Could research on "peacekeeper" T-cells offer a new path to autoimmune treatment?
Autoimmune diseases occur when the immune system mistakenly attacks healthy cells and tissue. T-cells—a type of white blood cell—are largely responsible for defending the body against viruses and bacteria. However, when T-cells have trouble distinguishing between foreign peptide antigens and self-peptides (pieces of protein from our own body), this can lead to autoimmunity.
New research from the University of Chicago studied a group of T-cells called Treg cells (short for regulatory T-cells), which essentially "keep the peace" within the body by preventing helper T-cells from attacking the body's own tissue. When self-peptides are presented, the peacekeeper Treg cells are trained to spot them and intervene to stop helper T-cells from being triggered and attacking those peptides.
In a study on mice, researchers removed Treg cells that specialize in recognizing a particular self-peptide from the prostate. In healthy mice, this change did not trigger an autoimmune response. However, in mice that were infected with a bacterium that expressed a peptide similar to the prostate self-peptide (or displayed a protein fragment that resembled it), helper T-cells became activated and attacked both the bacterium and the prostate, triggering autoimmunity. Without the Treg cells to control self-reactive responses and prevent "friendly fire," the helper T-cells attacked the mice's prostate cells.
From the study, researchers concluded that for each type of helper T-cell that is capable of triggering autoimmunity through a specific protein, there is a "doppelganger" or corresponding set of Treg cells that can suppress or regulate that response to prevent attacks on the self-peptides. Where conventional autoimmune treatment has focused on suppressing the immune system and indiscriminately purging helper and Treg T-cells, this research offers a more efficient path forward. Dr. Pete Savage proposes that "instead of having to delete all helper T-cells reactive to self-antigens, you simply generate enough of these Treg peacekeeper cells instead." The idea is to identify the specific helper T-cells involved in an autoimmune response and then expand or introduce their matching Treg cells to restore immune balance and prevent self-attacking.
A treatment based on these findings could be a game-changer for patients. It not only offers an alternate path for drug development, but also offers a more targeted solution that could lead to safer long-term outcomes. While the research is still in its early stages, its potential to transform autoimmune disease treatment is promising and exciting.
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