PD-L2 modulates asthma severity by directly decreasing dendritic cell IL-12 production View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-07

AUTHORS

I P Lewkowich, S Lajoie, S L Stoffers, Y Suzuki, P K Richgels, K Dienger, A A Sproles, H Yagita, Q Hamid, M Wills-Karp

ABSTRACT

Studies examining the role of programmed death 1 (PD-1) ligand 2 (PD-L2)/PD-1 in asthma have yielded conflicting results. To clarify its role, we examined the PD-L2 expression in biopsies from human asthmatics and the lungs of aeroallergen-treated mice. PD-L2 expression in bronchial biopsies correlated with the severity of asthma. In mice, allergen exposure increased PD-L2 expression on pulmonary myeloid dendritic cells (DCs), and PD-L2 blockade diminished allergen-induced airway hyperresponsiveness (AHR). By contrast, PD-1 blockade had no impact, suggesting that PD-L2 promotes AHR in a PD-1-independent manner. Decreased AHR was associated with enhanced serum interleukin (IL)-12 p40, and in vitro stimulation of DCs with allergen and PD-L2-Fc reduced IL-12 p70 production, suggesting that PD-L2 inhibits allergen-driven IL-12 production. In our model, IL-12 did not diminish T helper type 2 responses but rather directly antagonized IL-13-inducible gene expression, highlighting a novel role for IL-12 in regulation of IL-13 signaling. Thus, allergen-driven enhancement of PD-L2 signaling through a PD-1-independent mechanism limits IL-12 secretion, exacerbating AHR. More... »

PAGES

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Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/mi.2012.111

DOI

http://dx.doi.org/10.1038/mi.2012.111

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053498656

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23149662


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