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Scientists from the La Jolla Institute for Immunology (LJI) and the Medical College of Georgia (MCG) at Augusta University have made important strides in identifying a previously elusive type of immune cell. Their research demonstrates how these cells contribute to inflammation and cardiovascular diseases, potentially opening doors to new avenues of treatment.
T cells have always been recognized for their crucial role in our immune system. Some T cells function as the body's frontline defenders, alerting other immune cells to threats or attacking infected host cells. Meanwhile, T regulatory cells (Tregs) act as referees, ensuring that other T cells don't release excessive inflammatory molecules while combating infections.
However, a mysterious player entered the scene when earlier studies led by Dr. Klaus Ley, co-director of MCG's Immunology Center of Georgia, discovered that certain T cells amplify their attacks on the apolipoprotein B (APOB) molecule—a key component of harmful cholesterol. Intriguingly, these T cells closely resembled the usually beneficial Tregs.
Their latest research unveils the true nature of these cells. Named ex-T regulatory cells (exTregs), these cells have undergone a genetic shift, turning them from helpful regulators into promoters of inflammation. The reason for this transformation remains unclear, but LJI Postdoctoral Researcher Antoine Freuchet, Ph.D., speculates that it might be the body's misdirected response to chronic diseases like heart conditions.
To investigate further, the researchers started with mice models prone to atherosclerosis. Utilizing fluorescent tagging techniques, they were able to visually trace the evolution of Tregs into exTregs. Advanced sequencing methods further differentiated the gene expressions of these cells, allowing the scientists to identify specific markers unique to exTregs.
Building upon this foundation, the team applied their findings to human blood samples. Collaborating with researchers from the University of Virginia and LJI's own clinical investigation center, they detected similar exTreg markers in humans, especially in those with atherosclerosis.
The discovery implies that these rogue exTregs could be more potent in humans with heart conditions. As LJI Postdoctoral Researcher Payel Roy, Ph.D., emphasizes, the ability to detect these cells paves the way to deeper insights into their role in human health. This could be especially valuable for monitoring patients over time, gauging the efficacy of medications, and understanding other chronic health issues, like autoimmune diseases.
As Freuchet optimistically notes, this research could prove instrumental in future medical studies, offering hope to millions affected by cardiovascular diseases and beyond.
T cells have always been recognized for their crucial role in our immune system. Some T cells function as the body's frontline defenders, alerting other immune cells to threats or attacking infected host cells. Meanwhile, T regulatory cells (Tregs) act as referees, ensuring that other T cells don't release excessive inflammatory molecules while combating infections.
However, a mysterious player entered the scene when earlier studies led by Dr. Klaus Ley, co-director of MCG's Immunology Center of Georgia, discovered that certain T cells amplify their attacks on the apolipoprotein B (APOB) molecule—a key component of harmful cholesterol. Intriguingly, these T cells closely resembled the usually beneficial Tregs.
Their latest research unveils the true nature of these cells. Named ex-T regulatory cells (exTregs), these cells have undergone a genetic shift, turning them from helpful regulators into promoters of inflammation. The reason for this transformation remains unclear, but LJI Postdoctoral Researcher Antoine Freuchet, Ph.D., speculates that it might be the body's misdirected response to chronic diseases like heart conditions.
To investigate further, the researchers started with mice models prone to atherosclerosis. Utilizing fluorescent tagging techniques, they were able to visually trace the evolution of Tregs into exTregs. Advanced sequencing methods further differentiated the gene expressions of these cells, allowing the scientists to identify specific markers unique to exTregs.
Building upon this foundation, the team applied their findings to human blood samples. Collaborating with researchers from the University of Virginia and LJI's own clinical investigation center, they detected similar exTreg markers in humans, especially in those with atherosclerosis.
The discovery implies that these rogue exTregs could be more potent in humans with heart conditions. As LJI Postdoctoral Researcher Payel Roy, Ph.D., emphasizes, the ability to detect these cells paves the way to deeper insights into their role in human health. This could be especially valuable for monitoring patients over time, gauging the efficacy of medications, and understanding other chronic health issues, like autoimmune diseases.
As Freuchet optimistically notes, this research could prove instrumental in future medical studies, offering hope to millions affected by cardiovascular diseases and beyond.