Targeting a key protein of the innate immune system called TLR4 could be a new way of treating people with pulmonary fibrosis and other fibrotic disorders, according to a Northwestern University study.
The study, “TLR4-dependent fibroblast activation drives persistent organ fibrosis in skin and lung,” was published in the journal JCI Insight.
Fibrosis (scarring), seen in several chronic inflammatory diseases, results from the buildup of components of the extracellular matrix (ECM), a collection of molecules that provide structural and biochemical support to cells. Fibrosis is part of the normal healing process — as scar tissue — but when this process turns uncontrolled and pathological it damages such organs as the lungs, liver, kidney, skin or the heart.
What drives the variability of fibrosis across different patients is still scarcely understood, but abnormal functioning of the innate immune system is viewed as a potential key contributor.