Antigen-Antibody Immune Complexes Empower Dendritic Cells to Efficiently Prime Specific CD8+ CTL Responses In Vivo

Dendritic cells (DCs) require a maturation signal to acquire efficient CTL-priming capacity. In vitro FcgammaR-mediated internalization of Ag-Ab immune complexes (ICs) can induce maturation of DCs. In this study, we show that IC-induced DC maturation in vitro enables DCs to prime peptide-specific CD...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2002-03, Vol.168 (5), p.2240-2246
Main Authors: Schuurhuis, Danita H, Ioan-Facsinay, Andreea, Nagelkerken, Bas, van Schip, Jolien J, Sedlik, Christine, Melief, Cornelis J. M, Verbeek, J. Sjef, Ossendorp, Ferry
Format: Article
Language:English
Subjects:
Animals
Antigen Presentation
Antigen-Antibody Complex - immunology
Cell Differentiation
Cell Line, Transformed
Cytotoxicity Tests, Immunologic
Dendritic Cells - immunology
Endocytosis
Female
Histocompatibility Antigens Class I - physiology
Hybridomas
Mice
Mice, Inbred C57BL
Microscopy, Confocal
Ovalbumin - immunology
Ovalbumin - metabolism
Peptides - immunology
T-Lymphocytes, Cytotoxic - immunology
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Summary:Dendritic cells (DCs) require a maturation signal to acquire efficient CTL-priming capacity. In vitro FcgammaR-mediated internalization of Ag-Ab immune complexes (ICs) can induce maturation of DCs. In this study, we show that IC-induced DC maturation in vitro enables DCs to prime peptide-specific CD8+ CTLs in vivo, independently of CD4+ Th cells. Importantly, OVA/anti-OVA IC-treated DCs not only primed CD8+ CTLs to an exogenously loaded peptide nonrelated to OVA, but also efficiently primed CTLs against the dominant CTL epitope derived from the OVA Ag present in the ICs. Our studies show that ICs fulfill a dual role in priming of CD8+ CTL responses to exogenous Ags: enhancement of Ag uptake by DCs and activation of DCs, resulting in "license to kill." These findings indicate that the presence of specific Abs can crucially affect the induction of cytotoxic cellular responses.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.168.5.2240