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Researchers have discovered that T-cells - a type of white blood cell that learns to recognize and attack microbial pathogens - are activated by a pain receptor, according to a new study. 

The findings of the study showed the receptor helps regulate  intestinal inflammation in mice and that its activity can be manipulated. These findings could offer a potential new target for treating certain autoimmune disorders, such as Crohn's disease and possibly multiple sclerosis. 

"We have a new way to regulate T-cell activation and potentially better control immune-mediated diseases," said senior author Eyal Raz, MD, professor of medicine.

The study is first to show that these channels are also present on T-cells, where they are involved in gating the influx of calcium ions into cells. The same process is also required for T-cell activation. 

"Our study breaks current dogma in which certain ion channels called CRAC are the only players involved in calcium entry required for T-cell function," said lead author Samuel Bertin, a postdoctoral researcher in the Raz laboratory, in the press release. "Understanding the physical structures that enable calcium influx is critical to understanding the body's immune response."

HIV viruses target T-cells, and their destruction leads to AIDS. Certain vaccines also exploit T-cells by harnessing their ability to recognize antigens and trigger the production of antibodies, conferring disease resistance, the press release added.

Researchers performing the experiments on mice models, were able to reduce colitis with a TRPV1-blocker, initially developed as a new painkiller. One of the most promising discoveries the study made is that colitis in mice could be treated with much lower doses than what is needed to dull pain. 

"This suggests we could potentially treat some autoimmune diseases with doses that would not affect people's protective pain response," Raz added.

The study was published in the journal Nature Immunology.