Researchers in Braunschweig have tracked down a natural inhibitor mechanism in our immune system. The molecule, known as GPR83, can block over-reactions by our immune system's defenses before these damage body tissues, according to scientists at the German Research Centre for Biotechnology (GBF). GPR83 manages to do this by switching immune cells from their aggressive defense posture into a more docile mode. A breakdown of this mechanism, the researchers say, could play a role in auto-immune diseases, such as rheumatoid arthritis or Type-1 diabetes, as well as in host defense against severe infections. A summary of the findings has been published in the most recent issue of the Journal of Immunology.
A constant back-and-forth between the encouragement and inhibition of signals directs the activities of the human immune system. When bacteria or viruses enter the human organism, immune cells must be in a position to act swiftly and effectively against the invaders. That is why immune responses have the tendency to quickly accelerate into overdrive with self-amplifying mechanisms, even when the threat is minor. In the case of a false alarm, this can lead to an attack on the body's own tissue and, in turn, cause serious damage. For this reason, it is indispensable that the immune system has specific inhibitor mechanisms to subdue over-reactions.
T cells are among the most potent defenders of the immune cells, which among others things can kill infected cells. "Some T cells appear to possess a built-in blocker on their surfaces," explains GBF researcher Dr. Wiebke Hansen. "The molecule GPR83 serves as a receptor - as a kind of antenna - that responds to strong immune system over-reactions. When GPR83 is activated, the T cells do not become killers but are transformed into docile regulatory T cells - TREGs for short," says Dr. Hansen. From then on, they induce an immune tolerance by deactivating other T cells. "However, just who in the body is stepping on the brakes, and under what circumstances, still has to be clarified more thoroughly," she says.
For the Braunschweig researchers, studying the functions and impact of the GPR83 T cell inhibitor is promising. "If, at some point, we are able to find a way to stimulate GPR83 with drugs, this could be used to treat over-reactions or malfunctions of the immune system; for example, in the case of auto-immune diseases and chronic inflammations," notes the GBF work group leader, Prof. Jan Buer. By contrast, a targeted blocking of GPR83 would make the immune system more aggressive, and that, says Buer, could some day be interesting for treating severe infections, or for tumor therapy.
Manfred Braun | alfa
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