Research shows how trained immunity links to cardiovascular disease

When thinking about the immune system, most people think about B and T cells and how they can be trained to recognize pathogens, preventing re-infections. Besides this "adaptive" immune system, we also have an "innate" immune system which acts as first line defense against e.g. bacteria and viruses. The textbook view is that the innate immune system is non-specific so that it's response always follows the same pattern, even for recurring infections. However, research published today in Stem Cell Reports provides evidence that brief exposure to certain "danger signals" can prime the body's innate immune system into a long-term hyperreactive and inflammatory state termed "trained innate immunity."

To test this, PhD student Daniela Flores-Gomez from the team of Niels Riksen and Siroon Bekkering at Radboud University Medical Center, Netherlands, isolated blood stem cells and white blood cells from human bone marrow and exposed them to the protein IL-1beta, which is one of the main inducers of trained immunity in mice. Just like their mouse counterparts, the human blood stem cells divided more and made more innate white blood cells when stimulated with IL-1beta. Further, the trained white blood cells were hyperreactive, meaning that they produced more inflammatory proteins and stuck more to blood vessels. Interestingly, IL-1beta levels are elevated in patients after heart attack and these patients have an increased risk of developing atherosclerosis. This might be explained by a trained, hyperreactive immune system with stickier, plaque-forming white blood cells. A fat and sugar-rich diet might worsen this effect, as it promotes trained immunity through IL-1beta signaling in lab animals.

Source:

International Society for Stem Cell Research

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