Airway inflammation in asthma: key players beyond the Th2 pathway
A KleinJan - Current opinion in pulmonary medicine, 2016 - journals.lww.com
A KleinJan
Current opinion in pulmonary medicine, 2016•journals.lww.comAsthma is generally known as a Th2 disease. It has become increasingly clear that IL-4 has
pathophysiological effects in asthma that extend far beyond the Th2 pathway [1, 2]. The Th2
pathway is initiated by the binding of IL-4 to the IL-4 receptor, followed by phosphorylation of
signal transducer and activator of transcription 6 and the activation of GATA3. This innate
immune response significantly contributes to the allergic airway inflammation, which is
linked to eosinophils, mast cells, basophils, and innate lymphoid cell type 2 (ILC2)[3].
pathophysiological effects in asthma that extend far beyond the Th2 pathway [1, 2]. The Th2
pathway is initiated by the binding of IL-4 to the IL-4 receptor, followed by phosphorylation of
signal transducer and activator of transcription 6 and the activation of GATA3. This innate
immune response significantly contributes to the allergic airway inflammation, which is
linked to eosinophils, mast cells, basophils, and innate lymphoid cell type 2 (ILC2)[3].
Asthma is generally known as a Th2 disease. It has become increasingly clear that IL-4 has pathophysiological effects in asthma that extend far beyond the Th2 pathway [1, 2]. The Th2 pathway is initiated by the binding of IL-4 to the IL-4 receptor, followed by phosphorylation of signal transducer and activator of transcription 6 and the activation of GATA3. This innate immune response significantly contributes to the allergic airway inflammation, which is linked to eosinophils, mast cells, basophils, and innate lymphoid cell type 2 (ILC2)[3].
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