Systemic activation of dendritic cells by Toll-like receptor ligands or malaria infection impairs cross-presentation and anti-viral immunity
Contribuinte(s) |
L. Miller J. Wilson et al. |
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Data(s) |
01/01/2006
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Resumo |
The mechanisms responsible for the immunosuppression associated with sepsis or some chronic blood infections remain poorly understood. Here we show that infection with a malaria parasite (Plasmodium berghei) or simple systemic exposure to bacterial or viral Toll-like receptor ligands inhibited cross-priming. Reduced cross-priming was a consequence of downregulation of cross-presentation by activated dendritic cells due to systemic activation that did not otherwise globally inhibit T cell proliferation. Although activated dendritic cells retained their capacity to present viral antigens via the endogenous major histocompatibility complex class I processing pathway, antiviral responses were greatly impaired in mice exposed to Toll-like receptor ligands. This is consistent with a key function for cross-presentation in antiviral immunity and helps explain the immunosuppressive effects of systemic infection. Moreover, inhibition of cross-presentation was overcome by injection of dendritic cells bearing antigen, which provides a new strategy for generating immunity during immunosuppressive blood infections. |
Identificador | |
Idioma(s) |
eng |
Publicador |
Nature Publishing Group |
Palavras-Chave | #Immunology #Herpes-simplex Virus #In-vivo #Antigen Presentation #Langerhans Cells #Cutting Edge #Positive Selection #Transgenic Mouse #Life-cycle #T-cells #Expression #C1 #320202 Cellular Immunology #730102 Immune system and allergy |
Tipo |
Journal Article |