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Toxicol. Sci. 113, 85-94 (2010)
Diesel exhaust particles (DEP) were described as potent adjuvant in the induction and maintenance of allergic diseases, suggesting that they might play a role in the increase of allergic diseases in the industrialized countries. However, the cellular basis by which these particles enhance allergic immune responses is still a matter of debate. Thus, we exposed immature murine bone marrow-derived dendritic cells (BMDC) to different particles or particle-associated organic compounds in the absence or presence of the maturation stimuli lipopolysaccharide (LPS) and analyzed the cellular maturation, viability, and cytokine production. Furthermore, we monitored the functionality of particle-exposed BMDC to suppress B cell isotype switching to immunoglobulin (Ig) E. Only highly polluted DEP (standard reference material 1650a [SRM1650a]) but not particle-associated organic compounds or less polluted DEP from modern diesel engines were able to modulate the dendritic cell phenotype. SRM1650a particles significantly suppressed LPS-induced IL-12p70 production in murine BMDC, whereas cell-surface marker expression was not altered. Furthermore, SRM1650a-exposed immature BMDC lost the ability to suppress IgE isotype switch in B cells. This study revealed that highly polluted DEP not only interfere with dendritic cell maturation but also additionally with dendritic cell function, thus suggesting a role in T(h)2 immune deviation.
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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Dendritic cells; B cells; IgE; Particles; Organic compounds
Language
english
Publication Year
2010
HGF-reported in Year
2010
ISSN (print) / ISBN
1096-6080
e-ISSN
1096-0929
Journal
Toxicological Sciences
Quellenangaben
Volume: 113,
Issue: 1,
Pages: 85-94
Publisher
Oxford University Press
Publishing Place
Oxford
Reviewing status
Peer reviewed
Institute(s)
Institute of Lung Health and Immunity (LHI)
Institute of Epidemiology (EPI)
Institute of Ecological Chemistry (IOEC)
Institute of Molecular Toxicology and Pharmacology (TOX)
Cooperation Group Comprehensive Molecular Analytics (CMA)
Institute of Epidemiology (EPI)
Institute of Ecological Chemistry (IOEC)
Institute of Molecular Toxicology and Pharmacology (TOX)
Cooperation Group Comprehensive Molecular Analytics (CMA)
POF-Topic(s)
30202 - Environmental Health
30203 - Molecular Targets and Therapies
30203 - Molecular Targets and Therapies
Research field(s)
Enabling and Novel Technologies
Enabling and Novel Technologies
PSP Element(s)
G-521200-001
FE 73991
G-505100-002
G-505200-001
FE 73991
G-505100-002
G-505200-001
PubMed ID
19805405
WOS ID
000272935700009
Scopus ID
75249089156
Erfassungsdatum
2009-10-04