Investigating the role of TGFβ in the functional imprinting of pulmonary macrophages in health and disease

All tissues of the body are populated with a mixture of immune cells that help protect the body from invasion by microbes. In many tissues the most abundant immune cell is the macrophage. Literally meaning ‘big eater’, macrophages capture and destroy microbial intruders, but also clear dead cells and orchestrate tissue repair after injury or infection. However, in some people the tissue repair functions of macrophages can become uncontrolled leading to excessive repair, unconstrained scar formation (fibrosis) and organ dysfunction. Idiopathic pulmonary fibrosis (IPF) is an incurable, devastating, deadly disease where progressive scarring of the lung is believed to be driven by overactive macrophages. Importantly, macrophages are very flexible cells and are easily influenced by their environment.

The aim of this study is to understand the signals that dictate macrophage behaviour in the normal lung and during successful tissue repair so that these signals can be promoted or targeted when macrophages begin to behave abnormally in disease.