February 1, 2001
Filed at 3:17 p.m. ET
NEW YORK (Reuters Health) - Researchers have moved one step closer to developing drugs that selectively target immune system cells, which may lead to better treatments for diseases that cause the body's defense mechanisms to go awry.
T-cells make up an important part of the body's immune system, but in people with autoimmune diseases like type 1 diabetes, multiple sclerosis and rheumatoid arthritis, something goes wrong and groups of T-cells destroy healthy tissue.
In a report in the February issue of the journal Nature Biotechnology, Dr. Sofia Casares, of Mount Sinai School of Medicine in New York, and colleagues point out that one strategy for treating autoimmune diseases is to suppress all T-cells. While this approach minimizes the damage of the T-cells that have gone haywire, it can cause unwanted side effects by weakening the immune system, the researchers note.
To avoid the unwanted side effects of a broad attack on T-cells, Casares and colleagues formulated molecules that target specific types of T-cells. In laboratory tests, they used the molecules to deliver a toxic chemotherapy drug, doxorubicin, to a subset of T-cells. The targeted treatment selectively killed off these cells, the researchers report. And the modified drug also reduced levels of the T-cells in mice.
The findings represent the "first truly specific targeting system" for drugs that treat autoimmune diseases such as type 1 diabetes, multiple sclerosis and rheumatoid arthritis, one of the study's authors told Reuters Health.
"The molecules that we have engineered are able to target the drug only to those cell subsets responsible for the diseases and not to the entire population of T-cells," according to Mt. Sinai's Dr. Teodor-D. Brumeanu.
"This will avoid first the side effects of the drug on other cells and tissues unrelated to the disease, and secondly will allow efficient concentration of the drug in the pathogenic cells," Brumeanu explained.
The researchers have already begun preliminary testing of the molecule in mice with type 1 diabetes.
SOURCE: Nature Biotechnology