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Plasmodium Infection and Endotoxic Shock Induce the Expansion of Regulatory Dendritic Cells¹

Department of Medical Parasitology, New York University School of Medicine, New York, NY 10010

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^lowCD45RB^high DCs become the prevalent CD11c-expressing cells in the spleen, overtaking the conventional CD11c^high DCs. Furthermore, the regulatory CD11c^lowCD45RB^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^lowCD45RB^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.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by Natural Sciences and Engineering Research Council of Canada (to K.W.). A.R. was supported by National Institutes of Health Grant AI053698.

² Address correspondence and reprint requests to Dr. Ana Rodriguez, Department of Medical Parasitology, 341 East 25th Street, New York, NY 10010. E-mail address: ana.rodriguez{at}nyu.edu

³ Abbreviations used in this paper: DC, dendritic cell; iRBC, infected erythrocyte.

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