They identify a new mechanism of control of inflammation
They identify a new mechanism of control of inflammation
When an infection or tissue damage occurs, the body reacts by activating the inflammatory immune response that rejects the infection or repairs the damaged tissue. However, sometimes an excess of inflammation can cause the opposite effect and cause greater damage, as happens in allergies or autoimmune diseases.
Now, researchers from the National Center for Cardiovascular Research (CNIC) (Spain) have discovered a new mechanism of inflammation control that can handle the damage associated with the immune response. The study is published today in the prestigious scientific journal Science.
Inflammation is a defense mechanism that facilitates the arrival of cells of the immune system to the place where the aggression has taken place, for example, to the pancreas during pancreatitis or to the heart in situations of infarction. The function of these immune cells is to eliminate the damage causing this inflammation and contribute to the repair of damaged tissue.
"Neutrophils are the first immune cells that reach the infectious or inflammatory focus, with the aim of eliminating the aggression. However, they are very destructive and do not only act on the infection, but also on the tissue they reach, "explains David Sancho, who heads the Immunobiology laboratory of the CNIC that has conducted the study.
According to Sancho, the elimination of the injury leads to damage to the tissues themselves. This process is known as immunopathology, since it is a tissue damage caused by our own immune system.
In mice deficient in DNGR-1, which are not able to correctly recognize tissue damage, there is an uncontrolled arrival of neutrophils that causes much greater edema (damage). (Photo: CNIC)
"It is therefore important to characterize how our immune system can control the inflammatory response of neutrophils so that it is not harmful to our body," he adds.
This work has identified that dendritic cells, in addition to being essential for directing the specific response of T lymphocytes, can also control the infiltration of neutrophils in tissues and thus attenuate inflammation to avoid excessive tissue damage.
The research has been carried out in mouse models, the only system that reproduces the complexity of the infections and inflammatory processes studied, and allows us to better understand how immunopathological (harmful) responses are generated by our own defenses.
Dendritic cells, says Carlos del Fresno, first author of the article, "produce factors that attract neutrophils to the inflammatory focus, as is the case of the chemokine Mip-2. And, at the same time, these dendritic cells also express on their surface a receptor called DNGR-1, capable of recognizing tissue damage. This is because it identifies components inside the cells, which are only accessible when the cell is damaged or 'broken'. "
"Thus, when DNGR-1 detects this lesion - clarifies the Fresno -, it stops the capacity of the dendritic cells to produce Mip-2 and, therefore, reduces the arrival of neutrophils to the damaged organ. In this way it prevents a greater injury is generated, which can even compromise the integrity of the body.
Understand how the regulation of the immune system works, both in its positive side of fighting infection or cancer or favoring tissue repair, and in its negative side in which it can cause excess inflammatory damage during an infection, allergic reaction or Autoimmune disease is very important, stresses Paula Saz, coprimera author of the work.
"In the immune system this balance always occurs, and learning to control it is the key to be able to fight against many diseases that have an immune component," he says.
According to the CNIC researchers, this knowledge could be applied to diseases in which the massive arrival of neutrophils contributes to the development of the pathology, both during infectious processes and in tissue damage as a consequence, for example, of a myocardial infarction. (Source: CNIC)
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