Abstract
BackgroundDuring infection, dendritic cells (DCs) encounter pathogenic microorganisms that can modulate their function and shape the T cell responses generated. During the process of T cell activation, DCs establish strong, long-lasting interactions with naïve T cells.MethodsUsing a mouse malaria model, the interactions of DCs and naïve CD4+ T cells have been analysed.ResultsDCs, either incubated in vitro with infected erythrocytes or isolated from infected mice, are able to present exogenous antigens by MHC-II, but are not able to establish prolonged effective interactions with naïve CD4+ T cells and do not induce T cell activation. It was also found that effective T cell activation of naïve CD4+ T cells is impaired during late Plasmodium yoelii infection.ConclusionThese data may provide a mechanism for the lack of effective adaptive immune responses induced by the Plasmodium parasite.
Highlights
During infection, dendritic cells (DCs) encounter pathogenic microorganisms that can modulate their function and shape the T cell responses generated
These data may provide a mechanism for the lack of effective adaptive immune responses induced by the Plasmodium parasite
DCs are able to cross-present exogenous antigens in the context of major histocompatibility complex (MHC)-I molecules to activate CD8+ T cells. It was determined whether MHC-II and MHC-I antigen presentation was affected during infection with P. yoelii
Summary
Dendritic cells (DCs) encounter pathogenic microorganisms that can modulate their function and shape the T cell responses generated. To initiate T cell-dependent immune responses to microbial infections, DCs phagocytose antigens in peripheral tissues and migrate to the draining lymph nodes, where they interact with antigen-specific T cells. Different effects have been described depending on the parasite strain used, time after infection or subpopulation of DC analysed, a number of reports found defective activation of T cells [3]. These findings may be related with the low parasite-specific T cell responses induced by human malaria infections [4,5]
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