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Sudarshan Anand, Pu Wang, Kiyoshi Yoshimura, In-Hak Choi, Anja Hilliard, Youhai H. Chen, Chyung-Ru Wang, Richard Schulick, Andrew S. Flies, Dallas B. Flies, Gefeng Zhu, Yanhui Xu, Drew M. Pardoll, Lieping Chen, Koji Tamada
Published in Volume 116, Issue 4
J Clin Invest. 2006; 116(4):1045–1051 doi:10.1172/JCI27083
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Figure 2
Essential role of the soluble form of LIGHT in liver inflammation.

(A) B6 mice were injected i.v. with 30 mg/kg of ConA. At the indicated time points, serum was collected from the recipient mice and measured for soluble LIGHT concentration by LIGHT-specific ELISA. (B and C) B6 mice were injected with a sublethal dose of ConA (12.5 mg/kg) alone (filled circles, n = 13) or together with 20 μg plasmids encoding control pcDNA3.1 (open circles, n = 13), wild-type LIGHT (filled squares, n = 11), or LIGHTΔL (open squares, n = 10) by hydrodynamic injection technique. Survival of mice (B) and liver sections stained with H&E 18 hours after injection (C) were examined. N, necrotic area. *P = 0.3, **P = 0.033 between the groups by log-rank test. (D) BALB/c mice were injected i.p. with 50 μg of soluble LIGHT-flag fusion protein or control protein. One hour later, the mice were injected i.v. with 25 mg/kg ConA, and serum ALT levels were measured 6 hours later. One representative result from 3 independent experiments is shown as mean ± SD.