PMID- 22311598
OWN - NLM
STAT- MEDLINE
DCOM- 20120706
LR  - 20171116
IS  - 1521-4141 (Electronic)
IS  - 0014-2980 (Linking)
VI  - 42
IP  - 5
DP  - 2012 May
TI  - Leishmania amazonensis impairs DC function by inhibiting CD40 expression via A2B 
      adenosine receptor activation.
PG  - 1203-15
LID - 10.1002/eji.201141926 [doi]
AB  - Dendritic cells (DCs) play an essential role in the modulation of immune 
      responses and several studies have evaluated the interactions between Leishmania 
      parasites and DCs. While extracellular ATP exhibits proinflammatory properties, 
      adenosine is an important anti-inflammatory mediator. Here we investigated the 
      effects of Leishmania infection on DC responses and the participation of 
      purinergic signalling in this process. Bone marrow-derived dendritic cells 
      (BMDCs) from C57BL/6J mice infected with Leishmania amazonensis, Leishmania 
      braziliensis or Leishmania major metacyclic promastigotes showed decreased major 
      histocompatibility complex (MHC) class II and CD86 expression and increased 
      ectonucleotidase expression as compared with uninfected cells. In addition, L. 
      amazonensis-infected DCs, which had lower CD40 expression, exhibited a decreased 
      ability to induce T-cell proliferation. The presence of MRS1754, a highly 
      selective A(2B) adenosine receptor antagonist at the time of infection increased 
      MHC class II, CD86 and CD40 expression in L. amazonensis-infected DCs and 
      restored the ability of the infected DCs to induce T-cell proliferation. Similar 
      results were obtained through the inhibition of extracellular ATP hydrolysis 
      using suramin. In conclusion, we propose that A(2B) receptor activation may be 
      used by L. amazonensis to inhibit DC function and evade the immune response.
CI  - (c) 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
FAU - Figueiredo, Amanda B
AU  - Figueiredo AB
AD  - Laboratorio de Imunoparasitologia, Departamento de Ciencias Biologicas, 
      ICEB/NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
FAU - Serafim, Tiago D
AU  - Serafim TD
FAU - Marques-da-Silva, Eduardo A
AU  - Marques-da-Silva EA
FAU - Meyer-Fernandes, Jose R
AU  - Meyer-Fernandes JR
FAU - Afonso, Luis C C
AU  - Afonso LC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Acetamides)
RN  - 0 (Adenosine A2 Receptor Antagonists)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD40 Antigens)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 
      (N-(4-cyanophenyl)-2-(4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)-phenoxy)acetamide)
RN  - 0 (Purines)
RN  - 0 (Receptor, Adenosine A2B)
RN  - 0 (Trypanocidal Agents)
RN  - 6032D45BEM (Suramin)
RN  - EC 3.1.3.- (Nucleotidases)
SB  - IM
MH  - Acetamides/pharmacology
MH  - Adenosine A2 Receptor Antagonists/pharmacology
MH  - Animals
MH  - B7-2 Antigen/biosynthesis/immunology
MH  - Bone Marrow Cells/immunology
MH  - CD40 Antigens/biosynthesis/*immunology
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology
MH  - Histocompatibility Antigens Class II/immunology
MH  - Leishmania/*immunology
MH  - Leishmaniasis/*immunology
MH  - Lymphocyte Activation/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nucleotidases/biosynthesis
MH  - Purines/pharmacology
MH  - Receptor, Adenosine A2B/*immunology
MH  - Suramin/pharmacology
MH  - T-Lymphocytes/immunology
MH  - Trypanocidal Agents/pharmacology
EDAT- 2012/02/09 06:00
MHDA- 2012/07/07 06:00
CRDT- 2012/02/08 06:00
PHST- 2012/02/08 06:00 [entrez]
PHST- 2012/02/09 06:00 [pubmed]
PHST- 2012/07/07 06:00 [medline]
AID - 10.1002/eji.201141926 [doi]
PST - ppublish
SO  - Eur J Immunol. 2012 May;42(5):1203-15. doi: 10.1002/eji.201141926.