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000049054 084__ $$2WoS$$aImmunology
000049054 1001_ $$0P:(DE-HGF)0$$aRughetti, A.$$b0
000049054 245__ $$aRecombinant tumor associated MUC1 impairs differentiation  and function of Dendritic    Cells
000049054 260__ $$aBethesda, Md.$$bSoc.$$c2005
000049054 300__ $$a7764 - 7772
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000049054 440_0 $$014664$$aJournal of Immunology$$v174$$x0022-1767$$y12
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000049054 520__ $$aTumors 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.
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000049054 7001_ $$0P:(DE-HGF)0$$aPellicciotta, I.$$b1
000049054 7001_ $$0P:(DE-HGF)0$$aBiffoni, M.$$b2
000049054 7001_ $$0P:(DE-HGF)0$$aBäckström, M.$$b3
000049054 7001_ $$0P:(DE-HGF)0$$aLink, T.$$b4
000049054 7001_ $$0P:(DE-Juel1)VDB1170$$aNoll, T.$$b5$$uFZJ
000049054 7001_ $$0P:(DE-HGF)0$$aHansson, G. C.$$b6
000049054 7001_ $$0P:(DE-HGF)0$$aClausen, H.$$b7
000049054 7001_ $$0P:(DE-HGF)0$$aBurchell, J. M.$$b8
000049054 7001_ $$0P:(DE-HGF)0$$aTaylor-Papadimitriou, J.$$b9
000049054 7001_ $$0P:(DE-HGF)0$$aNuti, M.$$b10
000049054 773__ $$0PERI:(DE-600)1475085-5$$gVol. 174, p. 7764 - 7772$$p7764 - 7772$$q174<7764 - 7772$$tThe @journal of immunology$$v174$$x0022-1767$$y2005
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000049054 9141_ $$y2005
000049054 915__ $$0StatID:(DE-HGF)0010$$aJCR/ISI refereed
000049054 9201_ $$0I:(DE-Juel1)VDB56$$gIBT$$kIBT-2$$lBiotechnologie 2$$x0$$zab 31.10.10 weitergeführt IBG-1
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