Study results show a genetic risk variant on astrocytes enhances the accessibility of the central nervous system (CNS) to peripheral immune cells, escalating the risk of autoimmune inflammation and multiple sclerosis.
A genetic risk variant, rs7665090G, located near NFKB1, on astrocytes enhances the accessibility of the central nervous system (CNS) to peripheral immune cells, escalating the risk of autoimmune inflammation and multiple sclerosis (MS), according to the results of a recent study.
One recent finding suggested that changes in immune enhancers such as lymphocytes may disrupt innate and adaptive immune pathways; however, investigators were still unsure whether they affected CNS function and thus increased MS risk. In this study, rs7665090G was used to determine whether dysregulation in astrocyte function will affect MS risk.
Nuclear factor-κ—light chain enhancer of activated B cells (NF-κB) is an essential part of innate and adaptive immunity and plays a role in autoimmunity. Changes in NF-κB signaling have been associated with cancer and inflammatory and autoimmune diseases. In this study, investigators compared induced pluripotent stem cells (iPSCs)–derived astrocytes from patients who were healthy and patients with MS who were had a homogenous risk variant (rs7665090GG) or protective variant (rs7665090AA). In unstimulated astrocytes, both groups had low NF-κB signaling. However, once NF-κB signaling was stimulated using tumor necrosis factor α and IL-1β, NF-κB activation was significantly higher in the astrocytes that carried the risk variant.
A version of this article was orginally published by the American Journal of Managed Care. Continue reading the full article at AJMC.com.