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Figure ①: Antitumor biology of γδ T cells

Figure 1 illustrates the antitumor function of γδ T cells and its regulatory mechanism. γδ T cells directly recognize tumor cells through T cell receptors (TCR) and natural killer cell receptors (NKRs), and regulate tumor cell killing through a variety of mechanisms, including antibody-dependent cytotoxicity and IFNγ production. The antitumor characteristics of γδ T cells are mainly enhanced by IL-15, IL-2, IL-18, and IL-21, but epigenetic drugs or molecular factors in the tumor microenvironment can damage the killing ability of γδ T cells.

 

Figure ②: Childhood cancer immunotherapy

Figure 2 summarizes the various immunotherapy approaches currently being tested for childhood cancer. Most childhood tumors are considered “cold tumors” (top right), and cell therapies including CAR-T cell therapy (bottom right) are being explored as potential options for immunotherapy in childhood cancer. The left picture depicts “hot tumors” and the mechanism by which immune checkpoint inhibitors enhance the antitumor activity of T cells at the tumor site.

 

Figure ③: Metabolism in the tumor microenvironment

Figure 3 shows the active metabolic pathways in the tumor microenvironment and their effects on tumor immunity. Tumor cells will form a tumor microenvironment that lacks glucose but is rich in lactic acid. This microenvironment will impair T cell function and anti-tumor immune response. Competition between T cells and tumor cells for amino acids can also suppress anti-tumor immunity. In the tumor microenvironment, competition from tumor cells also affects the availability of fatty acids by T cells. Tumor cells and other metabolites produced by other immunoregulatory cells (such as adenosine and prostaglandin E2) are also involved in the suppression of T cell-mediated antitumor responses.

 

Figure ④: Tumor-immune classification

According to the existence and distribution of T cells, tumors can be divided into four main subtypes: hot, altered-excluded, altered-immunosuppressed, and cold. Figure 4 provides an overview of the major components, pathways, and features (green) of the immunogram that have been identified, as well as potential targets (blue) that may represent the most successful treatment options. A lowercase “i” refers to an inhibitor and a lowercase “a” refers to an agonist.

 

Figure ⑤: Glioblastoma immunotherapy

Figure 5 provides an overview of different immunotherapeutic models currently under development for the treatment of glioblastoma, including vaccine therapies, immune checkpoints that rely on dendritic cell (DC) -mediated presentation of glioblastoma-related antigens Blocking antibody drugs, CAR-T cell therapy targeting tumor-associated antigens, oncolytic virus therapy that allows the virus to selectively replicate in tumor cells and induce anti-tumor immunity.

 

Figure ⑥: Tumor immunotyping tools

Figure 6 shows a variety of resources that can be used to investigate tumor immunotyping for molecular information (gene expression profiling, DNA methylation profiling, or immunohistochemistry) and computational tools.

 

Figure ⑦: Basic targets for combination therapy

Figure 7 illustrates the potential of combination therapy in preventing the development of resistance to anti-cancer immunotherapy. Potential synergistic mechanisms include immune cell activation and T cell activation (a), alleviation of immune suppression induced by the tumor microenvironment (b), and support for effector functions of immune cells in the tumor microenvironment (c).

 

Figure ⑧: T cell response in bladder cancer

Figure 8 represents multiple ligand-receptor interactions between T cells and antigen presenting or tumor cells in bladder cancer. This ligand-receptor interaction regulates the response of T cells to antigens and represents a potential immunotherapy target that enhances T cell responses and promotes immune system-mediated cancer cell killing.

 

Figure ⑨: Biomaterials for targeted cancer immunotherapy

Some biomaterials and methods are being explored to achieve local delivery of cancer immunotherapy. On the left side of Figure 9, mesoporous silica rods spontaneously assemble and recruit host cells in vivo; in the middle of Figure 9, a microneedle-based transdermal drug delivery platform is loaded with a self-assembled immunotherapy nanocarrier; right of Figure 9 The side shows a scaffold for delivery of porous biomaterials, which releases a chemical attractant that recruits naive dendritic cells (DCs) into its voids, resulting in a major histocompatibility complex (MHC) -peptide complex The presentation of peptides in the body is increased.

 

Figure ⑩: Barriers to cancer oncolytic virus therapy

Figure 10 depicts the barriers (light blue) that limit the clinical benefits of oncolytic viruses. In order to optimize the treatment response, bioengineering, molecular and immunological methods (dark blue) should be adopted to achieve the following goals: 1) avoid virus vectors being neutralized by antibodies; 2) avoid oncolytic viruses by avoiding cell types other than tumor cells “Seizure” improves tumor absorption of oncolytic viruses; 3) increases the spread of oncolytic viruses by regulating the extracellular matrix (ECM); 4) enriches T cells’ response to tumor antigens.

 

Figure ⑪: Identification of cancer neoantigens

Figure 11 (a) depicts the process by which neoantigen originates from mutant proteins expressed by cancer cells and is displayed on the surface of antigen-presenting cells to be recognized by T cell receptors (TCRs) of CD8 + T cells; Figure 11 (b) ) Shows a computational route for predicting candidate new antigens based on next-generation sequencing data.

 

Figure ⑫: CAR-T cell therapy

Figure 12 provides an overview of CAR-T cell therapy. CAR-T cell therapy refers to the isolation of T cells from the patient’s peripheral blood, and the use of viral or non-viral vectors to insert a gene encoding a chimeric antigen receptor (CAR) into the T cell genome. CAR-T cells are then expanded in vitro and then returned to the patient. CAR expressed on the surface of CAR-T cells will recognize an antigen expressed on the surface of tumor cells, and then activate CAR-T cells to kill tumor cells.

 

Write at the end

Cancer-Immunotherapy-2020-Calendar cover image | The above image shows the adaptive immune system that forms the tumor’s immune environment and the multiple immune cell types of the innate immune system. The following figure shows the successive steps of the cancer immune cycle: antigen generation → dendritic cells present antigens to T cells → initiate and activate effector T cell responses against cancer specific antigens → T cells enter the tumor site, identify and kill cancer cells (Image source: Nat. Rev. Genet. [6])

The above 12 pictures are from Cancer-Immunotherapy-2020-Calendar, a theme of cancer immunotherapy published by Nature Reviews Clinical Oncology.

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