Your lungs and airways need to be stretchy, sort of like balloons. Take a big breath, and they’ll open right up.
Damaged lungs can’t open properly. Patients with asthma, idiopathic pulmonary fibrosis and systemic sclerosis suffer from fibrosis and tissue remodeling, where a build-up of tissue and immune cells, and proteins that form a glue-like substance, keep the airways from expanding. As fibrosis gets worse, taking a breath feels like blowing up a balloon filled with concrete.
In a new study, researchers at La Jolla Institute for Immunology (LJI) report that a protein called TL1A drives fibrosis in several mouse models, triggering tissue remodeling, and making it harder for lungs and airways to function normally.
“Our new study suggests that TL1A and its receptor on cells could be targets for therapeutics aimed at reducing fibrosis and tissue remodeling in patients with severe lung disease,” says LJI Professor Michael Croft, Ph.D., director of scientific affairs at LJI and senior author of the new study in The Journal of Immunology.
Croft’s laboratory is focused on understanding the importance of a family of proteins, called tumor necrosis factors (TNF) and tumor necrosis factor receptors (TNFR), in inflammatory and autoimmune diseases. By investigating these molecules, researchers hope to track down the root causes of inflammation and stop tissue damage before it’s too late.
Previous research had shown that a TNF protein called TL1A can act on immune cells involved in allergic reactions and drive those immune cells to make inflammatory molecules. The Croft Lab wondered-;if TL1A leads to inflammation, could it contribute to fibrosis in the lungs?
For the new study, Croft and his colleagues used genetic and therapeutic interventions, tissue staining, and fluorescence imaging techniques to study protein interactions in mouse models of severe