Reversal of Remimazolam-Mediated Inhibition of Jurkat T Cell Activation by TGFBI Depletion

GABAA receptors are well-recognized targets for intravenous anesthetics and have been identified in T lymphocytes. Remimazolam, a GABAA receptor-binding agent, enhances the inhibitory effects of γ-aminobutyric acid (GABA) and provides a rapid onset and offset of sedation, making it suitable for procedural sedation and anesthesia. However, the impact of remimazolam on T cell function remains poorly understood. In this study, we used mass spectrometry analysis to confirm that Jurkat T cells produce and secrete GABA de novo. Consequently, treatment with remimazolam inhibited Jurkat T cell activation, even in the absence of exogenous GABA. Transcriptomic profiling of remimazolam-treated Jurkat T cells exhibited a significant upregulation of TGFBI expression. Furthermore, CRISPR/Cas9-mediated knockout of TGFBI reversed the inhibitory effects of remimazolam on Jurkat T cell activation. These findings highlight the profound influence of anesthetics on T cell activation and could be crucial for optimizing their clinical application.