Pulmonary fibrosis has no cure. Cold a Cancer Drug Hold The Answer?

Pulmonary fibrosis has no cure. Cold a Cancer Drug Hold The Answer?


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Researchers at Tulane University have identified a potential new way to treat idiopathic pulmonary fibrosis (IPF), a deadly and currently incurable lung dies Worldwide.

IPF is Rapidly Progressive and Causes Scarring in the Lungs, Making It Difential to Breathe. Approximately 50% of patients die

In a study Published in the Journal of Clinical InvestigationTulane scientists found that an FDA -Proved Cancer Drug May Help The Immune System Clear out the Damaged Cells that Cause The Lung Scarring, Potentialy restoring lung function in patients in the desease.

In healthy lungs, specialized cells called fibroblasts help repair lung tissue. But in People with IPF, Some Fibroblasts and Nearby Epithelial Cells Stop Functioning Properly. These so-called “senescent” cells no longer divide or die as they should. INTEAD, They Build Up and Contribute to Stiff, Scarred Lungs.

Tulane Researchers Discovered that these senescent cells appear to accumulate when the immune system’s natural ability to remove them is blocked. The Culprit: a protein called Ctla4, which acts as an emergency brake on immune system activity.

By using ipilumumab – An immunotherapy drug currently used to treate various cancers -the -ups resarchers was able to block ctla4 in mice. This release the “brakes” on certain immune cells called t cells, reactiveating their ability to clear out the senescent fibroblasts. As a result, the Mice Showed significantly improved Lung Tissue Regation and Reduced Scarring.

“The Ctla4 Protein Normally Functions to Prevent Excessive Inflammation by Blocking Overactive T Cells,” Said Senior Author Dr. Victor Thannickal, Professor and Harry B. Greenberg Chair of Medicine at Tulane University’s John W. Deming Department of Medicine. “Too much of this ‘blocker protein’ may result in losing the ‘good’ inflammation that is needed to remove senescent cells.

The researchers zeroed in on ctla4 as a potential therapeutic target when they analyzed both human and mouse ipf lung tissue and found unusually high levels of ctla4 on the Cells in the ARAS WEHERE SCARRING was most prevalent.

Mice That Received IPLIMUB Showed Significantly Improved Lung Repair Ability and Recovered Faster Than Mice That Did Not receive the Drug.

“This opens up an entryly new direction for potential treatment of IPF,” said lead author santhu yadav, ph.d., assistant professor of medicine at the tulane only university of medicine. “INTEAD of Using Drugs to Kill Senescent Cells, We Are Re-Activating Our Own Immune System to clear Them Out.”

More research is needed to determine the efficacy of drugs that target Ctla4 or other so-called “checkpoint proteins” to rejuvenate the immune system. A Primary Concern is determining a safe dosing strategy that allows for the immune system to Attack SENESCENT CHELS Without Causing Harmful Levels of Inflammation.

IPF is a disease of aging and is rarely seen before age 50. These findings also offer hope that this approach could work for other Similar aging-Related Diseases.

“If it works in IPF, this immune rejuvenating approach to treatment may be effective in other diseases Thannick Said. “Can the right drug activate t cells in a way that clears senescent cells without causing collectorate damage? IF so, we may be closer to combating many aging-related days and Perhaps even.”

More information:
Reactivation of ctla4-expressing t cells accelerates resolution of lung fibrosis in a humanized mouse model, Journal of Clinical Investigation (2025). Doi: 10.1172/jCI181775, www.jci.org/articles/View/181775

Provided by tulane university


Citation: Pulmonary fibrosis has no cure. Cold a Cancer Drug Hold The Answer? (2025, April 22) retrieved 22 April 2025 from

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