Researchers have designed a protein that activates and increases the number of special, regulatory T cells called Tregs, which help prevent diseases such as rheumatoid arthritis and multiple sclerosis.
Autoimmune disorders like these happen when the immune system is inadvertently activated, mistakenly attacking the body’s tissues and organs. Though it is known that genetics play a role in their development, prevention, and treatment approaches also focus on external factors, such as nutrition and environment.
The team of engineers believes one answer to prevention and treatment lies inward, at the cellular level.
“Tregs are critical for keeping our immune system in balance, and when they get out of whack, people can develop autoimmune diseases,” says Jamie Spangler, assistant professor in the departments of chemical and biomolecular engineering. “(The study) showed that this molecule helps to prevent autoimmune diseases.”
“In the case of autoimmune disease, your own immune system is essentially attacking itself, so these Tregs are used to suppress that attack.”
The molecule, which fuses the interleukin-2 cytokine and the anti-cytokine antibody F5111, promoted Treg activation and expansion and protected non-obese diabetic mice against autoimmune disease development to a statistically significant degree.
“The way in which it does this is by specifically targeting and expanding Tregs, which are used to suppress an immune response,” says Derek VanDyke, a PhD candidate in the chemical and biomolecular engineering department and lead author of the study in the journal Cell Reports.
“In the case of autoimmune disease, your own immune system is essentially attacking itself, so these Tregs are used to suppress that attack.”
Because symptoms of autoimmune diseases are a result of the body’s defense system malfunctioning, suppressing this reaction could help in preventing the disease from manifesting, the researchers say.
Since early detection and prevention is not always possible, however, future work will explore the possibility of using this approach to reverse active disease.
Additional coauthors are from the University of California, San Francisco; the Academy of Sciences of the Czech Republic; the University of Oxford; the University of Pennsylvania; the University of California, Los Angeles; and Johns Hopkins.
The National Institutes of Health, the Department of Defense, the Juvenile Diabetes Research Foundation, the Czech Science Foundation, the Institute of Biotechnology of the Czech Academy of Sciences, the EU Horizon project, ReSHAPE, and the Mark Foundation for Cancer Research funded the work.
Source: for Johns Hopkins University
