White Blood Cells Attack Pain Receptors Activated By Microbial Pathogens

Recent findings published in the journal Nature Immunology show that T-cells--a type of white blood cells that are taught to recognize and attack microbial pathogens--can be activated via a pain receptor that help to regulate intestinal regulation found in mice that are manipulated and helped in the treatment of certain autoimmune disorders, such as Crohn's disease and potentially multiple sclerosis (MS).

"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, in a news release.

For the findings, researchers used channels to present T-cells involved in gating the influx of calcium ions into cells via the same process as 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," added lead study author Samuel Bertin, a postdoctoral researcher in the Raz laboratory. "Understanding the physical structures that enable calcium influx is critical to understanding the body's immune response."

HIV viruses target T-cells, with destruction that leads to AIDS. Furthermore, certain vaccines exploit T-cells by harnessing their ability to recognize antigens that trigger the production of antibodies that confer disease resistance.

Researchers performed the experiments on mice models who were able to reduce colitis via the TRPV1-blocker that initially developed as a new painkiller. They discovered promising achievements when the mice were treated with much lower doses that were 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 concluded.