UT Southwestern researchers engineer cells that may hold key to treating inflammatory diseases


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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.

© 1998 The University of Texas Southwestern Medical Center at Dallas

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