Immune changes may help reveal disease activity in cardiac sarcoidosis
Study links distinct immune-cell patterns to heart involvement and ECG changes
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Several types of immune cells and immune signaling molecules are altered in people with cardiac sarcoidosis, a new study shows.
These findings “may further elucidate the complex, and yet not well understood, [disease-driving] pathways in cardiac sarcoidosis,” the researchers wrote.
Although more studies are needed to validate the findings, the researchers suggested that this immune signature may eventually help predict clinical outcomes and identify new treatment targets in people with cardiac sarcoidosis.
The study, “The inflammatory fingerprint reveals immune cell populations associated with disease activity in cardiac sarcoidosis,” was published in Clinical Research in Cardiology.
How sarcoidosis can affect the heart
Sarcoidosis is an inflammatory disorder marked by granulomas, or abnormal clumps of immune cells. When sarcoidosis affects the heart, it is called cardiac sarcoidosis and can cause problems such as abnormal heart rhythms and heart failure.
Although immune-system dysfunction is known to play a role in sarcoidosis, the specific patterns of immune dysregulation are not fully understood.
In this study, a team of scientists in Germany analyzed immune activity in 22 people with cardiac sarcoidosis and four people who had sarcoidosis without heart involvement. Samples from 29 healthy people were also analyzed as controls.
Among cardiac sarcoidosis patients, 14 were classified as having active disease, marked by heart inflammation, while the remaining eight had chronic disease, marked by scarring in the heart.
The researchers’ analysis included dozens of immune-cell subtypes, along with many different immune signaling molecules. Results showed that many of these were altered in people with cardiac sarcoidosis.
First, the relative abundance of 18 immune cell populations was significantly increased in sarcoidosis patients compared with healthy controls, while eight populations were significantly decreased.
“Clustering of sarcoidosis patients showed a perceptible separation compared to the healthy controls indicating a crucial alteration of the inflammatory [profile],” the researchers wrote.
When comparing patients with and without heart involvement, those with cardiac sarcoidosis had a significantly higher relative abundance of antibody-producing immune cells called plasmablasts.
Immune-cell patterns differ with disease activity
In addition, several subsets of T cells, immune cells that can kill infected or abnormal cells and help regulate other parts of the immune system, were significantly reduced in people with active cardiac sarcoidosis compared with those with chronic disease. In contrast, several other immune cell types, including monocytes, were found at higher levels in people with active disease.
In analyses of immune signaling involved in inflammation and granuloma formation, expression of an inflammatory signaling receptor was significantly increased in certain blood cells from people with active cardiac sarcoidosis compared with sarcoidosis patients without heart involvement.
Further analyses showed that the abundance of immune cell populations linked to cardiac sarcoidosis was significantly associated with clinical parameters at the study’s start, as well as new electrocardiographic (ECG) changes during follow-up.
The scientists stressed that this was a small study and further work is needed to validate their findings, but they said these results may help better understand the biological underpinnings of cardiac sarcoidosis.
“These findings of an altered immune cell landscape in patients with sarcoidosis might contribute to the understanding of [biological changes] promoting adverse cardiovascular events,” the team wrote. “Determination of the immune signature in patients with [cardiac sarcoidosis] might enable novel diagnostic perspectives and potential new pharmacological targets to modify disease progression.”
