Saint Louis University researcher Daniel Hawiger, M.D., Ph.D., received more than $600,000 from the National Multiple Sclerosis Society to gain a better understanding of how the autoimmune process that causes multiple sclerosis (MS) may be stopped or slowed down.
Multiple sclerosis, a chronic disease of the central nervous system, occurs when some of the immune system’s “T-cells” mistake the nerve fiber coating called myelin as a foreign tissue to be destroyed.
Normally, T-cells that react to the body’s own proteins undergo a process called “immunological tolerance” in which they are educated to ignore “self.” When the tolerance process goes wrong, the self-reactive T-cells go on the attack.
Hawiger, who is assistant professor of molecular microbiology and immunology at SLU, aims to understand how immunological tolerance works and why it sometimes fails in order to design better clinical treatments that selectively suppress immune-mediated damage to the nervous system in people with MS.
Researchers will focus on understanding how different types of lymphocytes, such as regulatory and effector T-cells, and also dendritic cells, interact with each other. Hawiger’s lab recently found that a method of delivering fragments of myelin proteins to dendritic cells results in the generation of regulatory T-cells expressing specific factors that are required to suppress autoimmune destruction. Researchers hope that by manipulating such regulatory T-cells, they may be able to develop new and more precisely targeted immune therapies with fewer side effects.
“We believe that this research can show us a way to be very specific in silencing only the reactive T-cells without causing damage to the patient,” Hawiger said. “In the future, my hope is to have a much more selective type of immune therapy that would specifically target functions of the immune system that lead to MS without the side effects that come with general immune suppression.