IPF is rapidly progressive and causes scarring in the lungs, making it difficult to breathe. Approximately 50% of patients die within three years of diagnosis, and current treatments can only slow the disease—not stop or reverse it.

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. Instead, 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 ipilimumab—an immunotherapy drug currently used to treat various cancers—the researchers were able to block CTLA4 in mice. This released the “brakes” on certain immune cells called T cells, reactivating their ability to clear out the senescent fibroblasts.