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@ARTICLE{Rughetti:49054,
      author       = {Rughetti, A. and Pellicciotta, I. and Biffoni, M. and
                      Bäckström, M. and Link, T. and Noll, T. and Hansson, G. C.
                      and Clausen, H. and Burchell, J. M. and
                      Taylor-Papadimitriou, J. and Nuti, M.},
      title        = {{R}ecombinant tumor associated {MUC}1 impairs
                      differentiation and function of {D}endritic {C}ells},
      journal      = {The journal of immunology},
      volume       = {174},
      issn         = {0022-1767},
      address      = {Bethesda, Md.},
      publisher    = {Soc.},
      reportid     = {PreJuSER-49054},
      pages        = {7764 - 7772},
      year         = {2005},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {Tumors exploit several strategies to evade immune
                      recognition, including the production of a large number of
                      immunosuppressive factors, which leads to reduced numbers
                      and impaired functions of dendritic cells (DCs) in the
                      vicinity of tumors. We have investigated whether a mucin
                      released by tumor cells could be involved in causing these
                      immunomodulating effects on DCs. We used a recombinant
                      purified form of the MUC1 glycoprotein, an epithelial
                      associated mucin that is overexpressed, aberrantly
                      glycosylated, and shed during cancer transformation. The
                      O-glycosylation profile of the recombinant MUC1 glycoprotein
                      (ST-MUC1) resembled that expressed by epithelial tumors in
                      vivo, consisting of large numbers of sialylated core 1
                      (sialyl-T, ST) oligosaccharides. When cultured in the
                      presence of ST-MUC1, human monocyte-derived DCs displayed a
                      modified phenotype with decreased expression of
                      costimulatory molecules (CD86, CD40), Ag-presenting
                      molecules (DR and CD1d), and differentiation markers (CD83).
                      In contrast, markers associated with an immature phenotype,
                      CD1a and CD206 (mannose receptor), were increased. This
                      effect was already evident at day 4 of DC culture and was
                      dose dependent. The modified phenotype of DCs corresponded
                      to an altered balance in IL-12/IL-10 cytokine production,
                      with DC expressing an IL-10(high)IL-12(low) phenotype after
                      exposure to ST-MUC1 These DCs were defective in their
                      ability to induce immune responses in both allogeneic and
                      autologous settings, as detected in proliferation and
                      ELISPOT assays. The altered DC differentiation and Ag
                      presentation function induced by the soluble sialylated
                      tumor-associated mucin may represent a mechanism by which
                      epithelial tumors can escape immunosurveillance.},
      keywords     = {J (WoSType)},
      cin          = {IBT-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)VDB56},
      pnm          = {Biotechnologie},
      pid          = {G:(DE-Juel1)FUEK256},
      shelfmark    = {Immunology},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000229791400037},
      url          = {https://juser.fz-juelich.de/record/49054},
}