Dan Nemeth, Ph.D., postdoctoral fellow, Charles E. Schmidt College of Medicine and Stiles-Nicholson Brain Institute, recently co-authored a study that reveals specific neural circuitries responsive to immune signaling. The article was published in the Journal of Neuroinflammation.
“Interleukin-1 Receptor 1 (IL-1R1) is known as the primary conductor of inflammatory processes; however, recent research shows that it is more involved in our day-to-day brain function than previously thought. IL-1R1 signaling has been implicated in normal brain functions like memory, sleep and cognition and, when excessive IL-1R1 signaling is present, it is thought to lead to mood, affective and memory disorders. It has yet to be discovered how IL-1R1 may control or modify normal brain function,” Nemeth said.
The study aimed to provide a more detailed analysis of which cells express IL-1R1 in the brain. Using state-of-theart genetic techniques, the researchers discovered that distinct neurons throughout the brain express IL-1R1. While we found neuronal IL-1R1 in brain regions related to mood, affect and cognition, an unexpected finding is that IL-1R1 is expressed in neurons in the sensory system.
“This new discovery opens questions about whether immune signals influence our sensory processing and whether IL-1R1- mediated alterations of sensory signals contribute to cognitive issues, anxiety or depression,” he said. “Furthermore, this study shows that neurons do not signal the same way other IL-1R1-expressing cells do. Using high-tech spatial transcriptomics, we identified that neuronal IL-1R1 regulates synapse organization without causing inflammation. This suggests that IL-1R1 has a role in synaptic formation and can modify neural circuits and their function.”