Grant: Travel Awards - Institute Community Support

The lung samples nearly ten liters of air each minute, continuously exposing the very large mucosal barrier surface to foreign molecules. Despite this, the lung is generally maintained in a quiescent, non-inflamed state. However, upon infection or exposure to allergens or hazardous materials, airway inflammation can result in life long asthma, asthma exacerbations, airway hyper reactivity (AHR) and tissue fibrosis. These pathologies result from a deregulated host immune response and have long been thought to originate from the adaptive branch of the immune system. However, recent experimental evidence demonstrated that innate immune cells play an essential role in the onset of pathogenesis of these conditions. The recently identified population of group 2 innate lymphoid cells (ILC2) has been shown to play a key role in orchestrating excessive airway pathologies. I am aiming to provide with my work a better understanding of ILC2 at steady state and upon activation. Balancing the immune response by modulating ILC2 function will help to prevent lung pathologies upon respiratory infection. Moreover, a better understanding of the regulatory mechanism will support the design of new therapeutics and aid to tailor treatments for asthma.