| Literature DB >> 20668438 |
D H Strickland1, S Judd, J A Thomas, A N Larcombe, P D Sly, P G Holt.
Abstract
The hallmark of atopic asthma is transient airways hyperresponsiveness (AHR) preceded by aeroallergen-induced Th-cell activation. This is preceded by upregulation of CD86 on resident airway dendritic cells (DCs) that normally lack competence in T-cell triggering. Moreover, AHR duration is controlled via T-regulatory (Treg) cells, which can attenuate CD86 upregulation on DC. We show that airway mucosal Treg/DC interaction represents an accessible therapeutic target for asthma control. Notably, baseline airway Treg activity in sensitized rats can be boosted by microbe-derived stimulation of the gut, resulting in enhanced capacity to control CD86 expression on airway DC triggered by aeroallergen and accelerated resolution of AHR.Entities:
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Year: 2010 PMID: 20668438 DOI: 10.1038/mi.2010.43
Source DB: PubMed Journal: Mucosal Immunol ISSN: 1933-0219 Impact factor: 7.313