Abstract

Asthma is a chronic inflammatorydisease of the airwaysthat causesbronchial hyperreactivity, mucus overproduction, airwayremodelling and narrowing. Allergic asthmatic patients generally present a predisposition toward Thelper (Th) 2 inflammation that is maintained by allergen-driven innate factors and downstream activation of Th2 cells. In this regard, Notch signalling activates the key Th2 transcription factor Gata-3.In fact, Notch is considered as a master regulator of Th cells to terminally differentiate into Th1, Th2, Th17 lineages by directly inducing the respective transcription factors and cytokines.1 The latest findings by Harb et al., further report how Notch signalling enables an inflammatory response in the allergic airways by altering T-regulatory (Treg) cells into effector Th2 and Th17 cells.2.

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