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This article is original by Translational Medicine.
Please indicate the source for reprinting.
Author: Yun Introduction: Although scientists know that tumors accumulate fat, and that this accumulation is related to immune dysfunction, the details of this relationship are still unclear
.
Therefore, scientists conducted research on this relationship
.
Tumor metastasis is an inefficient process
.
Generally speaking, only a small percentage of tumor cells can successfully spread, migrate, and grow remotely
.
Tumor metastasis depends on the metastatic microenvironment-a special microenvironment that can promote the occurrence of metastatic events and the formation of the microenvironment of distant metastases
.
The characteristics of tumor microenvironment can be divided into three main categories: hypoxia, chronic inflammation and immunosuppression
.
One of the members of the “family” of tumor microenvironment is tumor-associated adipocytes, which participate in the formation of tumor microenvironment by secreting lipids, adipokines and cytokines, which promote the adhesion, migration and invasion of tumor cells, and regulate inflammatory response.
, Affect the malignant progression and proliferation of tumors
.
Although scientists know that tumors accumulate fat and that this accumulation is related to immune dysfunction, the details of this relationship are unclear
.
Recently, researchers published a study titled "Uptake of oxidized lipids by the scavenger receptor CD36 promotes lipid peroxidation and dysfunction in CD8+ T cells in tumors" in "Immunity"
.
Scientists proposed to improve the immune system's anti-cancer ability by reducing oxidized lipid damage in killer T cells, and identifying factors that cause immunosuppression in the tumor microenvironment can help develop new cancer immunotherapies
.
The team worked with Joseph Witztum's laboratory at the University of California, San Diego, and determined that tumors contain large amounts of lipids, especially oxidized lipids, which are usually found in oxidized low-density lipoproteins (low-density lipoproteins) and are generally considered It is "bad" fat
.
Then, they observed how killer T cells respond to oxidized low-density lipoproteins in tumors, and found that killer T cells increase CD36 (the scavenger receptor for oxidized lipids) on their surface and take up large amounts of oxidized lipids.
Quality to adapt to the tumor microenvironment
.
In collaboration with Brinda Emu's laboratory at Yale University, they discovered that this process can act as a catalyst to drive more lipid oxidation inside killer T cells and ultimately inhibit their defenses
.
Next, the team used various methods to study how CD36 impairs the function of killer T cells
.
They created a mouse model that lacked CD36 on T cells and used antibodies to block CD36
.
They confirmed that CD36 promotes T cell dysfunction in tumors by increasing the input of oxidized lipids, which leads to greater lipid oxidation and damage in T cells, and triggers the activation of stress response protein p38
.
"We found that when T cells are'stressed' by oxidized lipids, they turn off their anti-tumor function
.
" said Shihao Xu, a Salk postdoctoral researcher and the first author of the paper
.
The team also discovered new therapeutic opportunities to reduce lipids by blocking CD36 through immunotherapy, antibody therapy, or by overexpressing glutathione peroxidase 4 (GPX4, a key molecule that removes oxidized lipids in cells).
Oxidizes and restores the function of killer T cells in tumors
.
Importantly, lipid oxidation does not only occur in T cells; it also occurs in tumor cells, and too much can cause cell death
.
In fact, cancer research that increases lipid oxidation in tumor cells to lethal levels is exciting, but Kaech and her team urge caution
.
"Now that we have discovered this vulnerability of T cells to lipid oxidative stress, we may need to find more selective methods to induce lipid oxidation in tumor cells rather than T cells," the chairman of NOMIS Kaech said, "Otherwise, we may destroy anti-tumor T cells in this process
.
" Reference: https:// %3A%2F%2Flinkinghub.
elsevier.
com%2Fretrieve%2Fpii%2FS1074761321002090%3Fshowall%3Dtrue Note: This article aims to introduce medical research progress and cannot be used as a reference for treatment options
.
If you need health guidance, please go to a regular hospital for treatment
.
