2007
DOI: 10.1016/j.exppara.2006.09.015
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Plasmodium yoelii: Distinct CD4+CD25+ regulatory T cell responses during the early stages of infection in susceptible and resistant mice

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Cited by 60 publications
(60 citation statements)
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“…Therefore, we postulate that the associations of maternal IL-10 produced by PBMCs, and the A allele of A-1082G, with the increased risk for clinical malaria in young children, were attributable to the increased IL-10 production with the consequent potential suppressive effects on protective immunity to clinical malaria. Consistent with our findings, there is evidence that Treg proliferation might be causally associated with the suppression of T H 1 responses during early malaria infection, thereby increasing parasitemia in BALB/c mice in an IL-10-dependent manner (30).…”
Section: Discussionsupporting
confidence: 78%
“…Therefore, we postulate that the associations of maternal IL-10 produced by PBMCs, and the A allele of A-1082G, with the increased risk for clinical malaria in young children, were attributable to the increased IL-10 production with the consequent potential suppressive effects on protective immunity to clinical malaria. Consistent with our findings, there is evidence that Treg proliferation might be causally associated with the suppression of T H 1 responses during early malaria infection, thereby increasing parasitemia in BALB/c mice in an IL-10-dependent manner (30).…”
Section: Discussionsupporting
confidence: 78%
“…The mice of the control group had a mild expression of IL-4 in the spleen, which is higher than that in the mice inoculated with Lm and HKLm. These data showed that live Lm inoculation greatly changed the early cytokine environment of PyLinfected mice and confirmed our previous finding that IFN-γ production at day 3 after PyL infection is essential for the development of protective Th1 response (Wu et al 2007). …”
Section: Live Lm Is Required To Induce a Th1-prone Cytokine Environmesupporting
confidence: 77%
“…Recent studies indicated that some pathogens stimulate Tregs as an immune evasion mechanism (9). When it comes to malaria, studies in rodent models (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) and humans (21)(22)(23) have demonstrated an increase in Treg frequency shortly upon blood stage infection, although Treg frequency during the course of infection did not correlate with disease severity. Furthermore, attempts to deplete Tregs or to increase Treg frequency in mice prior to infection with a variety of parasite strains (Plasmodium yoelii, P. berghei, or P. chabaudi) have led to conflicting results.…”
mentioning
confidence: 99%