Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-7-13
pubmed:abstractText
Clinical and epidemiological studies have shown the contribution of viral infection to the development of allergic asthma. Many RNA viruses, pathogenic for the respiratory tract, generate double-stranded (ds)RNA during their replication. Typical innate immune responses triggered by dsRNA involve the endosomal and cytoplasmic pathways. The former is mediated by Toll/IL-1R domain-containing adaptor inducing IFN-? (TRIF), and the latter by IFN-? promoter stimulator 1 (IPS-1). We explored the effect of polyinocinic polycytidilic acid, a synthetic dsRNA, on the development of an asthma phenotype in mice. Administration of dsRNA during ovalbumin sensitization augmented airway eosinophilia and airway hyperresponsiveness after an antigen challenge, which was associated with enhanced induction of IL-13-producing CD8(+) T cells. The augmentation was induced in IPS-1-deficient mice but not in TRIF-deficient mice. The interactions between dendritic cells (DCs) and T cells are regulated by B7-family costimulatory molecules, including B7-H1 (also known as PD-L1), a putative ligand for programmed death-1 (PD-1). Treatment of bone marrow-derived DCs with dsRNA enhanced B7-H1 expression in a TRIF-dependent manner. Additionally, dsRNA increased B7-H1 expression on DCs in the draining lymph nodes of ovalbumin-sensitized mice. The augmentation of the asthma phenotype was prevented by the treatment of mice with anti-B7-H1 mAb but not with anti-PD-1 mAb. The augmentation was not induced in B7-H1-deficient mice. These results suggest that dsRNA-triggered activation of the innate immune system in sensitization leads to augmentation of the asthma phenotype via IL-13 mainly from CD8(+) T cells. B7-H1 plays a crucial role in the process without requiring interaction with PD-1.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing, http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Vesicular..., 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/IPS-1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin, http://linkedlifedata.com/resource/pubmed/chemical/Peptides, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Double-Stranded, http://linkedlifedata.com/resource/pubmed/chemical/TICAM-1 protein, mouse
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1535-4989
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:20802088-Adaptor Proteins, Signal Transducing, pubmed-meshheading:20802088-Adaptor Proteins, Vesicular Transport, pubmed-meshheading:20802088-Animals, pubmed-meshheading:20802088-Antigens, CD274, pubmed-meshheading:20802088-Antigens, CD80, pubmed-meshheading:20802088-Asthma, pubmed-meshheading:20802088-CD8-Positive T-Lymphocytes, pubmed-meshheading:20802088-Dendritic Cells, pubmed-meshheading:20802088-Immunity, Innate, pubmed-meshheading:20802088-Interleukin-13, pubmed-meshheading:20802088-Membrane Glycoproteins, pubmed-meshheading:20802088-Mice, pubmed-meshheading:20802088-Mice, Knockout, pubmed-meshheading:20802088-Ovalbumin, pubmed-meshheading:20802088-Peptides, pubmed-meshheading:20802088-Phenotype, pubmed-meshheading:20802088-Pulmonary Eosinophilia, pubmed-meshheading:20802088-RNA, Double-Stranded
pubmed:year
2011
pubmed:articleTitle
Essential role of B7-H1 in double-stranded RNA-induced augmentation of an asthma phenotype in mice.
pubmed:affiliation
Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan.
pubmed:publicationType
Journal Article