ILC2 Cells May Serve as A Power Weapon to Fight against Cancer Metastasis

Abstract It is well known that cancer immunotherapy utilizes the body's own immune system to kill cancer cells. In the past few years, cancer immunotherapy has entered a period of rapid development. Clinical trials have shown that it is effective for some blood or blood-diffusing cancers (such as lymphoma), however, this therapy is also accompanied by some serious side effects, and has had little success in the treatment of most solid tumors. A recent study at the University of British Columbia shows that the ILC2 cells that were ignored by scientists for almost 10 years may become a powerful tool to prevent the spread of cancer cell. Related research results are published online in the Journal of Scientific Reports. ILC2 - The Mysterious immune cells In 2016, Professor Wilf Jefferies, an expert in genetics and microbiology, discovered that a cancer cell can escape the surveillance of the immune system in the absence of interleukin 33 (IL-33), which in turn causes tumors‘ proliferation and metastasis. This strange phenomenon prompted him to focus on those cells that are activated by IL-33, that is, type 2 congenital lymphocytes (ILC2). ILC2 is a recently discovered new member of the ILC family, which was discovered by scientists while studying the pathogenesis of asthma diseases. Asthma is an autoimmune disease. Recent studies have shown that ILC2 cells are closely related to the onset of asthma, acritical part of the innate immune response can cause respiratory inflammation. Just like many other immune cells, ILC2 cells have both negative and positive effects. Specific experimental methods and conclusions Professor Jefferies and his team created a series of genetically engineered mice that lack ILC2 cells and then implanted lung cancer cells into mouse models. Their initial research focused on implanting cancer cell populations in the hind legs of genetically engineered mice and then observing whether lung cancer cells grow faster in genetically engineered mice (lack of ILC2 cells) than in normal control mice (with ILC2 cells). The results of the study are consistent with the initial experimental expectations: Tumors actually transferred faster in genetically engineered mice lacking ILC2 cells. However, Dr. Jefferies and professor Fumio Takei in pathology laboratory found that the biggest difference between genetically engineered mice and controls is that where cancer spreads in the body. Normally, primary lung cancer cells at the injection site will spread in genetically engineered mice and appear in tissues or organs such as the lungs, brain, adrenal glands, and lymphoid tissues. Metastasis of cancer cells is almost unlimited, and the number of cancer cells in the brain of genetically engineered mice is more than 1000 times that of mice in the control group. Dr. Jefferies et al. concluded from this observation that ILC2 cells prevent or slow the metastasis of lung and prostate cancers through tumor immune responses. It is another ‘mysterious’ immune cell that kills cancer cells. The further research on ILC2 cells Currently, Jefferies is further developing the human participation in clinical trials - to investigate whether the injection of ILC2 cells can prevent the proliferation of transplanted cancer cells. He injected ILC2 cells into cancer patients to determine if ILC2 cells could slow the spread of the tumor. ILC2 cells may become a promising immunocyte therapy as they do not need to be activated by specific tumor antigens. More importantly, there is no need to pre-treat ILC2 cells in the laboratory before applying them for treatment, which is different from the current CAR-T immune cell therapy. Dr. Jefferies et al. speculated that its mechanism: IL-33-bearing ILC2 cells are more efficiently activated, either simply because there are more ILC2 cells or both. Anyway, these results increase the possibility of utilizing the immune system to fight cancer. We will look forward the further process and updates.