These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Attenuation of graft arterial disease by manipulation of the LIGHT pathway.
    Author: Kosuge H, Suzuki J, Kakuta T, Haraguchi G, Koga N, Futamatsu H, Gotoh R, Inobe M, Isobe M, Uede T.
    Journal: Arterioscler Thromb Vasc Biol; 2004 Aug; 24(8):1409-15. PubMed ID: 15178556.
    Abstract:
    OBJECTIVE: The tumor necrosis factor (TNF) superfamily member LIGHT, which binds herpes virus entry mediator (HVEM) and lymphotoxin beta receptor (LTbetaR), plays important roles in regulating the immune response. To clarify the mechanism underlying graft arterial disease (GAD), we investigated the role of the LIGHT pathway in the progression of GAD. METHODS AND RESULTS: Hearts from Bm12 mice were transplanted into C57BL/6 (B/6) mice (class II mismatch). Recipients were injected intraperitoneally with HVEMIg (100 microg per treatment) every 7 days for 8 weeks. Treatment with HVEMIg significantly attenuated GAD (luminal occlusion=16.5+/-7.7% versus control allograft=62.6+/-12.1%, P<0.05), and significantly decreased intragraft IL-4, IL-6, and interferon-gamma (IFN-gamma) mRNA expression compared with controls. LTbetaR was expressed in smooth muscle cells (SMCs) with or without cytokine stimulation, whereas HVEM was detected in SMCs stimulated by IFN-gamma. Coculture of SMCs with T cells after transplantation induced SMC proliferation, and addition of HVEMIg resulted in inhibition of SMC proliferation. CONCLUSIONS: These results indicate that the LIGHT pathway plays important roles in the regulation not only of T-cell activation but also of SMC proliferation. Blockade of the LIGHT pathway is a promising avenue for the prevention of GAD.
    [Abstract] [Full Text] [Related] [New Search]