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New nanoparticles are being developed to combat cancer immunotherapy resistance

Scientists at Hokkaido University in Japan and their colleagues have discovered a method that may be able to help some cancer patients overcome their resistance to immunotherapy treatment. The approach, which has been demonstrated in mice experiments, was published in the Journal for Immunotherapy of Cancer.

The activation of checkpoint proteins on the surfaces of immune cells aids in the regulation of the immune response by preventing the cells from attacking other cells in the body without being specifically targeted. The problem is that some cancer cells are able to hijack this mechanism, which prevents the immune system from responding effectively against them. Scientists have recently discovered immune checkpoint inhibitors that can be used to counteract this strategy, but some people are resistant to the medications..

Fortunately, scientists at Hokkaido University and Aichi Institute of Technology have devised a method of circumventing this problem by developing a specially designed lipid nanoparticle that can transport immunity-triggering molecules into immune cells found in the liver known as macrophages.

The lipid in question, known as YSK12-C4, has a strong affinity for immune cells. Interferon-producing type 1 interferons were stimulated in the liver macrophages of mice with metastatic melanoma after being injected intravenously with the drug. This was accomplished by delivering signaling molecules known as cyclic dinucleotides across the cell membranes. This was accomplished by using the stimulator of an interferon gene (STING) pathway. In the spleen and lungs, these were released into the bloodstream, activating another type of immune cell known as natural killer cells, which secreted interferon-gamma within the lung metastases.

This treatment alone had only a mild anti-tumor effect, and it was not combined with other treatments. This is due to the fact that type 1 interferons and interferon-gamma induced the expression of a protein known as PD-L1 on cancer cells as a result of the treatment. Natural killer cells that express the tumor-killing protein PD-1 are prevented from mounting a powerful tumor-killing immune response by PD-L1. In contrast, administering an anti-PD-1 immunotherapy treatment prevented the cancer cells from turning off those natural killer cells, which then became armed and capable of launching a full-scale attack against the cancer cells.

In the study, Takashi Nakamura of Hokkaido University's faculty of pharmaceutical sciences discovered that lipid nanoparticles containing immune-signaling molecules were able to change the immune status from immunologically cold to immunologically hot. According to the researchers, this could pave the way for the development of a promising adjuvant that could reduce resistance to anti-PD-1 antibody treatment in certain cancer patients.

Further research will be required to determine whether or not the treatment can cause liver toxicity and whether or not different signaling molecules can be used in the treatment.

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