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Distinct host‐related dendritic cell responses during the early stage of Plasmodium yoelii infection in susceptible and resistant mice
Author(s) -
ZHENG W.,
WANG Q.H.,
LIU Y.J.,
LIU J.,
FENG H.,
WU J.J.,
CAO Y.M.
Publication year - 2010
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.2009.01190.x
Subject(s) - plasmodium yoelii , biology , host (biology) , immunology , developmental stage , stage (stratigraphy) , plasmodium (life cycle) , host response , immune system , malaria , virology , parasite hosting , plasmodium falciparum , genetics , parasitemia , developmental psychology , psychology , paleontology , world wide web , computer science
Summary The diverse outcomes of experimental murine infection with Plasmodium parasites, ranging from spontaneous cure to death, depend largely on the establishment of an effective Th1 immune response during the early stages of infection. However, the molecular and cellular factors responsible for the induction and regulation of this response are poorly understood. As immunity is initiated by dendritic cells (DCs), we compared their phenotype and function during the early stages of infection with Plasmodium yoelii 17XL ( P.y 17XL) strain in susceptible (BALB/c) and resistant (DBA/2) mice. Resistant DBA/2 mice developed a greater number of myeloid (CD11c + CD11b + ) and mature DCs, which were fully functional and capable of secreting IL‐12p40. In contrast, susceptible BALB/c mice produced more plasmacytoid (CD11c + CD45R/B220 + ) and less mature DCs, resulting in high levels of IL‐10 and TGF‐β1. In addition, an in vitro experiment confirmed that splenic DCs from the two strains of mice differ in their ability to prime CD4 + T cells in response to P.y 17XL stimulation. These findings indicate that the subset, the phenotype and the type of inflammatory and anti‐inflammatory signals of splenic DCs are critical factors responsible for the discrepancy in the ability to induce or regulate Th1 immune responses in different hosts.