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micrograph of a T cell
Image from NIAID
The “asymmetric division” of T cells could provide new ways to enhance cancer immunotherapy, according to researchers.
When a T cell divides, the activity of the enzyme mTORC1, which controls protein production, splits unevenly between the progeny.
Results of a new study suggest this uneven division reprograms the daughter cells so that one goes on to become an effector T cell and the other becomes a memory T cell.
This study was published in Nature Immunology.
“One of the critical steps needed to improve cancer immunotherapy, in general, is finding out ways to make antitumor T cells persist or hang around in the body longer,” said study author Jonathan Powell, MD, PhD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland.
With that in mind, Dr Powell and his colleagues analyzed murine T cells. They found that when a “mother” T cell that is naïve to immune threats encounters such a threat and divides, one of its daughter cells inherits far more mTORC1 activity than the other daughter cell.
The researchers activated mouse T cells using a virus. Once the T cells divided, the team used antibodies to detect mTORC1 activity in each of the daughter cells.
Then, the researchers sorted the daughter cells and examined their function by injecting them into mice given two identical infections and tracking the cells’ activity.
The team found the difference in mTORC1 activity levels between the daughter cells varied depending on the population of cells studied.
And the lopsided distribution of mTORC1 activity appeared to reprogram the use of energy and other metabolic activities of each daughter cell.
The cells with high levels of mTORC1 activity were found to be potently activated, killer/effector T cells, while the cells with low mTORC1 levels behaved like memory T cells, persisting for long periods of time and rapidly activating upon reinfection.
The researchers said this finding could be used to improve immunotherapy, but another aspect of this discovery is the prospect that asymmetric partitioning of mTORC1 might be widespread across cells in many biological systems.
Dr Powell said it’s possible the mechanism may help explain how stem cells develop into more specialized cells in the bone marrow, for instance, or how cells differentiate to become hair, skin, or brain cells in a growing embryo.
“We think there will be implications for biology well beyond the immune system,” he concluded. 
micrograph of a T cell
Image from NIAID
The “asymmetric division” of T cells could provide new ways to enhance cancer immunotherapy, according to researchers.
When a T cell divides, the activity of the enzyme mTORC1, which controls protein production, splits unevenly between the progeny.
Results of a new study suggest this uneven division reprograms the daughter cells so that one goes on to become an effector T cell and the other becomes a memory T cell.
This study was published in Nature Immunology.
“One of the critical steps needed to improve cancer immunotherapy, in general, is finding out ways to make antitumor T cells persist or hang around in the body longer,” said study author Jonathan Powell, MD, PhD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland.
With that in mind, Dr Powell and his colleagues analyzed murine T cells. They found that when a “mother” T cell that is naïve to immune threats encounters such a threat and divides, one of its daughter cells inherits far more mTORC1 activity than the other daughter cell.
The researchers activated mouse T cells using a virus. Once the T cells divided, the team used antibodies to detect mTORC1 activity in each of the daughter cells.
Then, the researchers sorted the daughter cells and examined their function by injecting them into mice given two identical infections and tracking the cells’ activity.
The team found the difference in mTORC1 activity levels between the daughter cells varied depending on the population of cells studied.
And the lopsided distribution of mTORC1 activity appeared to reprogram the use of energy and other metabolic activities of each daughter cell.
The cells with high levels of mTORC1 activity were found to be potently activated, killer/effector T cells, while the cells with low mTORC1 levels behaved like memory T cells, persisting for long periods of time and rapidly activating upon reinfection.
The researchers said this finding could be used to improve immunotherapy, but another aspect of this discovery is the prospect that asymmetric partitioning of mTORC1 might be widespread across cells in many biological systems.
Dr Powell said it’s possible the mechanism may help explain how stem cells develop into more specialized cells in the bone marrow, for instance, or how cells differentiate to become hair, skin, or brain cells in a growing embryo.
“We think there will be implications for biology well beyond the immune system,” he concluded.
micrograph of a T cell
Image from NIAID
The “asymmetric division” of T cells could provide new ways to enhance cancer immunotherapy, according to researchers.
When a T cell divides, the activity of the enzyme mTORC1, which controls protein production, splits unevenly between the progeny.
Results of a new study suggest this uneven division reprograms the daughter cells so that one goes on to become an effector T cell and the other becomes a memory T cell.
This study was published in Nature Immunology.
“One of the critical steps needed to improve cancer immunotherapy, in general, is finding out ways to make antitumor T cells persist or hang around in the body longer,” said study author Jonathan Powell, MD, PhD, of the Johns Hopkins University School of Medicine in Baltimore, Maryland.
With that in mind, Dr Powell and his colleagues analyzed murine T cells. They found that when a “mother” T cell that is naïve to immune threats encounters such a threat and divides, one of its daughter cells inherits far more mTORC1 activity than the other daughter cell.
The researchers activated mouse T cells using a virus. Once the T cells divided, the team used antibodies to detect mTORC1 activity in each of the daughter cells.
Then, the researchers sorted the daughter cells and examined their function by injecting them into mice given two identical infections and tracking the cells’ activity.
The team found the difference in mTORC1 activity levels between the daughter cells varied depending on the population of cells studied.
And the lopsided distribution of mTORC1 activity appeared to reprogram the use of energy and other metabolic activities of each daughter cell.
The cells with high levels of mTORC1 activity were found to be potently activated, killer/effector T cells, while the cells with low mTORC1 levels behaved like memory T cells, persisting for long periods of time and rapidly activating upon reinfection.
The researchers said this finding could be used to improve immunotherapy, but another aspect of this discovery is the prospect that asymmetric partitioning of mTORC1 might be widespread across cells in many biological systems.
Dr Powell said it’s possible the mechanism may help explain how stem cells develop into more specialized cells in the bone marrow, for instance, or how cells differentiate to become hair, skin, or brain cells in a growing embryo.
“We think there will be implications for biology well beyond the immune system,” he concluded.