PMID- 21609335
OWN - NLM
STAT- MEDLINE
DCOM- 20111128
LR  - 20181201
IS  - 1365-3024 (Electronic)
IS  - 0141-9838 (Linking)
VI  - 33
IP  - 9
DP  - 2011 Sep
TI  - Intraperitoneal murine Echinococcus multilocularis infection induces 
      differentiation of TGF-beta-expressing DCs that remain immature.
PG  - 471-82
LID - 10.1111/j.1365-3024.2011.01303.x [doi]
AB  - Intraperitoneal larval infection (alveolar echinococcosis, AE) with Echinococcus 
      multilocularis in mice impairs host immunity. Metacestode metabolites may 
      modulate immunity putatively via dendritic cells. During murine AE, a relative 
      increase of peritoneal DCs (pe-DCs) in infected mice (AE-pe-DCs; 4% of total 
      peritoneal cells) as compared to control mice (naive pe-DCs; 2%) became apparent 
      in our study. The differentiation of AE-pe-DCs into TGF-beta-expressing cells and 
      the higher level of IL-4 than IFN-gamma/IL-2 mRNA expression in AE-CD4+pe-T cells 
      indicated a Th2 orientation. Analysis of major accessory molecule expression on 
      pe-DCs from AE-infected mice revealed that CD80 and CD86 were down-regulated on 
      AE-pe-DCs, while ICAM-1(CD54) remained practically unchanged. Moreover, AE-pe-DCs 
      had a weaker surface expression of MHC class II (Ia) molecules as compared to 
      naive pe-DCs. The gene expression level of molecules involved in MHC class II 
      (Ia) synthesis and formation of MHC class II (Ia)-peptide complexes were 
      down-regulated. In addition, metacestodes excreted/secreted (E/S) or 
      vesicle-fluid (V/F) antigens were found to alter MHC class II molecule expression 
      on the surface of BMDCs. Finally, conversely to naive pe-DCs, an increasing 
      number of AE-pe-DCs down-regulated Con A-induced proliferation of naive CD4+pe-T 
      cells. These findings altogether suggested that TGF-beta-expressing immature 
      AE-pe-DCs might play a significant role in the generation of a regulatory immune 
      response within the peritoneal cavity of AE-infected mice.
CI  - (c) 2011 Blackwell Publishing Ltd.
FAU - Mejri, N
AU  - Mejri N
AD  - Institute of Parasitology, University of Berne, Bern, Switzerland.
FAU - Muller, J
AU  - Muller J
FAU - Gottstein, B
AU  - Gottstein B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Parasite Immunol
JT  - Parasite immunology
JID - 7910948
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (Cytokines)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - Alveolar echinococcosis
SB  - IM
MH  - Animals
MH  - B7-1 Antigen/immunology
MH  - B7-2 Antigen/immunology
MH  - Blotting, Western
MH  - Bone Marrow Cells/immunology
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - *Cell Differentiation
MH  - Cell Proliferation
MH  - Cytokines/metabolism
MH  - Dendritic Cells/cytology/*immunology
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Echinococcosis
MH  - Echinococcosis, Hepatic/immunology/parasitology
MH  - Echinococcus multilocularis/*immunology/pathogenicity
MH  - Female
MH  - Flow Cytometry
MH  - Gene Expression Regulation
MH  - Histocompatibility Antigens Class II/immunology
MH  - Host-Parasite Interactions
MH  - Lymphocyte Activation
MH  - Membrane Proteins/isolation & purification
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Peritoneal Cavity/cytology/*parasitology
MH  - RNA, Messenger/metabolism
MH  - Transforming Growth Factor beta/*immunology
EDAT- 2011/05/26 06:00
MHDA- 2011/12/13 00:00
CRDT- 2011/05/26 06:00
PHST- 2011/05/26 06:00 [entrez]
PHST- 2011/05/26 06:00 [pubmed]
PHST- 2011/12/13 00:00 [medline]
AID - 10.1111/j.1365-3024.2011.01303.x [doi]
PST - ppublish
SO  - Parasite Immunol. 2011 Sep;33(9):471-82. doi: 10.1111/j.1365-3024.2011.01303.x.