Lung cancer is the leading cause of cancer-related deaths worldwide and

has a poor prognosis. The influence of inflammation on tumorigenicity has

mostly been studied in the context of its contribution to primary tumor

initiation and promotion, with a strong focus on type-1 antitumor immunity.

However, the contribution of type-2 immunity, hallmarked by eosinophilia,

epithelial remodeling and repair driven by IL-4, IL-5, IL-9, and IL-13 from

innate lymphoid cells (ILC2), is still unclear. Here, we will investigate the

impact of local type-2 inflammation on the progression of NSCLC. Our

preliminary data show that treatment with the type-2 alarmin IL-33 results in

lower tumor burden in this model. Within this proposal we will use various

newly generated mouse lines and therapeutic intervention strategies in a

model of NSCLC to advance our understanding on the role of type-2

inflammation in antitumor immunity. Ultimately helping to develop new

strategies for immunotherapeutic interventions.