DALLAS - August 4, 1999 - Researchers at UT Southwestern Medical Center at Dallas have converted specialized cells that normally trigger an immune response into cells that trigger cell death.
The research, reported in this month's issue of Nature Medicine, involved the molecular engineering of cells in mice - a procedure that could eventually lead to the prevention and treatment of inflammatory diseases such as rheumatoid arthritis.
"What we did was to change the concept entirely. We tried to convert dendritic cells (which signal for an immune response) into cells that deliver death signals instead of activation signals," said Dr. Akira Takashima, the Thomas L. Shields, M.D., Professor in Dermatology.
Dendritic cells are specialized white blood cells that serve an important function within the immune system. Normally they send activation signals to T lymphocytes to begin multiplying and initiate an immune response.
"Sometimes the dendritic cells that can help a person acquire protective immunity are also involved in the induction of harmful immune responses," said Takashima. "There are many diseases, especially inflammatory diseases, where T cells play a pathogenic role."
For example, rheumatoid arthritis is a common inflammatory joint disease believed to be caused by an autoimmune response. Patients' immune systems form antibodies that improperly attack the lining surrounding joints, causing chronic inflammation.
"The next step is to translate our knowledge of dendritic cells and apply this technology into clinical trials for treating the various diseases caused by T cells," Takashima said.
Dr. Hiroyuki Matsue, assistant professor of dermatology at UT Southwestern and primary author of the study, collaborated with Takashima and other researchers from UT Southwestern, including Keiko Matsue, postdoctoral researcher, and Michael Walters, research technician.
National Institutes of Health grants supported the study.
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Contact: Ione Echeverria
ione.echeverria@email.swmed.edu
214-648-3404
UT Southwestern Medical Center
4-Aug-1999