PMID- 21906792
OWN - NLM
STAT- MEDLINE
DCOM- 20120412
LR  - 20120130
IS  - 1097-6825 (Electronic)
IS  - 0091-6749 (Linking)
VI  - 129
IP  - 2
DP  - 2012 Feb
TI  - Monocyte-derived dendritic cell recruitment and allergic T(H)2 responses after 
      exposure to diesel particles are CCR2 dependent.
PG  - 483-91
LID - 10.1016/j.jaci.2011.07.051 [doi]
AB  - BACKGROUND: The inhalation of diesel exhaust particles (DEPs) is associated with 
      increased sensitization toward inhaled allergens. Dendritic cells (DCs) are 
      important mediators in immune regulation. We previously showed that the 
      inhalation of DEPs increased the accumulation of DCs in the lung and enhanced the 
      T(H)2 response in the mediastinal lymph node. OBJECTIVE: We hypothesized that CC 
      chemokine receptors CCR2, CCR5, and CCR6 critically mediate the DC recruitment 
      upon exposure to DEPs and that these CC chemokine receptors are important in the 
      DEP-induced T(H)2 response. METHODS: We exposed CCR2 knockout, CCR5 knockout, 
      CCR6 knockout, and wild-type mice to DEPs and examined the pulmonary monocyte and 
      DC accumulation. By an adoptive transfer experiment, we assessed the direct 
      involvement of CCR2 and CCR6 in the recruitment of blood monocytes toward the 
      lung upon exposure to DEPs. We also examined the T(H)2 cytokine production in the 
      mediastinal lymph nodes of DEP-exposed CCR2 knockout and CCR6 knockout mice. 
      RESULTS: We observed that the DEP-induced monocyte and monocyte-derived DC 
      recruitment was completely abolished in CCR2 knockout mice. CCR6 knockout mice 
      also showed impaired monocyte recruitment upon exposure to DEPs. In contrast, 
      monocyte and DC recruitment was comparable between DEP-exposed wild-type and CCR5 
      knockout mice. The impaired monocyte-derived DC recruitment in DEP-exposed CCR2 
      knockout, not CCR6 knockout, mice resulted in an abolished T(H)2 response in the 
      mediastinal lymph node. CONCLUSION: These data suggest that monocyte-derived DCs, 
      recruited in a CCR2-dependent manner, are critical in inducing T(H)2 responses 
      upon inhalation of DEPs.
CI  - Copyright (c) 2011 American Academy of Allergy, Asthma & Immunology. Published by 
      Mosby, Inc. All rights reserved.
FAU - Provoost, Sharen
AU  - Provoost S
AD  - Laboratory for Translational Research in Obstructive Pulmonary Diseases, 
      Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium. 
      sharen.provoost@UGent.be
FAU - Maes, Tania
AU  - Maes T
FAU - Joos, Guy F
AU  - Joos GF
FAU - Tournoy, Kurt G
AU  - Tournoy KG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110908
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Air Pollutants)
RN  - 0 (CCR6 protein, mouse)
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Chemokines)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, CCR5)
RN  - 0 (Receptors, CCR6)
RN  - 0 (Vehicle Emissions)
SB  - IM
MH  - Air Pollutants/*toxicity
MH  - Animals
MH  - Bronchoalveolar Lavage
MH  - Chemokines/immunology
MH  - Dendritic Cells/*drug effects/immunology
MH  - Gene Expression/drug effects
MH  - Lung/cytology/drug effects/immunology
MH  - Lymph Nodes/drug effects/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Phagocytes/*drug effects/immunology
MH  - Receptors, CCR2/deficiency/genetics/*immunology
MH  - Receptors, CCR5/deficiency/genetics/immunology
MH  - Receptors, CCR6/deficiency/genetics/immunology
MH  - Th2 Cells/*drug effects/immunology
MH  - Vehicle Emissions/*toxicity
EDAT- 2011/09/13 06:00
MHDA- 2012/04/13 06:00
CRDT- 2011/09/13 06:00
PHST- 2011/03/15 00:00 [received]
PHST- 2011/06/01 00:00 [revised]
PHST- 2011/07/22 00:00 [accepted]
PHST- 2011/09/13 06:00 [entrez]
PHST- 2011/09/13 06:00 [pubmed]
PHST- 2012/04/13 06:00 [medline]
AID - S0091-6749(11)01244-9 [pii]
AID - 10.1016/j.jaci.2011.07.051 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2012 Feb;129(2):483-91. doi: 10.1016/j.jaci.2011.07.051. 
      Epub 2011 Sep 8.