We have something to thank our immunesystem, because it always protects us from bacteria, viruses and even cancer. Quite a lot is already known about how exactly immune cells work. But how do such powerful "fighters" avoid the destruction of themselves and their own kind in the "attack on the invaders"? Researchers at the Peter McCallum Center for Cancer and University College London seem to have found the answer. Moreover, it allows not only to better learn the capabilities of our body, but also to develop new methods of treatment of dangerous diseases. For example, cancer.
Why immune cells don't kill their own kind
The discovery was made while studying the principlesthe work of cells of the immune system at the time of the fight against cancer. In particular, we studied cytotoxic T-lymphocytes (CTLs) - a type of immune cells that “hunt” for cancer cells, as well as cells infected with viruses or otherwise damaged. Once they capture the target, they use a protein called perforin, which punches holes in the outer membrane of the cell. If this protective layer is broken, toxic molecules from T-lymphocytes can penetrate into the problem cell and kill it from the inside.
But there is a catch in how this works. By all accounts, CTLs should fall prey to their own attacks, since they do not have specific “identities” for their own kindred. Moreover, they do not always “win the battle” with the same cancer, which may be one of the reasons for the onset and development of oncology in the body.
All cells in our body are surrounded by a membrane,made up of millions of tiny lipid molecules, ”said lead author Dr. Ilya Voskoboinik in an interview with New Atlas. We found that the lipids in the membranes of CTLs are more densely packed compared to the cells they are trying to kill. The denser the lipids are packed, the less permeable is the membrane for the action of perforin.
As part of a new study, scientists thought thatthe answer seems to lie in the outermost shell. Not only is the CTLs membrane denser than in target cells, but also some of the lipid molecules that make them up are negatively charged. This allows them to reflect the proteins of perforin (which also has a negative charge), preventing their damage.
Read also: Toshiba's new device drops 13 types of cancer by a drop of blood
To test this hypothesis, researchersartificially destroyed lipids in CTLs cell membranes. Of course, these immune cells lost some of their resistance to perforin, after which they became vulnerable to "normal" lymphocytes. The team says some cancer cells can strengthen their own membranes in a similar way, making them look like the ones on cytotoxic lymphocytes. And those who didn’t “do it” just remain unprotected. We often write about such discoveries on the pages of our portal. So sign up so you don’t miss anything.
The effectiveness of modern approaches toimmunotherapy depends on the ability of CTLs to kill tumor cells, says Jesse Rudd-Schmidt, another author of this work. If some cancer cells can rearrange their outer membranes to resemble tightly packed and negatively charged CTLs, this can protect them from death by the immune system. But you can fight it.
Now scientists are aiming to identify waysdamage to the cell wall of cancer cells in order to make them vulnerable to the effects of immune cells. In this case, you need to be careful, since similar techniques can cause deterioration of the immune system itself. But if scientists succeed, then this discovery can lead to the creation of new cancer treatments.