Feb. 27, 2006 The failure of programming that sparks the death of dendritic cells -- those that activate the immune system -- can initiate autoimmune disease, said researchers from Baylor College of Medicine in a report that appears in the current issue of the journal Science.
The problem begins with a process called programmed cell death or apoptosis, said Dr. Jin Wang, assistant professor of immunology at Baylor College of Medicine. Mice bred to have a defect in apoptosis of their dendritic cells went on to develop autoimmune disease, he said.
"This suggests that defective apoptosis of dendritic cells can be a critical component of autoimmune diseases," said Wang.
Autoimmune diseases, such as juvenile diabetes and lupus, result when the immune system begins attacking the body's own tissues rather than foreign bodies.
"We knew that autoimmunity in general can be caused when dendritic cells are unchecked, either by programmed cell death or overactivation," said Wang.
"Dendritic cells are the initiators of immunity," said Wang.
They do this by showing or presenting foreign antigens from invading bacteria or viruses to the immune system, which then activates lymphocytes to attack.
Previously, many people thought autoimmunity occurred through apoptosis because of accumulating lymphocytes or white blood cells -- key elements of the immune system.
"If they didn't die, we thought they would start to accumulate and do damage to the body's own tissues," he said. However, at least eight studies that suppressed programmed cell death in lymphocytes did not induce autoimmune disease in animals.
In the future, Wang said, he and his colleagues plan to fill in the gaps between what happens when apoptosis is hindered in the dendritic cells and the occurrence of autoimmune disease.
Others who participated in this research include: Drs. Min Chen, Li Huang and Hector Sandoval of BCM, and Drs. Yui-Hsi Wang, Yihong Wang, and Yong-Jun Liu of The University of Texas M.D. Anderson Cancer Center.
Funding for this project came from the Cancer Research Institute, American Society of Hematology, the National Institutes of Health and a Ruth L. Kirschstein National Research Service Award.
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