https://scholars.lib.ntu.edu.tw/handle/123456789/160549
Title: | Enhanced Proliferation and Increased Interferon-g Production in T Cells by Signal Transduced Through Tumor Necrosis Factor -Related Apoptosis- Inducing Ligand (TRAIL) | Authors: | CHOU, AI-HSIANG HSU, PING-NING |
Issue Date: | 2001 | Journal Volume: | v.167 | Start page/Pages: | 134-7 | Source: | Journal of Immunology | Abstract: | TNF-related apoptosis-inducing ligand (TRAIL, also called Apo2L), a novel member of TNF superfamily, induces apoptosis in transformed cell lines of diverse origin. TRAIL is expressed in most of the cells, and the expression is up- regulated in activated T cells. Four receptors for TRAIL have been identified, and there is complex interplay between TRAIL and TRAIL receptors in vivo. The actual biological function of TRAIL/TRAIL receptor is still not clear. Growing evidence has demonstrated that members of TNF superfamily transduce signals after engagement with their receptors. Cross-linking of TRAIL by plate-bound rTRAIL receptor, death receptor 4-Fc fusion protein enhanced T cell proliferation and increased IFN- production in conjunction with immobilized suboptimal anti-CD3 stimulation in mouse splenocytes. The increase of T cell proliferation by death receptor 4-Fc was dose dependent, and this effect could be blocked by soluble rTRAIL proteins, indicating the occurrence of reverse signaling through TRAIL on T cell. The enhanced secretion of IFN- mediated via TRAIL could be blocked by SB203580, a p38 mitogen-activated protein kinase - specific inhibitor. Thus, in addition to its role in inducing apoptosis by binding to the death receptors, TRAIL itself can enhance T cell proliferation after TCR engagement and signal the augmentation of IFN- secretion via a p38- dependent pathway. This provides another example of reverse signaling by a member of TNF superfamily. In conclusion, our data suggest that TRAIL can itself transduce a reverse signal, and this may shed light on the biological function of TRAIL. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/87877 |
Appears in Collections: | 免疫學研究所 |
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