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Editor-in-Chief | Enzyme Beauty In the past few decades, researchers have been committed to developing vaccines that support tumor treatment.
Currently, two preventive tumor vaccines have been approved (HPV vaccine and hepatitis B vaccine), which play an important role in the prevention of related tumors.
However, this preventive vaccine has no effect on tumors that have already developed.
So far, the FDA has only approved a dendritic cell-based vaccine (Sipuleucel-T) to treat existing cancers, and its overall clinical benefit is still low.
Investigating the reasons, there are two main obstacles hindering the development of cancer vaccines: the high variability of tumor-associated antigens (TAA) and the immunosuppressive tumor microenvironment.
In situ tumor immunity is considered to be a promising alternative cancer vaccination strategy, which does not require identification and isolation of patient-specific TAA.
Through local application of therapeutic agents or immunomodulators, in situ tumor immunity can produce a large amount of TAA and activate the immune response in the tumor microenvironment.
A variety of in situ vaccination strategies, including oncolytic virus, photothermal therapy (PTT), radiotherapy (RT), agonist immunotherapy, and in situ chemotherapy, can all induce effective immune responses.
However, these strategies are still limited by a low antigen cross-presentation and immunosuppressive environment.
Recently, the research group of Professor Qiaobing Xu from Tufts University in the United States published an article titled In situ cancer vaccination using lipidoid nanoparticles on Science Advances.
This study uses liposome molecules to significantly increase the effect of in situ immunotherapy.
Specifically, the researchers found that liposome 93-O17S can capture TAA produced by chemotherapy and deliver TAA to the draining lymph nodes.
In addition, this liposome also enhances the cross-presentation of antigens and promotes the activation of interferon gene stimulating protein (STING), which has achieved significant effects in the treatment of mouse melanoma tumor models.
First, the researchers screened out the adjuvant liposome molecule 93-O17S from dozens of types of liposome molecules, and further found that 93-O17S can activate Th1-type helper T cell responses and promote antigen crossover.
Submit.
In addition, 93-O17S can also activate the STING pathway of antigen-presenting cells through intracellular delivery of the STING agonist cGAMP, thereby promoting the secretion of type I interferon factor.
93-O17S (93-O17S/cGAMP) encapsulating cGAMP can significantly improve the humoral and cellular immune response of the model antigen in the body, showing a high potential.
Then, the researchers verified in vivo that 93-O17S/cGAMP can effectively capture and deliver model antigens to draining lymph nodes, thereby promoting STING activation of tumor tissues.
In addition, 93-O17S/cGAMP combined with the chemotherapy drug doxorubicin can significantly promote the infiltration of antigen presenting cells and T lymphocytes.
Further cell typing analysis showed that the therapy can promote the activation of dendritic cells and promote the M1 polarization of macrophages.
Finally, 93-O17S/cGAMP combined with low-dose doxorubicin showed a significant effect in the treatment of mouse melanoma models, and about 30% of mouse tumors were completely eliminated.
Further research showed that the in situ immunization method caused a certain immune memory effect, and about 70% of the recovered mice prevented the invasion of the tumor by the second vaccination.
In summary, 93-O17S can deliver TAA and the STING agonist cGAMP intracellularly, thereby effectively promoting the cross-presentation of TAA and the activation of STING, and finally showing outstanding tumor chemotherapy and immunotherapy effects.
The first author of this article is Dr.
Chen Jinjin. Original link: https://advances.
sciencemag.
org/lookup/doi/10.
1126/sciadv.
eabf1244 Platemaker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article, personal forwarding and sharing are welcome, and it is prohibited without permission Reprinted, the author has all legal rights, offenders must be investigated.
Currently, two preventive tumor vaccines have been approved (HPV vaccine and hepatitis B vaccine), which play an important role in the prevention of related tumors.
However, this preventive vaccine has no effect on tumors that have already developed.
So far, the FDA has only approved a dendritic cell-based vaccine (Sipuleucel-T) to treat existing cancers, and its overall clinical benefit is still low.
Investigating the reasons, there are two main obstacles hindering the development of cancer vaccines: the high variability of tumor-associated antigens (TAA) and the immunosuppressive tumor microenvironment.
In situ tumor immunity is considered to be a promising alternative cancer vaccination strategy, which does not require identification and isolation of patient-specific TAA.
Through local application of therapeutic agents or immunomodulators, in situ tumor immunity can produce a large amount of TAA and activate the immune response in the tumor microenvironment.
A variety of in situ vaccination strategies, including oncolytic virus, photothermal therapy (PTT), radiotherapy (RT), agonist immunotherapy, and in situ chemotherapy, can all induce effective immune responses.
However, these strategies are still limited by a low antigen cross-presentation and immunosuppressive environment.
Recently, the research group of Professor Qiaobing Xu from Tufts University in the United States published an article titled In situ cancer vaccination using lipidoid nanoparticles on Science Advances.
This study uses liposome molecules to significantly increase the effect of in situ immunotherapy.
Specifically, the researchers found that liposome 93-O17S can capture TAA produced by chemotherapy and deliver TAA to the draining lymph nodes.
In addition, this liposome also enhances the cross-presentation of antigens and promotes the activation of interferon gene stimulating protein (STING), which has achieved significant effects in the treatment of mouse melanoma tumor models.
First, the researchers screened out the adjuvant liposome molecule 93-O17S from dozens of types of liposome molecules, and further found that 93-O17S can activate Th1-type helper T cell responses and promote antigen crossover.
Submit.
In addition, 93-O17S can also activate the STING pathway of antigen-presenting cells through intracellular delivery of the STING agonist cGAMP, thereby promoting the secretion of type I interferon factor.
93-O17S (93-O17S/cGAMP) encapsulating cGAMP can significantly improve the humoral and cellular immune response of the model antigen in the body, showing a high potential.
Then, the researchers verified in vivo that 93-O17S/cGAMP can effectively capture and deliver model antigens to draining lymph nodes, thereby promoting STING activation of tumor tissues.
In addition, 93-O17S/cGAMP combined with the chemotherapy drug doxorubicin can significantly promote the infiltration of antigen presenting cells and T lymphocytes.
Further cell typing analysis showed that the therapy can promote the activation of dendritic cells and promote the M1 polarization of macrophages.
Finally, 93-O17S/cGAMP combined with low-dose doxorubicin showed a significant effect in the treatment of mouse melanoma models, and about 30% of mouse tumors were completely eliminated.
Further research showed that the in situ immunization method caused a certain immune memory effect, and about 70% of the recovered mice prevented the invasion of the tumor by the second vaccination.
In summary, 93-O17S can deliver TAA and the STING agonist cGAMP intracellularly, thereby effectively promoting the cross-presentation of TAA and the activation of STING, and finally showing outstanding tumor chemotherapy and immunotherapy effects.
The first author of this article is Dr.
Chen Jinjin. Original link: https://advances.
sciencemag.
org/lookup/doi/10.
1126/sciadv.
eabf1244 Platemaker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article, personal forwarding and sharing are welcome, and it is prohibited without permission Reprinted, the author has all legal rights, offenders must be investigated.
