Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 19, 2026 1 hour, 44 minutes ago
Medical News: Breakthrough insights into how a key fibrosis drug reshapes immune responses
Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease that slowly scars the lungs, making it increasingly difficult for patients to breathe. Scientists have long known that the anti-fibrotic drug nintedanib helps slow disease progression, but exactly how it influences the immune system has remained unclear. Now, researchers from the Department of Pharmaceutical Sciences and the Department of Health Sciences at the University of Piemonte Orientale in Novara, Italy, along with the Division of Respiratory Diseases at Maggiore della Carità University Hospital, have uncovered compelling new evidence that the drug fundamentally alters immune cell behavior in patients with IPF.
Nintedanib reshapes immune cells, reducing harmful fibrosis signals in lung disease patients
Study tracked immune cells before and after treatment
The research team closely examined blood samples from 20 patients diagnosed with IPF before starting nintedanib therapy and again after six months of treatment. Each patient received the standard dose of 150 mg twice daily. The investigators focused on two important immune cell types—monocytes and macrophages—which play a crucial role in inflammation and tissue repair. These immune cells can either worsen lung scarring or help slow it, depending on their biological state. This
Medical News report highlights that the researchers discovered a striking shift in immune cell balance following treatment.
Macrophages derived from treated patients showed significantly higher levels of CD80 and CD86, markers linked to anti-fibrotic and protective immune activity. At the same time, harmful pro-fibrotic markers such as CD206 and CD163 were reduced.
Dangerous fibrosis-promoting signals sharply declined
One of the most important discoveries involved TGF-beta, a powerful signaling molecule known to drive fibrosis. After six months of treatment, both gene expression and release of TGF-beta from immune cells dropped significantly. This suggests that nintedanib may help reduce the harmful biological signals responsible for excessive scarring in the lungs. The study also found that treated macrophages showed increased oxidative activity, a sign that these immune cells had shifted toward a more active, disease-fighting state. Interestingly, monocytes themselves did not show major changes initially, but they appeared to be “primed” in a way that caused them to later develop into healthier, anti-fibrotic macrophages.
Immune system reprogramming could explain clinical benefits
These findings offer a critical explanation for why nintedanib helps slow lung damage in IPF patients. Instead of merely blocking fibrosis directly, the drug appears to reprogram immune cells, encouraging them to fight scarring rather than promote it. This immune rebalancing could help reduce ongoing tissue damage and improve disease stability over time. Researchers also observed that patients with worse lung function tended to have more harmful immune patterns
, further highlighting the importance of immune cell behavior in disease progression.
Conclusion reveals promising implications for future therapies
The study provides strong evidence that nintedanib does far more than previously understood. By altering how immune cells develop and behave, the drug appears to create a biological environment less favorable to fibrosis and more supportive of healing. This discovery opens the door to future therapies that specifically target immune cell polarization, potentially improving outcomes not only in pulmonary fibrosis but also in other chronic fibrotic diseases. Importantly, understanding these immune mechanisms could help physicians refine treatment strategies and identify which patients may benefit the most from therapy.
The study findings were published in the peer reviewed journal: Biomolecules.
https://www.mdpi.com/2218-273X/16/2/319
For the latest drug news, keep on logging to Thailand
Medical News.
Read Also:
https://www.thailandmedical.news/articles/med-news
Share
Tweet
Share
