Australian researchers have identified the master regulator of the immune response signaling pathway that is out of sync in multiple sclerosis and other inflammatory diseases.
The lynchpin in the process is the xIAP protein, the team said. Their discovery that it triggers the NOD2 pathway’s faulty inflammation signaling could lead to new therapies for MS.
Their study, “IAPs Regulate Distinct Innate Immune Pathways to Co-ordinate the Response to Bacterial Peptidoglycans,” appeared in the journal Cell Reports.
Another protein, NOD2, also helps control the signaling pathway. But xIAP plays a larger role, the team said.
Defects in the signaling pathway lead to MS and the bowel disease Crohn’s, whose hallmarks include uncontrolled inflammation.
When the NOD2 pathway is working as it should, it detects invaders such as bacteria, triggering the release of inflammatory signals to fight the infection. But defects in the pathway’s control system lead to immune cells continuing to generate inflammation after an infection is cleared. The result is a chronic inflammatory disease.
“Inflammation occurs when our immune cells release inflammatory messengers, or cytokines, which is a normal response to disease,” Ueli Nachbur of the Walter and Eliza Hall Institute of Medical Research said in a press release. “However when too many cytokines are produced, inflammation can get out of control and damage our own body — a hallmark of inflammatory diseases,” said Nachbur, the co-lead author of the study.
The researchers were intent on identifying the master regulator of the inflammation that the NOD2 pathway triggers.
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