Reduction of conventional dendritic cells during Plasmodium infection is dependent on activation induced cell death by type I and II interferons.

Abstract

Dendritic cells (DCs) play critical roles in innate and adaptive immunity and in pathogenesis during the blood stage of malaria infection. The mechanisms underlying DC homeostasis during malaria infection are not well understood. In this study, the numbers of conventional DCs (cDCs) and plasmacytoid DCs (pDCs) in the spleens after lethal rodent malaria infection were examined, and were found to be significantly reduced. Concomitant with up-regulation of maturation-associated molecules, activation of caspase-3 was significantly increased, suggesting induction of cell death. Studies using neutralizing antibody and gene-deficient mice showed that type I and II interferons were critically involved in activation induced cell death of cDCs during malaria infection. These results demonstrate that DCs rapidly disappeared following IFN-mediated DC activation, and that homeostasis of DCs was significantly impaired during malaria infection.

• Authors: Takahiko Tamura, Kazumi Kimura, Katsuyuki Yui, Shigeto Yoshida
• Journal: Experimental parasitology (Exp Parasitol) Vol. 159 Pg. 127-35 (Dec 2015) ISSN: 1090-2449 [Electronic] United States
• PMID: 26420463 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier Inc. All rights reserved.

Chemical References

• Adaptor Proteins, Vesicular Transport
• Ifnar1 protein, mouse
• Interferon Type I
• Myeloid Differentiation Factor 88
• TICAM-1 protein, mouse
• Receptor, Interferon alpha-beta
• Caspase 3

Topics

• Adaptor Proteins, Vesicular Transport (genetics)
• Animals
• Apoptosis
• Caspase 3 (metabolism)
• Cells, Cultured
• Dendritic Cells (cytology, enzymology, immunology)
• Enzyme Activation
• Interferon Type I (immunology, physiology)
• Malaria (immunology)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Myeloid Differentiation Factor 88 (genetics)
• Plasmodium berghei (immunology)
• Plasmodium yoelii (immunology)
• Receptor, Interferon alpha-beta (immunology)
• Spleen (cytology)