New Immunological Mechanisms of PANDAS and Sydenham’s chorea Revealed
Principal investigator Dritan Agalliu, Ph.D., Chair of the PANDAS Network Scientific Advisory Board and Postdoctoral Research Fellow Ugur Akcan PhD, and Charlotte Wayne have worked to understand how streptococcal bacteria underlie the acute encephalitic onset in children with PANDAS and Sydenham’s chorea.
Below is a pre-recorded interview of Dr. Akcan explaining the step-by-step processes for isolating the role of Th17 pathways and their effects on the brain.
This publication brings us one step closer to opening the door to new diagnostic and treatment approaches for those suffering from PANDAS and Sydenham’s chorea.
Briefly, the paper identifies that Group A Strep (GAS) infection causes specialized white blood cells frequently associated with autoimmunity (Th17 cells) to make a signaling molecule (IL-17A) that directly communicates with the brain’s resident white blood cells (microglia) and indirectly transmits the inflammatory signals to critical blood-brain barrier cells (endothelial cells). Their data suggest that this Th17 communication underpins the neuroinflammation observed in children and adolescents exposed to repeated GAS infections (PANDAS) by causing the brain’s blood vessels to become leaky. Communication between Th17 cells alters how microglia and endothelial cells behave by inducing extensive transcriptional changes (turning genes on and off) following repeated group A strep (GAS) infections.
The authors state, “Together, these findings support a role for IL-17A–IL17RA signaling in microglia and macrophages in shaping BBB dysfunction after GAS infection, and suggest that targeting this pathway may complement existing therapeutic strategies for chronic SC/PANDAS in the absence of active infection.”
View the publication by clicking the link below. The final publication will come out in the next few weeks.
