Proven successful in mice, this protocol could lead to new ways to treat autoimmune diseases such as MS, rheumatoid arthritis, and type 1 diabetes in humans. As it stands, the main therapy for autoimmune diseases involves suppressing inflammation by inhibiting immune cells with anti-inflammatory medications and steroids. While they temporarily relieve symptoms, these drugs can hamper the immune system at the same time and leave patients susceptible to infections. That’s why scientists are looking to develop a new type of treatment that targets the autoimmune and inflammatory immune cells without compromising the immune system’s function. New research, highlighted in Science Translational Medicine, details how researchers developed special T-cells that can destroy disease-causing immune cells without eliminating good immune cells needed to protect against infections. Get the Facts About Autoimmune Disease »

Reprogramming the Immune System The research was led by Shimpei Kasagi of the National Institutes of Health (NIH), who figured out how to produce regulatory T-cells, or Tregs, that can treat autoimmune diseases. The researchers created a suppressed immune environment in mice with either experimental autoimmune encephalomyelitis or non-obese diabetes using an immune-regulating molecule called TGF-beta. Then they injected autoantigenic-peptides into the animals; these peptides are molecules that produce specific Tregs and resulted in antigen-specific T-cell differentiation. The Tregs then stopped inflammatory responses by traveling into the tissues and organs of the mice. In essence, the researchers reprogrammed the immune system with the Tregs. The scientists found that the newly generated Tregs not only stopped the autoimmune disease, but the animals were able to stay disease-free long after stopping the peptide injection. Related News: Severe Headaches Not Linked to Lupus, Study Shows » The key for this treatment is the introduction of autoantigen-specific Tregs. The procedures aim to reprogram the native T-cells to differentiate into immunosuppressive regulatory T-cells, not to pro-inflammatory effector T-cells, said Dr. WanJun Chen, one of the researchers with the NIH. Once reprogrammed, these autoantigen-specific Tregs regenerate, which is probably why the mice in the study continued to experience disease remission after the treatment. It still needs to be confirmed if more peptides would need to be administered for long-term remission, Chen said. “The long and dramatic effectiveness and duration of the suppression of the autoimmune diseases is better than we expected,” Chen said. As a result of the treatment, the mice had normal immune system defense when exposed to bacterial antigens.