Authors:
Strickland, D. H.; Judd, S.; Thomas, J. A.; Larcombe, A. N.; Sly, P. D.; Holt, P. G.
Authors notes:
Mucosal Immunology. 2011;4(1):43-52
Keywords:
atopic asthma, transient airways hyperresponsiveness (AHR), aeroallergen-induced Th-cell activation, CD86, airway dendritic cells (DCs), T-regulatory (Treg)
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.