In a ground-breaking discovery, scientists have unveiled the mysteries surrounding a particular type of human T cell that has long eluded detection. This revelation, spearheaded by the combined efforts of the La Jolla Institute for Immunology (LJI) and the Medical College of Georgia (MCG) at Augusta University, sheds light on the elusive ex-T regulatory cells (exTregs) and their potential role in inflammation and cardiovascular ailments.
ExTregs, although rare, play a pivotal role in the human immune system. Their elusive nature has made them difficult to detect in human samples until now. The recent study has not only provided a reliable method to identify these cells but also offers insights into their contribution to inflammation and cardiovascular diseases.
To trace these cells, scientists employed fluorescent tags on mice susceptible to atherosclerosis. This allowed them to pinpoint specific markers unique to exTregs. Leveraging these findings, they successfully identified exTregs in human blood samples. “These cells are likely causing damage,” remarked LJI Postdoctoral Researcher Payel Roy, Ph.D., emphasizing the significance of the discovery.
T cells, the defenders of our body, have various roles. While some alert other immune cells to potential threats or eliminate infected host cells, T regulatory cells (Tregs) ensure that other T cells don’t release excessive inflammatory molecules during their defensive operations.
Interestingly, some T cells, which were previously believed to be beneficial Tregs, were found to be contributing to atherosclerosis by targeting a molecule known as apolipoprotein B (APOB). This molecule is a primary component of the “bad” cholesterol responsible for the formation of hazardous plaques in arteries.
The recent study has unveiled the true identity of these cells: they are, in fact, exTregs. These cells undergo a genetic “deprogramming,” losing their ability to regulate inflammation. The transformation of these cells might be the body’s misguided attempt to adapt to chronic diseases.
“When there’s excessive chronic inflammation, like in heart disease, the body might reconfigure itself, causing these Tregs to turn rogue. Instead of controlling inflammation, they become inflammatory,” explained LJI Postdoctoral Researcher Antoine Freuchet, Ph.D.
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The study’s initial phase was conducted on mice, as exTregs had been identified in them for quite some time. The researchers tagged both Tregs and the harmful exTregs in a mouse model. These tags would glow, indicating the normal functioning of Tregs. A shift from a dual-color glow to a single color would signify the transformation of Tregs to exTregs.
By employing techniques like flow cytometry and bulk RNA sequencing, the team discerned vast differences in gene expression between Tregs and exTregs. This led to the identification of specific exTreg markers.
Using these markers, the team successfully identified biomarkers for human exTregs in blood samples. The findings were consistent across samples from both the University of Virginia and LJI’s John and Susan Major Center for Clinical Investigation. The discovery that exTregs in humans with atherosclerosis might be more potent is particularly intriguing.
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With the ability to detect exTregs in blood, scientists can now specifically identify these cells and understand their molecular fingerprints. The future holds promising avenues for using these biomarkers to study their roles in other chronic health conditions, including autoimmune diseases.
The potential applications of this discovery are vast. For instance, monitoring how exTreg biomarkers change over time in individual patients could provide invaluable insights. Would there be a decrease in exTreg signs if a patient were administered effective medication? Only time and further research will tell.
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This monumental research was supported by various esteemed institutions, including the National Institutes of Health and the American’s Heart Association.
Article Reference:
- https://theprint.in/science/study-reveals-when-regulatory-t-cells-go-bad/1710636/
- https://www.sciencedaily.com/releases/2023/08/230810141015.htm
