PMID- 26420463
OWN - NLM
STAT- MEDLINE
DCOM- 20160421
LR  - 20151215
IS  - 1090-2449 (Electronic)
IS  - 0014-4894 (Linking)
VI  - 159
DP  - 2015 Dec
TI  - Reduction of conventional dendritic cells during Plasmodium infection is 
      dependent on activation induced cell death by type I and II interferons.
PG  - 127-35
LID - S0014-4894(15)30044-8 [pii]
LID - 10.1016/j.exppara.2015.09.010 [doi]
AB  - 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.
CI  - Copyright (c) 2015 Elsevier Inc. All rights reserved.
FAU - Tamura, Takahiko
AU  - Tamura T
AD  - 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.
FAU - Kimura, Kazumi
AU  - Kimura K
AD  - Division of Immunology, Department of Molecular Microbiology and Immunology, 
      Graduate School of Biomedical Sciences, Nagasaki University, 1-12-4, Sakamoto, 
      Nagasaki 852-8523, Japan.
FAU - Yui, Katsuyuki
AU  - Yui K
AD  - 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.
FAU - Yoshida, Shigeto
AU  - Yoshida S
AD  - Laboratory of Vaccinology and Applied Immunology, Kanazawa University, School of 
      Pharmacy, Kakuma-machi, Kanazawa 920-1192, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150928
PL  - United States
TA  - Exp Parasitol
JT  - Experimental parasitology
JID - 0370713
RN  - 0 (Adaptor Proteins, Vesicular Transport)
RN  - 0 (Ifnar1 protein, mouse)
RN  - 0 (Interferon Type I)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (TICAM-1 protein, mouse)
RN  - 156986-95-7 (Receptor, Interferon alpha-beta)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Adaptor Proteins, Vesicular Transport/genetics
MH  - Animals
MH  - Apoptosis
MH  - Caspase 3/metabolism
MH  - Cells, Cultured
MH  - Dendritic Cells/cytology/enzymology/*immunology
MH  - Enzyme Activation
MH  - Interferon Type I/immunology/physiology
MH  - Malaria/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myeloid Differentiation Factor 88/genetics
MH  - Plasmodium berghei/*immunology
MH  - Plasmodium yoelii/immunology
MH  - Receptor, Interferon alpha-beta/immunology
MH  - Spleen/cytology
OTO - NOTNLM
OT  - Dendritic cells
OT  - Interferons
OT  - Malaria
EDAT- 2015/10/01 06:00
MHDA- 2016/04/22 06:00
CRDT- 2015/10/01 06:00
PHST- 2015/05/09 00:00 [received]
PHST- 2015/07/26 00:00 [revised]
PHST- 2015/09/24 00:00 [accepted]
PHST- 2015/10/01 06:00 [entrez]
PHST- 2015/10/01 06:00 [pubmed]
PHST- 2016/04/22 06:00 [medline]
AID - S0014-4894(15)30044-8 [pii]
AID - 10.1016/j.exppara.2015.09.010 [doi]
PST - ppublish
SO  - Exp Parasitol. 2015 Dec;159:127-35. doi: 10.1016/j.exppara.2015.09.010. Epub 2015 
      Sep 28.