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Erratum

Erratum

Page 1037 | Published online: 12 Jun 2008

Figures & data

Figure 5. Schematic model of the mechanism involved in the antitumor effect of vaccination with complexes consisting of ECDHER2 and anti-HER2/neu IgG3-(IL-2) in DC. Anti-HER2/neu IgG3-(IL-2) can bind HER2/neu expressed as soluble antigen ECDHER2. This soluble antigen is poorly processed because of its high level of glycosylation that results in its binding to the mannose receptor, early endosomal retention, and recycling back to the cell surface. However, the interaction between the complex of ECDHER2 plus anti-HER2/neu IgG3-(IL-2) with IL-2 receptor (IL-2R) expressed on the cell surface induces ECDHER2 internalization and trafficking to the late endosome/lysosome MHC class II pathway facilitating the processing and presentation to CD4+ T cells via MHC class II molecules in order to stimulate the immune response against HER2/neu positive tumor cells.
Figure 5. Schematic model of the mechanism involved in the antitumor effect of vaccination with complexes consisting of ECDHER2 and anti-HER2/neu IgG3-(IL-2) in DC. Anti-HER2/neu IgG3-(IL-2) can bind HER2/neu expressed as soluble antigen ECDHER2. This soluble antigen is poorly processed because of its high level of glycosylation that results in its binding to the mannose receptor, early endosomal retention, and recycling back to the cell surface. However, the interaction between the complex of ECDHER2 plus anti-HER2/neu IgG3-(IL-2) with IL-2 receptor (IL-2R) expressed on the cell surface induces ECDHER2 internalization and trafficking to the late endosome/lysosome MHC class II pathway facilitating the processing and presentation to CD4+ T cells via MHC class II molecules in order to stimulate the immune response against HER2/neu positive tumor cells.

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