In:
The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 88.13-88.13
Abstract:
To elucidate the role of Axl on the regulation of LIGHT expression, we established the stably over-expressing Axl T lymphoma cells in mouse EL4 (EL4-Axl) and human Jurkat T lymphoma cells (Jurkat-Axl). The expression of LIGHT and its receptor, herpes virus entry mediator (HVEM) was remarkably increased both in EL4-Axl and Jurkat-Axl compared with the individual controls. Furthermore, the expression of LIGHT, HVEM and IFN-γ was reduced in the various tissues of Axl-/- mice. The proliferation of EL4-Axl cells was inhibited by treatment of Axl-Ig in a concentration and LIGHT expression-dependent manner. In LIGHT promoter assay using a transient transfection of Jurkat-Axl cells with 5¡ deletion mutants, luciferase reporter activity showed the highest transcriptional activity in the gene segment -190/+1. Electrophoretic mobility shift assay (EMSA) and Western blot analysis revealed that Sp1 was able to directly bind to its binding site on LIGHT promoter upon triggering AKT/PI3K signaling pathway. These results suggest that Sp1 plays a crucial role in the regulation of LIGHT expression by Axl signaling in T lymphoma. This work was supported by the SRC/ERC program of MOST/KOSEF (RESEARCH CENTER FOR WOMEN'S DISEASES)
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.182.Supp.88.13
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2009
detail.hit.zdb_id:
1475085-5
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