HMGB1 and Huntington disease: To test the role of the thioredoxin system in the regulation of the HMGB1 redox status in the extracellular space, we specifically inhibited the TrxR activity in monocytes from HD pre-treated with PGE2. Indeed, the TrxR inhibitor Auranofin led to a fast oxidation of HMGB1, similarly to what observed in the supernatant of untreated monocytes, proving the relevance of the thioredoxin system in the modulation of the redox status of HMGB1.