Our immune system is the first line of defense against disease, but unfortunately it can go rogue and attack healthy tissues. Scientists at Johns Hopkins University have now engineered a protein that may help prevent these autoimmune diseases by boosting the number of regulatory T cells (Tregs).
The immune system keeps a vigilant watch over our bodies at all times, tagging and destroying foreign pathogens or problematic cells to prevent illness. However, sometimes it can get a little overzealous and start attacking the body’s own cells, which can trigger a range of autoimmune diseases like type 1 diabetes, lupus and rheumatoid arthritis.
To prevent these issues from arising, immune cells called Tregs play the vital role of keeping the immune system responses in check, but they can fail at this job. So for the new study, the researchers set out to boost their numbers, following previous studies that have shown promise in doing so to help treat autoimmune diseases like multiple sclerosis and Crohn’s disease.
In this case, the team created a molecule that fuses a cytokine called interleukin-2 with an anti-cytokine antibody called F5111. This had the effect of promoting the activation and expansion of Tregs. The researchers tested the molecule in mice engineered to be susceptible to colitis and diabetes, and found that the protein bestowed the animals with significant protection against developing the respective autoimmune diseases.
“Tregs are critical for keeping our immune system in balance, and when they get out of whack, people can develop autoimmune diseases," said Jamie Spangler, corresponding author of the work. "(The study) showed that this molecule helps to prevent autoimmune diseases.”
Of course, results from mouse studies don’t always cross over to humans, so clinical use would still be many years away, if ever. And while it’s currently weighted towards preventing disease, the team hopes to investigate whether it or a similar technique could be developed to reverse an autoimmune condition that’s already active.
The research was published in the journal Cell Reports.
Source: Johns Hopkins University
