title: 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.affiliation: Division of Immunology, Department of Molecular Microbiology and Immunology, Graduate School of Biomedical Sciences, Nagasaki University, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan; Global COE Program, Nagasaki University, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan; Laboratory of Vaccinology and Applied Immunology, Kanazawa University, School of Pharmacy, Kakuma-machi, Kanazawa 920-1192, Japan. Electronic address: tamura99@p.kanazawa-u.ac.jp.
authors.forename: Takahiko
authors.initials: T
authors.lastname: Tamura
authors.affiliation: Division of Immunology, Department of Molecular Microbiology and Immunology, Graduate School of Biomedical Sciences, Nagasaki University, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan.
authors.forename: Kazumi
authors.initials: K
authors.lastname: Kimura
authors.affiliation: Division of Immunology, Department of Molecular Microbiology and Immunology, Graduate School of Biomedical Sciences, Nagasaki University, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan; Global COE Program, Nagasaki University, 1-12-4, Sakamoto, Nagasaki 852-8523, Japan.
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Yui
authors.affiliation: Laboratory of Vaccinology and Applied Immunology, Kanazawa University, School of Pharmacy, Kakuma-machi, Kanazawa 920-1192, Japan.
authors.forename: Shigeto
authors.initials: S
authors.lastname: Yoshida
mesh_terms: D033942:Adaptor Proteins, Vesicular Transport / Q000235:genetics; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology / Q000201:enzymology / Q000276:immunology*; D004789:Enzyme Activation; D007370:Interferon Type I / Q000276:immunology / Q000502:physiology; D008288:Malaria / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics; D010962:Plasmodium berghei / Q000276:immunology*; D010967:Plasmodium yoelii / Q000276:immunology; D053633:Receptor, Interferon alpha-beta / Q000276:immunology; D013154:Spleen / Q000166:cytology
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D053148:Caspase 3; D007370:Interferon Type I; D053594:Myeloid Differentiation Factor 88; D053633:Receptor, Interferon alpha-beta; C508032:Ifnar1 protein, mouse; C476286:Ticam1 protein, mouse
keywords: Dendritic cells; Interferons; Malaria