T-cells are expected to become targets for drugs that inhibit atherosclerosis.

In fact, one in four Americans will die from a series of effects of atherosclerosis, namely the accumulation of fat and cholesterol in the arteries.statins help reduce mortality, millions of people are still at risk.researchers at the La Jolla Institute of Immunology (LJI) in the United States are working on a way to stop plaque formation.in a new study, researchers found that some T lymphocytes, a type of white blood cell, initially tried to fight the disease, but could eventually exacerbate inflammation and make atherosclerosis worse."Your immune system usually responds to itself with anti-inflammatory, but once the disease starts, it's bad for you." "" professor, Professor Klaus Ley, said the paper was published in Circulation on July 24.Ley's lab specializes in T-cells, which identify specific peptides or protein fragments.researchers also found that each person can produce T-cells that identify ApoB, the main protein for LDL cholesterol.LDL, sometimes referred to as "bad" cholesterol, is important for transporting fat molecules where the body needs them, but too much LDL can lead to plaque formation, leading to atherosclerosis.Ley hopes to one day be able to control T-cells by designing a vaccine that can target LDLs to prevent the formation of dangerous plaques.in a 2018 study, the team showed that an atherosclerosis vaccine could reduce plaque levels in mice.in the new study, the researchers hope to find the antigen episophe on the ApoB protein, the target of T cells.this allows researchers to build "quads" to look for a very small number of Molecules that can identify These table bits of T cells.using the new tracking method, Ley and colleagues identified a set of regulated T-cells that usually help reduce inflammation in the body.but something seems to be wrong with atherosclerosis, which changes the function of these cells.regulatory T cells do not reduce inflammation, but instead secrete an immune molecule called cytokine, which increases inflammation and further narrows the diseased arteries. "These T-cells don't cause plaques in the arteries, but they accelerate disease, ". ," Ley said. researchers also found that genes and dietplay in transforming regulatory T-cells from auxiliary cells to disease-causing cells. in fact, in just four weeks, diet led to harmful T-cell metastasis in mice. now, researchers are studying more patientS's T cells in more detail to find out what drives regulatory T-cells to become pathogenic. "You can protect patients only if you know the mechanism." ," Ley said. ()