Kunz and E. Socher and S. E. Autenrieth$^*$
                      and A. Purbojo and H. Sirbu and A. Hartmann and C. Alexiou
                      and R. Cesnjevar and D. Dudziak},
      title        = {{XCR}1 expression distinguishes human conventional
                      dendritic cell type 1 with full effector functions from
                      their immediate precursors.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {120},
      number       = {33},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2023-01629},
      pages        = {e2300343120},
      year         = {2023},
      abstract     = {Dendritic cells (DCs) are major regulators of innate and
                      adaptive immune responses. DCs can be classified into
                      plasmacytoid DCs and conventional DCs (cDCs) type 1 and 2.
                      Murine and human cDC1 share the mRNA expression of XCR1.
                      Murine studies indicated a specific role of the XCR1-XCL1
                      axis in the induction of immune responses. Here, we describe
                      that human cDC1 can be distinguished into XCR1- and XCR1+
                      cDC1 in lymphoid as well as nonlymphoid tissues.
                      Steady-state XCR1+ cDC1 display a preactivated phenotype
                      compared to XCR1- cDC1. Upon stimulation, XCR1+ cDC1, but
                      not XCR1- cDC1, secreted high levels of inflammatory
                      cytokines as well as chemokines. This was associated with
                      enhanced activation of NK cells mediated by XCR1+ cDC1.
                      Moreover, XCR1+ cDC1 excelled in inhibiting replication of
                      Influenza A virus. Further, under DC differentiation
                      conditions, XCR1- cDC1 developed into XCR1+ cDC1. After
                      acquisition of XCR1 expression, XCR1- cDC1 secreted
                      comparable level of inflammatory cytokines. Thus, XCR1 is a
                      marker of terminally differentiated cDC1 that licenses the
                      antiviral effector functions of human cDC1, while XCR1- cDC1
                      seem to represent a late immediate precursor of cDC1.},
      keywords     = {DC differentiation (Other) / IL-12 (Other) / XCR1 (Other) /
                      antiviral immunity (Other) / cDC1 (Other)},
      cin          = {F171},
      ddc          = {500},
      cid          = {I:(DE-He78)F171-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37566635},
      doi          = {10.1073/pnas.2300343120},
      url          = {https://inrepo02.dkfz.de/record/278395},
}