Scientists discover mechanism synods immune cells to avoid self-harm when attacking ‘intruders’

According tomedia reports, our immune system can protect us from cancer and infection. But how on earth do immune cells avoid harming themselves when they attack “intruders”? Researchers at Australia’s Peter McCallum Cancer Centre and University College London have now found that they form a hard barrier around themselves, a finding that could lead to new cancer treatments.

Scientists discover mechanism synods immune cells to avoid self-harm when attacking 'intruders'

Cytotoxic T lymphocytes (CTL) are immune cells that have a lethal effect on certain viruses, tumor cells and other antigens. Once locked to the target, they use a protein called perforatin that “punchs” the outer membrane of the cell. When the protective layer is damaged, toxic molecules enter and kill the cells in question.

But there has always been a mystery about how these cells work. CtLs are known to be the victims of their own attacks, but they can always win the battle, and scientists aren’t sure why. For the new study, researchers at Peter Mac and UCL set out to investigate. The answer seems to lie in the outer membrane itself. The membranes of CTL are not only denser than the target cells, but also some lipid molecules that make up them are negatively charged. This allows them to capture perforatin proteins, thus preventing them from causing any damage.

“All the cells in our body are surrounded by a membrane of millions of tiny lipid molecules,” said Ilia Voskoboinik, a senior author of the study. We found that lipids in the CTL membrane were piled up more closely than the cells that CTL was trying to kill. The tighter the lipid builds up, the harder the membrane’s effect on perforator is to penetrate. “

To examine this mechanism, the researchers artificially destroyed lipids in the CTL membrane. Sure enough, these immune cells lose some resistance to perforatin. Some cancer cells may strengthen the defenses of their own membranes, and removing that action could lead to new anti-cancer treatments, the team said.

“The effectiveness of current immunotherapy depends on CTL’s ability to kill tumor cells through the activity of perforatin,” said lead author Jesse Rudd-Schmidt of the study. “If some cancer cells can recombine their outer membranes to resemble a close-stacked, negatively charged membrane of CTL, they can be protected from being killed by the immune system.” This part explains the huge difference in patients’ responses to cancer immunotherapy. “

The study was published in the journal Nature Communications.

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