To investigate how apolipoproteins modify immune cell function in innate and adaptive airway inflammatory cells

Asthma is the world’s commonest chronic lung disease, affecting 350 million people worldwide. The advent of novel ‘biologic’ therapies targeting specific phenotypes of asthma is currently revolutionizing the treatment of patients with type 2 inflammation. However, there are no specific treatments available for the 50% of patients with type 2 low disease. The Levine group has identified a novel pathobiologic mechanism involving dysregulation of apoplipoproteins, which may play an important role in this phenotype by regulating the recruitment and function of innate and adaptive immune cells, which may have relevance for resistance to corticosteroids. Peptide mimetics of these molecules have potential as novel therapies for asthma, especially for patients with type 2 low neutrophilic inflammation. Dr Hinks group uses in vitro, murine and ex vivo human studies on highly phenotyped asthmatics to explore the biology of the inflamed airway mucosa, particularly innate and adaptive immune cells. Through this collaboration the student would use a range of techniques and a mix of wet lab science and human experimental medicine to understand the translational potential of apolipoprotein biology in human asthma.