They discover a key factor that protects the heart after a heart attack

Regulatory T lymphocytes are cells responsible for controlling other elements of the immune system to prevent uncontrolled inflammatory responses from causing damage.

In a recent study, it has been shown that the expression of the CD69 receptor on regulatory T lymphocytes confers protection after suffering a myocardial infarction, since it acts as a control point for the exacerbated inflammation responsible for heart damage in the medium term.

The research has been carried out by a team that includes Dr. Pilar Martín, head of the Group of Regulatory Molecules of Inflammatory Processes of the National Center for Cardiovascular Research (CNIC) in Spain and Dr. Rafael Blanco-Domínguez, from the CNIC and first job signer. Researchers from the Biomedical Research Network Center for Cardiovascular Diseases (CIBERCV) in Spain belonging to the group of Dr. Francisco Sánchez-Madrid at the CNIC and the University Hospital of La Princesa in Madrid, and the group of Dr. José Martínez have also participated. -González, at the Barcelona Institute for Biomedical Research (IIBB) and the Sant Pau Research Institute in Barcelona.

The new study also reveals that levels of expression of the CD69 receptor in peripheral blood could predict the development of heart failure, that is, of serious consequences in the functionality of the heart.

The researchers, through the analysis of blood immunological markers of 283 patients with myocardial infarction, ischemic heart disease and the main cause of death in the world, have discovered that there is an increase in the expression of this CD69 receptor in regulatory T lymphocytes in the first hours after the ischemic event.

Rafael Blanco-Dominguez and Pilar Martin. (Photo: CNIC)

Thanks to experiments with mouse models, this team of scientists has revealed that the absence of CD69 leads to an increase in inflammation, cardiac dysfunction and the rate of death after infarction.

This phenomenon, explains Dr. Martín, “is due to the fact that the regulatory T cells that express CD69 are recruited at the site of the infarction and are necessary to inhibit the gamma-delta T cells, which secrete the proinflammatory interleukin-17. The presence of CD69 makes regulatory T cells more efficient at inducing death and inhibiting interleukin-17 secretion through a novel antigen-specific independent mechanism.”

The research has also seen that a very relevant fact: therapy with regulatory T cells that express CD69 after a heart attack in CD69-deficient mice is sufficient to make up for the deficiency of this molecule and thus reduce cardiac inflammation and improve survival.

The follow-up of patients with infarction from two independent cohorts, in close collaboration with the Cardiology Departments of the Hospital Universitario de La Princesa in Madrid and the Hospital de la Santa Creu i Sant Pau in Barcelona, ​​confirmed that the expression levels of CD69 in peripheral blood are used to predict the development of heart failure, that is, serious sequelae in the functionality of the heart. In other words, as explained by Dr. Blanco-Domínguez, those patients in the study who had low levels of CD69 during the first hours after the infarction had a higher risk of developing heart failure during the first two and a half years after admission at the hospital.

The results of the study open the door to developing diagnostic methods and therapies for this global heart problem based on what has been discovered about CD69.

The study is titled “CD69 expression on regulatory T cells protects from immune damage after myocardial infarction.” And it has been published in the academic journal Journal of Clinical Investigation. (Source: CNIC)