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In the study, UAB scientists 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 2 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, M.D., Ph.D., UAB professor of
medicine and 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, Ph.D. an assistant professor in the UAB Division of
Clinical Immunology and Rheumatology and lead author on the study.
The research team included UAB investigators from the departments of
Medicine, Cell Biology, Pathology, Microbiology and Dermatology and
from Children�s Hospital of Pittsburgh and the University of Tennessee
Health Science Center in Memphis.
Funding for the 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.
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