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Centre d’Immunologie de Marseille-Luminy, Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, Université de la Méditerranée, and Centre National de la Recherche Scientifique Groupement de Recherche 2352 "Immunociblage des Tumeurs," Marseille, France
We investigated interactions between CD4+ T cells and
dendritic cells (DC) necessary for presentation of exogenous Ag by DC
to CD8+ T cells. CD4+ T cells responding to
their cognate Ag presented by MHC class II molecules of DC were
necessary for induction of CD8+ T cell responses to MHC
class I-associated Ag, but their ability to do so depended on the
manner in which class II-peptide complexes were formed. DC derived from
short-term mouse bone marrow culture efficiently took up Ag
encapsulated in IgG FcR-targeted liposomes and stimulated
CD4+ T cell responses to Ag-derived peptides associated
with class II molecules. This CD4+ T cell-DC interaction
resulted in expression by the DC of complexes of class I molecules and
peptides from the Ag delivered in liposomes and permitted expression of
the activation marker CD69 and cytotoxic responses by naive
CD8+ T cells. However, while free peptides in solution
loaded onto DC class II molecules could stimulate IL-2 production by
CD4+ T cells as efficiently as peptides derived from
endocytosed Ag, they could not stimulate induction of cytotoxic
responses by CD8+ T cells to Ag delivered in liposomes into
the same DC. Signals requiring class II molecules loaded with
endocytosed Ag, but not free peptide, were inhibited by
methyl-
-cyclodextrin, which depletes cell membrane cholesterol.
CD4+ T cell signals thus require class II molecules in
cholesterol-rich domains of DC for induction of CD8+ T cell
responses to exogenous Ag by inducing DC to process this Ag for class I
presentation.
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