Kathleen W. Schleifer

TL;DR: Data suggest that resistance to allergen-driven AHR is mediated in part by CD4+CD25+ T reg cell suppression of DC activation and that the absence of this regulatory pathway contributes to susceptibility.

TL;DR: Children with ASD had increased activation of both Th2 and Th1 arms of the adaptive immune response, with a Th2 predominance, and without the compensatory increase in the regulatory cytokine IL-10.

TL;DR: The results suggest that there are independent gene expression signatures reflective of cells and genes poised or committed to activation by an asthma attack, and exacerbated asthma status is readily distinguished based on the occurrence of strong gene Expression signatures in nasal epithelial samples.

TL;DR: Results provide a potential explanation for the dominant role of IL-13 in induction of goblet cell hyperplasia and airway hyperresponsiveness in asthma.

TL;DR: Resistance to allergen-driven AHR is mediated in part by CD4, and dendritic cells from T reg cell‐depleted mice demonstrated an increased capacity to stimulate T cell proliferation and Th2 cytokine production, which was concomitant with reduced IL-12 expression.