Protein's New Role in Autoimmune Disease
Blocking immunity protein interleukin 17 slows disease-causing B cell actions
Posted 1/3/08
Investigators at the University of Alabama at Birmingham (UAB) have identified the previously unknown role of a chemical messenger leading to autoimmune disorders, such as rheumatoid arthritis and lupus. The new findings have been published in the journal Nature Immunology.
The messenger is the naturally occurring chemical interleukin 17 (IL-17), an immunity protein.
The researcher team, including Arthritis Foundation-funded scientist, Hui-Chen Hsu, PhD, pinpointed a role IL-17 plays in autoimmune and inflammatory responses, aside from its commonly known effects within immunity. Future research will home in on IL-17's unwanted actions and preserve its benefits within the immune system.
In the study, the team blocked messenger signals from the IL-17 protein to the immune system of mice. This disruption significantly reduced the number of white blood cells, namely disease-causing B cells, clustered in the mice's spleen.
The number of B-cell clusters dropped from 17 percent to two percent when the IL-17 protein signals were blocked, the study authors said. The drop was a clear sign that IL-17 plays a major role on shaping B cells' ability to create more and more disease-causing antibodies.
"The effect of IL-17 to slow down B cells, thereby enhancing their interaction with other immune regulatory cells a new and exciting discovery," said John D. Mountz, MD, PhD, senior author on the study.
"This is surprising since previously IL-17 was thought to increase, but not decrease, cell motion. Now the effects of IL-17 on B cells can be explored more fully," Mountz said.
Many types of B cells make up the human immune system, which is regulated to sense and fight infection without attacking normal, healthy tissue. In autoimmune diseases that regulatory process becomes imbalanced.
"Knowing more about IL-17's ability to regulate unwanted B-cell migration will generate new ideas in the ongoing search for better drug targets in preventing and treating autoimmune disease," said Hui-Chen Hsu, PhD, an assistant professor in the UAB Division of Clinical Immunology and Rheumatology and lead author on the study.
Funding for this study came from the Arthritis Foundation, the American College of Rheumatology, the U.S. Department of Veterans Affairs, the National Institutes of Health and Tokyo-based Daiichi Sankyo Co., Ltd.
This article was adapted from a press release issued by the University of Alabama at Birmingham.
