The HMGB1 is increased in CSF of patients with an Anti-NMDAR encephalitis

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune disorder of the central nervous system (CNS). Interleukin (IL)-6 and IL-17A may play important roles in the pathogenesis of this disease. High-mobility group box protein 1 (HMGB1), a small but highly conserved ubiquitous protein, is recognized to be a potent innate inflammatory mediator that can activate the nuclear factor light chain enhancer of activated B cells and release cytokines such as IL-6 and IL-17A when released extracellularly. However, whether cerebrospinal fluid (CSF) HMGB1 levels are altered in anti-NMDAR encephalitis is still unclear.

The aim of this study was to determine whether a correlation exists between the CSF concentrations of HMGB1 and IL-6 and IL-17A in anti-NMDAR encephalitis patients. We also sought to assess whether HMGB1 influences the clinical outcomes in anti-NMDAR encephalitis patients.

Thirty-three patients with anti-NMDAR antibodies and 38 controls were recruited. CSF HMGB1 was measured using an enzyme-linked immunosorbent assay. The main clinical outcomes were evaluated using the modified Rankin scale (mRS). The data were extracted using microarray analysis software.

Our results showed significant increases in CSF HMGB1, IL-6, and IL-17A (P < .05) in anti-NMDAR encephalitis patients. But between 3 months' mRS scores in anti-NMDAR encephalitis patients and CSF data, there was no correlation. Our study suggests that HMGB1 CSF levels are increased in patients with anti-NMDAR encephalitis and reflect the underlying neuroinflammatory process.