Nature sub-journal: In addition to cancer, immunotherapy is expected to benefit patients with this type of lung disease.

Iexclusiveidal pulmonary fibrosis is a form of depotified pulmonary disease, with approximately 3 million patients worldwide.
the patient's lung function will continue and irreversibly decline due to progressive scarring in the lungs, which is life-threatening.
unfortunately, there are currently few treatments other than lung transplants that can change the progression of the disease, with a three-year survival rate of only 50%, with a prognosis comparable to some serious malignant tumors.
an important reason for this treatment challenge is that it is not clear why scars in the lungs began to spread.
, a study published by scientists at Stanford University gave us a new understanding of the pathological mechanisms of the disease.
researchers found that the fibroblasts that make up the scar multiply like cancer cells, escaping the surveillance of the immune system.
based on this result, immunotherapy is used to reactivate immune function, which is expected to be a boon for patients with iexclusivefluidpulmonary fibrosis.
research published in Nature's Nature Communications Nature.
study leader Professor Gerlinde Wernig of Stanford University and her colleagues in previous work found that a gene called JUN is a key regulator of the fibrosis process, expressing the gene that causes severe fibrosis in the lungs, liver, skin, bone marrow and kidneys of mice.
when they examined tissue samples from patients with advanced pulmonary fibrosis, they not only confirmed that there was an active JUN in a large number of fibrosis fibrosis fibrosis cells, but also found that the transcription factor signal directly regulated the genes that encode CD47 and PD-L1, which increased the two proteins. readers who
know about cancer may know that cancer cells often use the molecules CD47 and PD-L1 to evade surveillance and removal by the immune system.
normally, immune cells that flow through the body identify and remove cells that can cause disease.
, however, when cancer cells express CD47, it is equivalent to signaling "don't eat me" to macrophages, while PD-L1, it blocks attacks by macrophages and T cells.
Now, researchers have found that fibroblasts also use these immunosuppressive proteins to evade the immune system.
"In iexclusiveized lung disease, these fibroblasts behave almost as well as cancer cells."
"They grow on a normal lung structure, block the respiratory tract and block air from entering and leaving the bloodstream, " says Professor Wernig. "In this work, the researchers also found that another inflammatory factor, called IL-6, plays a key role in fibrosis disease."
"When we looked at clinical tissue samples from patients with pulmonary fibrosis, we found a significant increase in IL-6," professor Wernig said.
further analysis
" showed that JUN activation resulted in more IL-6 secretion of fibroblasts, which in turn increased the production of CD47, resulting in further increased resistance of fibroblasts to immune cell regulation.
when researchers blocked both IL-6 and CD47 signaling in pneumoconiosis mice, they found that they had a synergistic anti-fibrosis effect that allowed the lung tissue in mice to improve faster.
"eliminate inflammation and cut off the 'Don't Eat Me' signal, allowing us to reverse late fibrosis in mice."
," the study authors concluded. Professor
Wernig said: "This study shows a new treatment that can help improve the condition of patients with pulmonary fibrosis.
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