All three studies help explain, each from a different angle, how "helper" T-cells can drive autoimmune diseases by creating inflammation. Salt seems to cause enzymes to stimulate the creation of the helper T-cells, escalating the immune response.
"We think of helper T-cells as sort of the orchestra leaders, helping the immune system know what the cells should be doing in response to different microbial pathogens," explained Dr. John O'Shea, director of intramural research at the U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases, in Bethesda, Md. "The strength of these papers is that they have found another factor that drives [helper T-cell] differentiation -- salt."
While salt may play a role in autoimmune diseases, the researchers said the picture is most likely complicated. "We don't think salt is the whole story. It's a new, unexplored part of it, but there are hundreds of genetic variants involved in autoimmune disease and environmental factors, too," said Hafler.
It's also unclear just how much salt is required to stimulate the autoimmune response, Hafler added.
In addition to salt, other factors have been shown to influence levels of helper T-cells, including microbes, diet, metabolism, environmental factors and cytokines (proteins that help regulate inflammatory responses), according to O'Shea, who was not involved with the new studies.
O'Shea said the studies provide a way to test -- hopefully soon in human trials -- whether a low-salt diet might help treat autoimmune disease.
"They have now identified a biomarker, so you could treat people wi
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