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Pulmonary fibrosis is a severe and chronic lung disease that predominantly affects older adults. With no specific treatments currently available, lung transplantation often remains the only option to extend patients’ lives. A research team from CeMM and MedUni Vienna has now uncovered that the aging immune system plays a crucial role in the onset and progression of the disease. Their study, published in the leading journal Science Immunology, lays the groundwork for developing new immune-based therapies.

In their investigation, the team led by Sylvia Knapp and Riem Gawish (Department of Medicine I, MedUni Vienna) demonstrated for the first time how the age of specific immune cells contributes to the development of idiopathic pulmonary fibrosis (IPF). IPF is characterized by excessive deposition of connective tissue in the lungs, leading to progressive stiffening of lung tissue, difficulty breathing, and ultimately, death. Until now, this age-related disease was primarily attributed to changes in lung structural cells. However, the new findings challenge this assumption.

Rejuvenating the Immune System: A Promising Therapeutic Strategy

As shown in the study, first-authored by CeMM PhD student Asma Farhat, it is not the aging lung tissue itself, but rather the aging immune system that drives the increased risk of IPF over time. Using a mouse model, the researchers found that transplanting aged immune cells into young animals aggravated fibrosis. In contrast, targeted rejuvenation of the immune system prevented disease onset in older animals.

The reason lies in a shift within the immune landscape: with age, certain immune cells—specifically profibrotic macrophages—accumulate in the lungs and promote pathological connective tissue formation. At the same time, the regulatory T cells that typically counteract inflammation become less active. These aging T cells produce less interleukin-10, a key anti-inflammatory molecule. “The interleukin-10 produced by T cells is important for suppressing the profibrotic effects of macrophages, and it is precisely this important mechanism that appears to no longer function in old age,” explains first author Asma Farhat.

These findings pave the way for a novel therapeutic approach focused on modulating immune cell function—offering a potential alternative to lung transplantation. Further studies will be necessary to validate the results and explore this promising path toward treatment.

The Study “An aging bone marrow exacerbates lung fibrosis by fueling profibrotic macrophage persistence” was published in Science Immunology (DOI: 10.1126/sciimmunol.adk5041) on 28 March 2025. 

Funding: This Study was supported by the Austrian Science Fund FWF.