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A critical role of TRAIL expressed on cotransplanted hepatic stellate cells in prevention of islet allograft rejection
Author(s) -
Yang HorngRen,
Hsieh ChingChuan,
Wang Lianfu,
Fung John J.,
Lu Lina,
Qian Shiguang
Publication year - 2010
Publication title -
microsurgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 63
eISSN - 1098-2752
pISSN - 0738-1085
DOI - 10.1002/micr.20697
Subject(s) - islet , apoptosis , hepatic stellate cell , medicine , transplantation , immune system , cancer research , microbiology and biotechnology , immunology , biology , pathology , endocrinology , diabetes mellitus , biochemistry
Hepatic stellate cells (HSCs) have demonstrated a strong T‐cell inhibitory activity. In a mouse islet transplantation model, cotransplanted HSCs can protect islet allografts from rejection. The involved mechanism is not fully understood. We showed in this study that expression of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL), an important apoptosis‐inducing ligand, on HSCs was crucial in protection of islet allografts, since HSCs derived from TRAIL knockout mice demonstrated less inhibitory activity towards T‐cell proliferative responses, and substantially lost their capacity in protecting cotransplanted islet allografts from rejection, suggesting that TRAIL‐mediated T cell apoptotic death is important in HSC‐delivered immune regulation activity. © 2009 Wiley‐Liss, Inc. Microsurgery 2010.