Researchers in Germany discovered that patients with idiopathic pulmonary fibrosis (IPF) have increased levels of myeloid-derived suppressor cells (MDSC) in the blood. The higher the number of MDSC, the more limited the lung function. The findings also indicate that MDSC may serve as IPF biomarkers.
The study, “Peripheral blood myeloid-derived suppressor cells reflect disease status in idiopathic pulmonary fibrosis,” was published in the European Respiratory Journal.
MDSC are a heterogeneous population of cells comprising myeloid cell progenitors and precursors of several immune system cells, such as granulocytes, macrophages, and dendritic cells. These cells are generally immature and are characterized by their role in the regulation of immune responses and tissue repair in healthy people, and their ability to suppress immune T-cell response. MDSC have been found to be associated with a poor prognosis in cancer, facilitating immune evasion.
“The role of MDSC has been most extensively studied in cancer, where they suppress the immune system and contribute to a poor prognosis,” first author Dr. Isis Fernandez, MD, said in a news release. The findings from the study indicate that identical mechanisms are also at work in IPF.
To understand the abundance and function of MDSC in IPF, Prof. Oliver Eickelberg and his colleagues at the Comprehensive Pneumology Center at Helmholtz Zentrum München, in partnership with the Department of Internal Medicine at Munich University Hospital in Germany, tested blood samples of 170 participants, including 69 IPF patients, for the composition of circulating immune cell types.
Researchers found that MDSC counts in patients with IPF were significantly higher than in the healthy group of participants. MDSC counts inversely correlated with lung function only in IPF, identifying them as potent biomarkers for disease progression. When researchers conducted the experiment in patients with chronic obstructive pulmonary disease (COPD) or other interstitial lung diseases, they observed that this inverse correlation was absent.
“We conclude that the number of MDSC reflects the course of the disease, especially in IPF,” Fernandez said.
The team then measured the activity of genes that are usually expressed by immune cells to determine if these cells could be the underlying cause of lung function deterioration. Researchers found that these genes were frequently less expressed in lung tissue samples with high counts of MDSC cells, suggesting that MDSC compromises the immune system in patients with IPF.
“We were able to show that MDSC are primarily found in fibrotic niches of IPF lungs characterized by increased interstitial tissue and scarring, that is, in regions where the disease is very pronounced,” Eickelberg said. “As a next step, we seek to investigate whether the presence of MDSC can serve as a biomarker to detect IPF and to determine how pronounced it is.”
The researchers also want to investigate the mechanisms of MDSC accumulation in more detail. “Controlling accumulation or expansion of MDSC or blocking their suppressive functions may represent a promising treatment options for patients with IPF,” Eickelberg said.
IPF is a chronic and disease characterized by a progressive decline in lung function. The term pulmonary fibrosis means scarring of lung tissue and is the cause of worsening dyspnea (shortness of breath). The fibrotic process in IPF is irreversible and researchers have been trying to discover new indicators or novel disease biomarkers that can be used for earlier diagnosis and to potentially slow or halt IPF progression.
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