In the study, researchers gave halofuginone to mice with experimental autoimmune encephalitis (EAE), an artificially induced immune disease that resembles multiple sclerosis in humans.
They found that low-doses of halofuginone inhibited the development of Th17 cells in the mice but did not alter other kinds of T cells important for normal immune function.
Tests in human cells in the lab showed a similar inhibition of Th17 cell formation.
The researchers believe that halofuginone acts by activating a biochemical pathway known as the amino acid starvation response, or AAR, which typically protects cells when amino acids, the essential building blocks of proteins, are in short supply.
When excess amino acids were added to cultured T cells that were exposed to halofuginone, the AAR didn't switch on, allowing Th17 cells to develop.
Conversely, the researchers were able to inhibit Th17 differentiation by depleting amino acids and causing the AAR to kick in.
"When a cell senses amino acid deprivation, it tries to conserve amino acids by preventing specific types of responses that are energetically expensive," Sundrud said. "In inflamed tissues, a lot of cells are producing a lot of protein, so it would make sense that a cell with amino acid deprivation would want to block signals that promote inflammation."
Halofuginone is one of the 50 "fundamental herbs" of traditional Chinese medicine, according to the study. It has also been used as an anti-malarial agent. Decades ago, according to background information in the news release, the U.S. Army tried to improve upon its anti-malarial properties without success.
Halofuginone is also used to treat scleroderma, an autoimmune disease of the connective tissue. Because the compound is now in the public domain, the pharmaceutical industry has not sh
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