Little changes can make a big difference.
In a paper published Sunday in the journal Nature Immunology, OMRF scientist Jose Alberola-Ila, M.D., Ph.D., found that a single missing protein in mice makes their immune systems unable to produce a potent defensive cell. The findings could be key to a deeper understanding of autoimmune disorders like type I (juvenile) diabetes.
When we get sick, our immune system needs time to marshal resources to stage a counter-attack against pathogens. But Natural Killer T cells (or NKT cells) are like the S.W.A.T. team, defusing the immediate danger to the body by shooting first and asking questions later.
Not all immune cells can become Natural Killer T cells, Alberola-Ila said. Many variables go into their creation, but they can’t exist without a particular protein (c-Myb), which binds to several genes to control the output of other proteins required for NKT cell development.
“Originally, we were looking at this protein because it helps control the development of conventional immune cells,” he said. “But during our research, we found that mice without the protein couldn’t produce Natural Killer T cells. It was serendipity.”
The discovery could have important implications for understanding the development of autoimmune diseases like type I diabetes and allergic disorders, Alberola-Ila said. In these illnesses, the body turns Natural Killer T cells and other weapons of its own defense system against itself.
The next step is to find out how the protein controls so many genes required for Natural Killer T cell development at once and if it plays a role in controlling the function of those cells, he said.
OMRF scientists Taishan Hu, Ph.D., and Amie Simmons and University of Virginia researcher Tim Bender, Ph.D., also contributed to the research, which was funded through grants from the National Institute of Allergy and Infectious Disease and the American Heart Association.
