Author: Lunding, Lars; Wegmann, Michael
Title: NK cells in asthma exacerbation Document date: 2015_7_8
ID: 0v17xscr_5
Snippet: NK cells are more frequent in the lung than in other organs [5] and their role in protecting against respiratory infections by viruses has been broadly described in animal models. Also they can directly react on TLR3 activation by ssRNA without support of antigen-presenting cells [6]. However, whether these important and beneficial functions may lead to aggravation of an already existing asthma remains unclear. Alike T cells NK cells can be divid.....
Document: NK cells are more frequent in the lung than in other organs [5] and their role in protecting against respiratory infections by viruses has been broadly described in animal models. Also they can directly react on TLR3 activation by ssRNA without support of antigen-presenting cells [6]. However, whether these important and beneficial functions may lead to aggravation of an already existing asthma remains unclear. Alike T cells NK cells can be divided into different subsets such as NK1/NK17 cells, NK2 cells, or NKreg cells according to their cytokine production [7]. Whether NK1/NK17 cells that are characterized by producing interferon (IFN) γ and IL-17A are actually the source of IL-17A and regulate the inflammatory response resulting in asthma exacerbation in our model remains to be investigated. Since we did neither observe enhanced production of IFNγ in wild type animals with acute asthma exacerbation nor an effect of NK cell depletion on IFNγ levels in BAL fluid, this hypothesis remains doubtful. Our data further suggest that the NK cells in our model require rather IL-6 then IL-23 or RORγt to express IL-17A and to exert their pathological function. Of course ongoing studies that characterize this NK cell subset in points of cytokine production, chemotaxis, survival, and interaction with other immune cells are necessary, but will help understanding the pathologic functions of NK cells and their potential as therapeutic targets in virus-induced asthma exacerbations.
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