American scientists have discovered one of the mechanisms responsible for the immune response to silicone implants. A key role came to senescent cells, which stimulate the formation of proinflammatory T lymphocytes. The researchers were able to slow the formation of fibrous capsule around the implant by using xenolitica drug that kills the “old” cells. Theoretically, this could be a method to prevent complications after placement of implants, including breast. A study published in the journal Science Translational Medicine.
Despite the fact that the implantation of synthetic materials into the human body turned into a routine operation, it continues to cause side effects and in some cases even disease. No matter how we tried to “hide” the surface of the implant from the immune system, from time to time, patients have a reaction to a foreign body: around it accumulate immune cells — primarily macrophages and fibroblasts from the surrounding connective tissue begins to secrete fibers of the intercellular substance. As a result, the implant is covered by a dense fibrous (connective tissue) capsule. Because of this, it can shrivel up and lose shape, but it’s not so bad — according to some, in the case of breast implants, the fibrosis increases the risk of developing rheumatic diseases and even tumors.
A group of scientists under the leadership of Jennifer Eliseeff (Jennifer Elisseeff) from the Medical school of Johns Hopkins University suggested that in the process of the body’s response to silicone implant involved the system not only innate but also acquired immunity, as they are closely related to each other. To test their assumptions, they took samples from 12 patients during surgery replacing breast implant. In the tissues surrounding the silicone, they counted the number of immune cells of various types. It turned out that among them is dominated by T helper 17 is a group of regulatory T-lymphocytes, which stimulate inflammation and often appear in allergies and autoimmune processes. In the samples also found elevated concentrations of interleukin-17 — a proinflammatory protein that produces this group of T cells.
The researchers then wondered whether this universal process for different implants. They implanted under the skin of mice, several types of synthetic materials — polycaprolactone (“standard” immunogenic implant), polyethylene, polyethylene glycol and silicone. The strength of the immune response (the level of expression of the proinflammatory proteins) differed depending on the material, but in all cases, scientists have found an increased production of interleukin-17. He was singled out by several cell types, but ultimately six weeks after implantation, the first among them took T helper 17.
To determine whether interleukin-17 in the formation of the fibrous capsule, the authors repeated the experiment on nokauti mice was absent or the Il-17 or the receptor for it. These animals have around the implant accumulated less connective tissue cells, and expression of extracellular matrix proteins in them was 1.5-2 times less than that of conventional mice with the implant. Then, the researchers suggested that it is sufficient to inhibit the activity of interleukin-17 in order to prevent fibrosis. And indeed, when they injected antibodies to the protein in the animal organism, expression of extracellular matrix proteins was decreased to approximately the same level as noauth for Il-17 mice.