Liver Non-Parenchymal Cells Induce Apoptosis in Activated T Cells in Vitro.
- Author:
Young Cheol LEE
1
;
Lina LU
;
Fumin FU
;
Wei LI
;
Angus W THOMSON
;
John J FUNG
Author Information
1. Department of Surgery, Hallym University College of Medicine, Anyang, Korea. yclee@www.hallym.or.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
T cell apoptosis;
Liver nonparenchymal cells;
Immune tolerance;
Transplantation
- MeSH:
Allografts;
Animals;
Apoptosis*;
DNA Fragmentation;
Heart;
Immune Tolerance;
In Situ Nick-End Labeling;
Liver*;
Mice;
Perforin;
Receptors, Tumor Necrosis Factor;
Skin;
T-Lymphocytes*;
Transplantation;
Transplants
- From:The Journal of the Korean Society for Transplantation
2001;15(1):73-78
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Liver, unlike heart or skin, allografts transplanted between MHC-disparate mouse strains are spontaneously accepted without any immunosuppressive therapy. Despite the allograft acceptance, the recipients continue to exhibit donor-specific immune responses in vitro (MLR and generation of CTL). High levels of CTL apoptosis evident within tolerated liver grafts have been postulated as a mechanism underlying this 'split' tolerance. METHODS and RESULTS: By using radiometric DNA fragmentation test ("JAM" assay) and TUNEL staining, we present the evidence here that liver nonparenchymal cells (NPC) are quite strong inducers of activated T cell apoptotic death in allogeneic mice. This phenomenon occurs the similar level in activated T cells of syngeneic or third-party mice. Liver cells from gld (FasL-deficient) mice exert similar apoptosis-inducing effect on activated T cells from normal mice. Tumor necrosis factor receptor (TNFR): Fc fusion protein, and concanamycin A, an inhibitor of perforin pathway, fail to inhibit the apoptotic activity. CONCLUSION: These data indicate that liver NPC play important role in causing active apoptosis in graft-infiltratingCTL which favors liver graft acceptance, and liver-induced activated T cell apoptosis may not mediated by Fas, TNF or perforin pathways.
