PMID- 19635909
OWN - NLM
STAT- MEDLINE
DCOM- 20090909
LR  - 20090807
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Linking)
VI  - 183
IP  - 4
DP  - 2009 Aug 15
TI  - Functional modulation of dendritic cells and macrophages by Japanese encephalitis 
      virus through MyD88 adaptor molecule-dependent and -independent pathways.
PG  - 2462-74
LID - 10.4049/jimmunol.0801952 [doi]
AB  - Dendritic cells (DCs) are potent initiators of T cell-mediated immunity that 
      undergo maturation during viral infections. However, few reports describing the 
      interactions of DCs with Japanese encephalitis virus (JEV), which remains the 
      most frequent cause of acute and epidemic viral encephalitis, are available. In 
      this study, we investigated the interaction of JEV with DCs and macrophages. JEV 
      replicated its viral RNA in both cells with different efficiency, and JEV 
      infection of macrophages followed the classical activation pathway of 
      up-regulation of tested costimulatory molecules and proinflammatory cytokine 
      production (IL-6, TNF-alpha, and IL-12). On the contrary, JEV-infected DCs failed 
      to up-regulate costimulatory molecules such as CD40 and MHC class II. Of more 
      interest, along with production of proinflammatory cytokines, DCs infected by JEV 
      released antiinflammatory cytokine IL-10, which was not detected in macrophages. 
      Moreover, signaling through MyD88 molecule, a pan-adaptor molecule of TLRs, and 
      p38 MAPK in JEV-infected DCs was found to play a role in the production of 
      cytokines and subversion of primary CD4(+) and CD8(+) T cell responses. We also 
      found that IL-10 released from JEV-infected DCs led to a reduction in the priming 
      of CD8(+) T cells, but not CD4(+) T cells. Taken together, our data suggest that 
      JEV induces functional impairment of DCs through MyD88-dependent and -independent 
      pathways, which subsequently leads to poor CD4(+) and CD8(+) T cell responses, 
      resulting in boosting viral survival and dissemination in the body.
FAU - Aleyas, Abi G
AU  - Aleyas AG
AD  - Laboratory of Microbiology, College of Veterinary Medicine and Bio-Safety 
      Research Institute, Chonbuk National University, Jeonju, Republic of Korea.
FAU - George, Junu A
AU  - George JA
FAU - Han, Young Woo
AU  - Han YW
FAU - Rahman, M M
AU  - Rahman MM
FAU - Kim, Seon Ju
AU  - Kim SJ
FAU - Han, Sang Bae
AU  - Han SB
FAU - Kim, Byung Sam
AU  - Kim BS
FAU - Kim, Koanhoi
AU  - Kim K
FAU - Eo, Seong Kug
AU  - Eo SK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090727
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - CD4-Positive T-Lymphocytes/immunology/metabolism/virology
MH  - CD8-Positive T-Lymphocytes/immunology/metabolism/virology
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology/metabolism/*virology
MH  - Encephalitis Virus, Japanese/*immunology
MH  - Encephalitis, Japanese/immunology/pathology/virology
MH  - Macrophage Activation/immunology
MH  - Macrophages/*immunology/metabolism/*virology
MH  - Mice
MH  - Mice, Transgenic
MH  - Molecular Sequence Data
MH  - Myeloid Differentiation Factor 88/*physiology
MH  - Signal Transduction/*immunology
MH  - Virus Replication/immunology
EDAT- 2009/07/29 09:00
MHDA- 2009/09/10 06:00
CRDT- 2009/07/29 09:00
PHST- 2009/07/29 09:00 [entrez]
PHST- 2009/07/29 09:00 [pubmed]
PHST- 2009/09/10 06:00 [medline]
AID - jimmunol.0801952 [pii]
AID - 10.4049/jimmunol.0801952 [doi]
PST - ppublish
SO  - J Immunol. 2009 Aug 15;183(4):2462-74. doi: 10.4049/jimmunol.0801952. Epub 2009 
      Jul 27.