Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 2, Pages 716-726Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.2.716
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- NIAID NIH HHS [R01 AI053698, AI053698, R01 AI053698-05] Funding Source: Medline
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During an acute Plasmodium infection, uncontrolled proinflammatory responses can cause morbidity and mortality. Regulation of this response is required to prevent immunopathology. We therefore decided to investigate a recently characterized subset of regulatory dendritic cells (DCs) that expresses low levels of CD11c and high levels of CD45RB. During a Plasmodium yoelii infection, these regulatory CD11c(low)CD45RB(high) DCs become the prevalent CD11c-expressing cells in the spleen, overtaking the conventional CD11c(high) DCs. Furthermore, the regulatory CD11c(low)CD45RB(high) DCs induce IL-10-expressing CD4 T cells. A similar change in splenic DC subsets is seen when mice are injected with sublethal doses of LPS, suggesting that shifting the splenic DC subsets in favor of regulatory CD11c(low)CD45RB(high) DCs can be triggered solely by a high inflammatory stimulus. This is the first time regulatory DCs have been observed in a natural immune response to an infectious disease or endotoxic shock.
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