Related Experiment Video
Updated: Aug 17, 2026
Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
Published on: November 8, 2015
Trichosanthin inhibits antigen-specific T cell expansion through nitric oxide-mediated apoptosis pathway
Fang Li1, Yunhua Mei, Ying Wang
1Joint Immunology Laboratory of Institute of Health Sciences and Shanghai Institute of Immunology, Shanghai Institutes for Biological Sciences/Chinese Academy of Sciences, and Shanghai Second Medical University, Shanghai 200025, China.
Abstract:
Trichosanthin (TCS) has been found to exhibit inflammation-suppressing effect but the underlying mechanisms are not clear. In this study, we found that TCS inhibited OVA-specific T cell proliferation in a dose-dependent manner. Such inhibition was correlated with enhanced cell death. At the same time, inducible nitric oxide synthase (iNOS) mRNA expression and protein levels were found increased in cells treated with TCS, and nitric oxide (NO) production by cells was elevated in the presence of TCS. When L-NIL, the specific inhibitor of iNOS, was added to suppress NO production induced by TCS, OVA-specific cell death was significantly inhibited, meanwhile, thymidine incorporation of cells was rescued towards normal levels. These results indicate that TCS could inhibit antigen-specific T cell activation via NO-mediated apoptosis pathway.
Insights
Trichosanthin (TCS) suppresses T cell activation by inducing cell death. This effect is mediated by nitric oxide (NO) production, highlighting a novel pathway for inflammation control.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- Trichosanthin (TCS) is known to possess anti-inflammatory properties.
- The precise molecular mechanisms underlying TCS's anti-inflammatory effects remain largely unelucidated.
Purpose of the Study:
- To investigate the mechanism by which TCS inhibits antigen-specific T cell activation.
- To explore the role of nitric oxide (NO) in TCS-mediated T cell modulation.
Main Methods:
- T cell proliferation assays using ovalbumin (OVA)-specific T cells.
- Assessment of T cell apoptosis and cell death.
- Measurement of inducible nitric oxide synthase (iNOS) mRNA and protein expression.
- Quantification of nitric oxide (NO) production.
- Inhibition of NO production using L-NIL, a specific iNOS inhibitor.
Main Results:
- TCS dose-dependently inhibited OVA-specific T cell proliferation.
- TCS treatment led to increased T cell death.
- TCS upregulated iNOS expression and enhanced NO production in T cells.
- Inhibition of NO production by L-NIL reversed TCS-induced T cell death and restored proliferation.
Conclusions:
- TCS inhibits antigen-specific T cell activation through a pathway involving NO-mediated apoptosis.
- The findings elucidate a novel mechanism for TCS's anti-inflammatory action.
- Targeting the NO pathway could be a therapeutic strategy for inflammation.
