July 12, 2018
New research shows that overreactive and tissue-damaging T-cells can transition into regulatory T-cells that help to control the immune system’s response.
These findings open the door to further understanding of the mechanism underlying this transition, knowledge that can help scientists in designing more effective, targeted immunotherapies for diseases like multiple sclerosis (MS).
The study, “A temporally dynamic Foxp3 autoregulatory transcriptional circuit controls the effector Treg programme” was published in the EMBO Journal.
In MS and other autoimmune diseases, immune system cells called T-cells overreact and begin to respond to non-threatening signals, leading to an uncontrolled activation of the immune system that ultimately damages a person’s own tissues. The same phenomenon underlies allergies like asthma.
T-cells are vital immune system cells, activating other cells in this system to strengthen the immune response against invaders like bacteria. However, every immune response needs to come to an end, and for that our body relies on a special group of cells called regulatory T-cells or Tregs. These cells act as negative regulators, and like “good police” they shut down the immune response triggered by overreacting T-cells.
Researchers have for long thought that Tregs were always Tregs — and no other cell type could become these beneficial “good police” cells. Now, a team of researchers at the Imperial College London, U.K., showed that overactive T-cells can transform and become Tregs, helping to suppress the immune system and prevent overactivation.
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