Sensing of lipids on macrophages by CD36 alters tuberculosis immune responses

Tuberculosis (TB) disease, caused by infection with the intracellular pathogen Mycobacterium tuberculosis (Mtb), is currently resurgent and is a pressing global health concern. The co-occurrence of type 2 diabetes is an increasing risk factor for the development of TB, but exactly how this condition alters the immune response against Mtb is unclear.

This work will assess if the increase in circulating lipids, which accompanies diabetes, alters the key components of the innate immune response against Mtb, chiefly the activity of the alveolar macrophage. By developing animal and in-vitro models of dyslipidemia and Mtb infection, we will examine how the receptor CD36 determines the nature of the immune response by modulating storage and hydrolysis of lipids.