Year: 2025
Type: article
Abstract: 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.
Source: Immune discovery.
Authors: Hao Wang, Ge Gao, Haoyuan Ma, Yingcheng Qi, Bowen Zhang, Tingting Liu, Yang Liu, Tianhan Li, Lichen Zhang, Hui Wang, Yinming Liang, Binhui Zhou
Institution: Henan Medical University
Language: English
Subfield: Developmental Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
Award: G4227146011
OpenAlex ID: W4412881966