Protein crystallization is an important feature of Type-2 inflammation, as evidenced by the convergent evolution of Galectin-10 (Gal10) crystals in humans, and Ym1/2 crystals in mice. Despite the prevalence of crystals as a principal feature of pathogenic mucus in human diseases such as asthma, chronic rhinosinusitis and allergic bronchopulmonary aspergillosis, their biological importance has not been explored, due to a substantial lack of tools. We have undertaken several novel approaches to investigate these crystals in an in vivo setting. We have developed several mouse lines to understand the role of Gal10, which is normally absent in mice, in contributing to various features of allergic diseases. Transgenic mice that endogenously express Gal10 demonstrate increased mucus production as well as crystal formation during house dust mite-induced asthma. Additionally, lung organoids of transgenic mice will be grown where parameters of crystallisation can be more precisely controlled and manipulated. Lastly, models of Type-2 lung inflammation in mice will be developed, to model Type-2 diseases in humans in which crystals are found. Understanding the causes and consequences of Gal10 crystallization in a physiological in vivo setting will allow a novel understanding into the pathogenesis of Type-2 diseases and particularly plugging. This will provide a unique platform to investigate Gal10 crystals as a therapeutic target for an impenetrable aspect of airway disease.