|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0009521,
umls-concept:C0035820,
umls-concept:C0155877,
umls-concept:C0205349,
umls-concept:C0332281,
umls-concept:C0441889,
umls-concept:C0965743,
umls-concept:C1527148,
umls-concept:C1705357,
umls-concept:C1824180,
umls-concept:C1956385
|
|
pubmed:issue |
8
|
|
pubmed:dateCreated |
2009-4-3
|
|
pubmed:abstractText |
The role of complement in the development of maladaptive immunity in experimental allergic asthma is unclear. In this study, we show that C3a receptor (C3aR)-deficient mice are protected from the development of Th2 immunity in a model of house dust mite-induced asthma. C5a receptor (C5aR)-targeting of C3aR-deficient mice during allergen sensitization not only reversed the protective effect but enhanced Th2 cytokine production, airway inflammation, and airway responsiveness, suggesting that the reduced allergic phenotype in C3aR-deficient mice results from protective C5aR signaling. In support of this view, C5aR expression in C3aR-deficient pulmonary dendritic cells (DCs) was increased when compared with wild-type DCs. Moreover, C5aR targeting regulated the frequency of pulmonary plasmacytoid DCs expressing costimulatory molecules B7-H1 and B7-DC. Ex vivo targeting of B7-H1 and B7-DC increased Th2 cytokine production from T cells of wild-type but not of C5aR-targeted mice, suggesting a protective role for C5a through regulation of B7 molecule expression on plasmacytoid DCs.
|
|
pubmed:grant |
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-10358194,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-10973279,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-10984054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-11067890,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-11086104,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-12421977,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-12853161,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-14764726,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15125219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15238608,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15286806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15322209,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15528378,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15634899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-15845447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-16314437,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-16439722,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-16511606,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-16870256,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-16889830,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-17044927,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-17475559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-18173375,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-18274560,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-18301423,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-2680973,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-9275149,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-9551945,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19342693-9856949
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD274,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Cd274 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C5a,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Pdcd1lg2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Programmed Cell Death 1 Ligand 2...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Anaphylatoxin C5a,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement,
http://linkedlifedata.com/resource/pubmed/chemical/complement C3a receptor
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Apr
|
|
pubmed:issn |
1550-6606
|
|
pubmed:author |
|
|
pubmed:issnType |
Electronic
|
|
pubmed:day |
15
|
|
pubmed:volume |
182
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
5123-30
|
|
pubmed:dateRevised |
2011-11-17
|
|
pubmed:meshHeading |
pubmed-meshheading:19342693-Animals,
pubmed-meshheading:19342693-Antigens, CD274,
pubmed-meshheading:19342693-Antigens, CD80,
pubmed-meshheading:19342693-Asthma,
pubmed-meshheading:19342693-Complement C5a,
pubmed-meshheading:19342693-Dendritic Cells,
pubmed-meshheading:19342693-Membrane Glycoproteins,
pubmed-meshheading:19342693-Mice,
pubmed-meshheading:19342693-Mice, Inbred BALB C,
pubmed-meshheading:19342693-Peptides,
pubmed-meshheading:19342693-Programmed Cell Death 1 Ligand 2 Protein,
pubmed-meshheading:19342693-Receptor, Anaphylatoxin C5a,
pubmed-meshheading:19342693-Receptors, Complement,
pubmed-meshheading:19342693-Signal Transduction,
pubmed-meshheading:19342693-Th2 Cells
|
|
pubmed:year |
2009
|
|
pubmed:articleTitle |
A protective role for C5a in the development of allergic asthma associated with altered levels of B7-H1 and B7-DC on plasmacytoid dendritic cells.
|
|
pubmed:affiliation |
Division of Molecular Immunology, Cincinnati Children's Hospital Medical Center and University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|
