Researchers in the Department of Immunology at St. Jude Children’s Research Hospital in Memphis were able to identify a faulty “brake” in immune cells which may be involved in the inflammation triggering multiple sclerosis (MS). This brake is believed to be able to control inflammation, offering the potential for the development of new treatments for MS.
The researchers were also able to identify a new model of MS symptoms, including balance control problems and movement disorders, which represent new tools to increase the understanding of MS and other autoimmune disorders.
In the study titled “The NLRP12 Sensor Negatively Regulates Auto-inflammatory Disease by Modulating Interleukin-4 Production in T Cells,” published in the journal Immunity, the team found that the Nlrp12 genetic mutation causes T cells to go “haywire.” A mutation in this specific gene, which produces a protein that can control T cells’ immune responses, usually disrupts this natural process and provokes severe inflammation. However, the researchers found the inflammation did not produce the paralysis that is usually associated with MS, but triggered other MS symptoms, specifically problems with balance control and movement disorders, which researchers have sought to reproduce in experimental settings.
“It’s important to note that MS is a spectrum disorder — some patients present with paralyzing conditions and some patients don’t,” said in a recent news release study author John Lukens, PhD, of the University of Virginia School of Medicine Department of Neuroscience and its Center for Brain Immunology and Glia. “Not everybody’s symptoms are the same, so this might give us a glimpse into the etiology or pathogenesis of that family of MS.”
Inflammation continues to be an emerging research focus in a wide range of diseases, including autoimmune diseases such as Multiple Sclerosis. Researchers now believe that blocking this exacerbated inflammatory response may potentially control MS symptoms as well as other conditions that cause hyper-inflammation.