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T-cell receptor ensures Treg functionality

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Regulatory T cells (Tregs) need T-cell receptors to fulfill their protective functions, according to research published in Immunity.

The researchers knew that Tregs need T-cell receptors to develop properly, but they were unsure of the receptors’ role after that.

To find out, the team deactivated T-cell receptors on mature Tregs in genetically modified mice.

They found these defective Tregs were not able to carry out their protective function without the T-cell receptors.

Furthermore, the Treg pool fell significantly, as these cells were no longer multiplying.

However, the researchers also discovered that two of Tregs’ most well-known central molecular properties—the production of Foxp3 protein and specific chemical changes to DNA—were still present in the defective T cells.

“Without their receptor, the Tregs are still clearly identifiable as Tregs,” said study author Christoph Vahl, PhD, of the Max Planck Institute of Biochemistry in Martinsried, Germany.

“However, they lose a large part of their cellular identity. They also lose their special ability to suppress excessive immune reactions.”

“The Tregs obviously need continuous contact with their environment to function correctly. This is presumably the reason why they need a receptor that recognizes endogenous substances and continuously sends signals.”

“During the course of our research, we uncovered a very important mechanism for suppressing excessive responses and responses targeted against the human body,” added Marc Schmidt-Supprian, PhD, also of the Max Planck Institute.

“These findings could be relevant for situations where it would be beneficial to weaken the control of Tregs over immune responses—for example, in the treatment of cancer.”

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Lab mouse

Regulatory T cells (Tregs) need T-cell receptors to fulfill their protective functions, according to research published in Immunity.

The researchers knew that Tregs need T-cell receptors to develop properly, but they were unsure of the receptors’ role after that.

To find out, the team deactivated T-cell receptors on mature Tregs in genetically modified mice.

They found these defective Tregs were not able to carry out their protective function without the T-cell receptors.

Furthermore, the Treg pool fell significantly, as these cells were no longer multiplying.

However, the researchers also discovered that two of Tregs’ most well-known central molecular properties—the production of Foxp3 protein and specific chemical changes to DNA—were still present in the defective T cells.

“Without their receptor, the Tregs are still clearly identifiable as Tregs,” said study author Christoph Vahl, PhD, of the Max Planck Institute of Biochemistry in Martinsried, Germany.

“However, they lose a large part of their cellular identity. They also lose their special ability to suppress excessive immune reactions.”

“The Tregs obviously need continuous contact with their environment to function correctly. This is presumably the reason why they need a receptor that recognizes endogenous substances and continuously sends signals.”

“During the course of our research, we uncovered a very important mechanism for suppressing excessive responses and responses targeted against the human body,” added Marc Schmidt-Supprian, PhD, also of the Max Planck Institute.

“These findings could be relevant for situations where it would be beneficial to weaken the control of Tregs over immune responses—for example, in the treatment of cancer.”

Lab mouse

Regulatory T cells (Tregs) need T-cell receptors to fulfill their protective functions, according to research published in Immunity.

The researchers knew that Tregs need T-cell receptors to develop properly, but they were unsure of the receptors’ role after that.

To find out, the team deactivated T-cell receptors on mature Tregs in genetically modified mice.

They found these defective Tregs were not able to carry out their protective function without the T-cell receptors.

Furthermore, the Treg pool fell significantly, as these cells were no longer multiplying.

However, the researchers also discovered that two of Tregs’ most well-known central molecular properties—the production of Foxp3 protein and specific chemical changes to DNA—were still present in the defective T cells.

“Without their receptor, the Tregs are still clearly identifiable as Tregs,” said study author Christoph Vahl, PhD, of the Max Planck Institute of Biochemistry in Martinsried, Germany.

“However, they lose a large part of their cellular identity. They also lose their special ability to suppress excessive immune reactions.”

“The Tregs obviously need continuous contact with their environment to function correctly. This is presumably the reason why they need a receptor that recognizes endogenous substances and continuously sends signals.”

“During the course of our research, we uncovered a very important mechanism for suppressing excessive responses and responses targeted against the human body,” added Marc Schmidt-Supprian, PhD, also of the Max Planck Institute.

“These findings could be relevant for situations where it would be beneficial to weaken the control of Tregs over immune responses—for example, in the treatment of cancer.”

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