Allergic asthma is a severe chronic airway disease affecting more than 300 million people worldwide. The disease arises in response to an excessive T cell immune response initiated by inhalation of environmental allergens, including house dust mite, pollen, and animal dander. While current treatments aim to control asthma symptoms, they are not curative; the basic mechanisms driving the disease are still not fully understood, and this impedes development of rational curative therapies. Recent work discovered that a resident memory Th2 cell (Th2RM) subset persists in the lung for months after allergen exposure. Generally, TRM provide long-term local protection against pathogens. However, in asthma, these types of T cells worsen disease severity by producing Th2 cytokines locally. Virtually nothing is known about the emergence of TRM in asthma, and unravelling the mechanisms by which these cells form, become dormant and propagate disease is the core aim of this proposal. By integrating cutting edge technologies and methodologies, I will elucidate molecular and cellular communication mechanisms leading to local retention of allergen-specific TRM, and understand how they contribute to the local inflammatory response. While this research will add insights to the broader T cell biology field, understanding these fundamental asthma pathways is crucial if clinical management of severe asthma is to shift from a syndrome focused disease towards personalized treatment regimens.