After repeated exposure to a fragment of the myelin protein — the target of autoimmune attack in multiple sclerosis (MS) — immune cells in mice were reprogrammed to be tolerant to myelin, suppressing the immune response associated with the disease, a study revealed.
Researchers showed that in these tolerant T-cells, genes that limit immune responses were enhanced, while genes that activated T-cells were repressed.
These findings support the development of therapies that directly address the underlying autoimmune response in MS patients.
The study, “Chromatin Priming Renders T Cell Tolerance-Associated Genes Sensitive to Activation below the Signaling Threshold for Immune Response Genes,” was published in the journal Cell Reports.
MS is characterized by the immune system mistakenly attacking myelin — the fatty protective coating that covers nerve fibers. T-cells are a type of immune cell that is involved in the autoimmune attack against the myelin sheath and represents a target for MS treatments.
The process of T-cell activation against an antigen — molecules capable of stimulating an immune response — is tightly regulated and depends on multiple signaling pathways to ensure an appropriate immune response.
A recent review analysis demonstrated that T-cell activation could be suppressed by repeated exposure to an antigen, leading to so-called T-cell tolerance against that antigen. This represents a type of immunotherapy with the potential to desensitize the immune system.
Understanding the mechanism of this phenomenon may help researchers find ways to reprogram T-cells to become tolerant and not attack the myelin sheath, which may lead to effective therapies to treat the underlying cause of MS.
We are sorry that this post was not useful for you!
Let us improve this post!
Tell us how we can improve this post?