Over the last 50 years, there has been a worldwide increase in the prevalence of allergic diseases, with more than 300 million people suffering from asthma, 400 million from some form of allergic rhinitis, and nearly 10% of children suffering from food allergies. In susceptible individuals, these pathologies are principally driven by aberrant type 2 immune responses to innocuous environmental proteins. Why only certain individuals mount inappropriate responses to otherwise harmless proteins has remained an unanswered question. It is thought that maladaptive innate sensing of these harmless environmental proteins leads to disease. We want to understand the pathways that either promote or protects against development of allergies.

Recent discoveries have raised the possibility that altered recognition of allergens, through pattern recognition receptors like toll-like receptors and c-type lectin receptors, may underlie disease susceptibility.  We know mediators like IL-33 and complement (C3a) are important drivers of allergy.

We primarily focus on how are allergens sensed and how they initiate aberrant type 2 inflammation that drives allergy.