Please indicate the source for reprinting.
Author: Yun Introduction: Although scientists know that tumors accumulate fat, and that this accumulation is related to immune dysfunction, the details of this relationship are still unclear
.
Therefore, scientists conducted research on this relationship
.
Tumor metastasis is an inefficient process
.
Generally speaking, only a small percentage of tumor cells can successfully spread, migrate, and grow remotely
.
Tumor metastasis depends on the metastatic microenvironment-a special microenvironment that can promote the occurrence of metastatic events and the formation of the microenvironment of distant metastases
.
The characteristics of tumor microenvironment can be divided into three main categories: hypoxia, chronic inflammation and immunosuppression
.
One of the members of the “family” of tumor microenvironment is tumor-associated adipocytes, which participate in the formation of tumor microenvironment by secreting lipids, adipokines and cytokines, which promote the adhesion, migration and invasion of tumor cells, and regulate inflammatory response.
, Affect the malignant progression and proliferation of tumors
.
Although scientists know that tumors accumulate fat and that this accumulation is related to immune dysfunction, the details of this relationship are unclear
.
Recently, researchers published a study titled "Uptake of oxidized lipids by the scavenger receptor CD36 promotes lipid peroxidation and dysfunction in CD8+ T cells in tumors" in "Immunity"
.
Scientists proposed to improve the immune system's anti-cancer ability by reducing oxidized lipid damage in killer T cells, and identifying factors that cause immunosuppression in the tumor microenvironment can help develop new cancer immunotherapies
.
The team worked with Joseph Witztum's laboratory at the University of California, San Diego, and determined that tumors contain large amounts of lipids, especially oxidized lipids, which are usually found in oxidized low-density lipoproteins (low-density lipoproteins) and are generally considered It is "bad" fat
.
Then, they observed how killer T cells respond to oxidized low-density lipoproteins in tumors, and found that killer T cells increase CD36 (the scavenger receptor for oxidized lipids) on their surface and take up large amounts of oxidized lipids.
Quality to adapt to the tumor microenvironment
.
In collaboration with Brinda Emu's laboratory at Yale University, they discovered that this process can act as a catalyst to drive more lipid oxidation inside killer T cells and ultimately inhibit their defenses
.
Next, the team used various methods to study how CD36 impairs the function of killer T cells
.
They created a mouse model that lacked CD36 on T cells and used antibodies to block CD36
.
They confirmed that CD36 promotes T cell dysfunction in tumors by increasing the input of oxidized lipids, which leads to greater lipid oxidation and damage in T cells, and triggers the activation of stress response protein p38
.
"We found that when T cells are'stressed' by oxidized lipids, they turn off their anti-tumor function
.
" said Shihao Xu, a Salk postdoctoral researcher and the first author of the paper
.
The team also discovered new therapeutic opportunities to reduce lipids by blocking CD36 through immunotherapy, antibody therapy, or by overexpressing glutathione peroxidase 4 (GPX4, a key molecule that removes oxidized lipids in cells).
Oxidizes and restores the function of killer T cells in tumors
.
Importantly, lipid oxidation does not only occur in T cells; it also occurs in tumor cells, and too much can cause cell death
.
In fact, cancer research that increases lipid oxidation in tumor cells to lethal levels is exciting, but Kaech and her team urge caution
.
"Now that we have discovered this vulnerability of T cells to lipid oxidative stress, we may need to find more selective methods to induce lipid oxidation in tumor cells rather than T cells," the chairman of NOMIS Kaech said, "Otherwise, we may destroy anti-tumor T cells in this process
.
" Reference: https:// %3A%2F%2Flinkinghub.
elsevier.
com%2Fretrieve%2Fpii%2FS1074761321002090%3Fshowall%3Dtrue Note: This article aims to introduce medical research progress and cannot be used as a reference for treatment options
.
If you need health guidance, please go to a regular hospital for treatment
.
