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How can cancer cells escape our immune system? Reveal the mysterious mechanism of tumor escape!
In today's biomedical research, cancer immunology is becoming a hot and important field. This interdisciplinary research direction focuses on understanding the role of the immune system in cancer progress and development, especially in cancer immunotherapy, allowing us to use our own immune system to fight tumors.
Cancer Immune Surveillance and Immune Editing reflects how our immune system protects us from tumor risk, the result of decades of research.
The key to tumor antigen
Tumor cells express tumor antigens that can be recognized by the immune system and trigger an immune response. These tumor antigens can be divided into tumor-specific antigens (TSA) and tumor-associated antigens (TAA). Tumor-specific antigens are only present in tumor cells, usually due to viral infections or gene mutations. Relatively speaking, tumor-related anti-principles also exist in normal healthy cells, except that the time, place or number of expression varies.
Immune editing process
Cancer immune editing is a complex process in which the interaction between the immune system and tumor cells goes through three stages: elimination, balance and escape. During the elimination phase, the immune system effectively destroys tumor cells. However, some tumor cells may evade this immune response through mutations or alterations, and eventually enter the escape stage, when tumor cells become the dominant growth and establish an immune suppression environment.
The process of immune editing can be compared to Darwin's theory of evolution, and tumor cells adapting to the environment gain advantages through time.
How does tumor escape the immune system?
Tumor cells use a variety of mechanisms to avoid detection by the immune system. First, they may reduce MHC I expression through gene mutations, which makes them unrecognizable to CD8+ cytotoxic T cells (Tc cells). Second, tumor cells can stop expressing synergistic stimulators that are critical to their detection, such as CD80 or CD86, which can affect the intensity of the immune response. In addition, some tumor cells express molecules that can induce apoptosis of T lymphocytes, such as FasL or PD-L1, further inhibiting the function of the immune system.
The impact of tumor microenvironment
The tumor microenvironment often promotes the formation of immunosuppression, which is caused by the interaction of tumor cells and other cells. Tumor cells can secrete transforming growth factor β (TGF-β), which transforms CD4+ T cells into inhibitory regulatory T cells, further weakening the anti-tumor immune response.
Non-classical MHC class I molecules such as HLA-G also play an important immunomodulatory role in the tumor microenvironment, which may become a new target for treatment.
Immunomodulation method
To improve our immune response to tumors, researchers have developed a variety of immune regulation methods. Immune checkpoint inhibitors, including anti-CTLA-4 and anti-PD-1 antibodies, enhance T cell activation and response by blocking inhibitory signals. These methods have been proven to be effective in the treatment of a variety of tumor types. Genetically engineered chimeric antigen receptor T cells (CAR T cells) are also an important advance in cancer treatment, which can accurately attack specific tumor antigens.
Immune links for chemotherapy
In terms of chemotherapy, researchers have found that inducing immunogenic cancer cell death during chemotherapy is the key to improving efficacy. While most standard chemotherapy options are based primarily on their direct destruction of cancer cells, they are equally important for activation of the immune system. For example, studies have shown that the use of certain chemotherapy drugs can promote the activation of dendritic cells, which is crucial for the response of tumor-specific T cells.
From the perspective of anti-tumor, how can we maintain and strengthen our immune system response so that it can accurately identify and eliminate tumor cells?
