Mouse anti Human TNFRSF6B monoclonal antibody, clone 330923 [Biotin]

The tumor necrosis factor receptor super-family member 6b (TNFRSF6B) is over-expressed in various human cancers, but its function in hepatocellular carcinoma (HCC) remains uncertain. The aim of the study was to investigate the relationship between TNFRSF6B expression and apoptosis in HCC and the effect of anti-TNFRSF6B neutralization monoclonal antibody (McAb) on HCC cells. TNFRSF6B mRNA and protein expression were compared with apoptosis in 78 cases of HCC. Proliferation, cell cycle, apoptosis, and migration ability of liver cancer cells co-cultured with anti-TNFRSF6B McAb were also detected. TNFRSF6B mRNA and protein expression in the tumor tissues negatively correlated with apoptosis. Cell proliferation was decreased, cell cycle was arrested in G1/S-phase, apoptosis was increased, and migration ability was inhibited by anti-TNFRSF6B McAb in vitro. Anti-TNFRSF6B McAb could be useful to suppress proliferation and induce apoptosis in HCC. Thus, TNFRSF6B might be a critical, targeted therapy strategy for HCC. (C) 2010 Elsevier GmbH. All rights reserved.

Background: Microglia mediate amyloid-beta peptide (A beta)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer's disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 anti-inflammatory phenotype. Based on its role as an immunosupressor, we examined whether DcR3 could alleviate neuroinflammation and AD-like deficits in the central nervous system. Method: We crossed human APP transgenic mice (line J20) with human DcR3 transgenic mice to generate wild-type, APP, DcR3, and APP/DcR3 mice for pathological analysis. The Morris water maze, fear conditioning test, open-field, and elevated-plus maze were used to access their cognitive behavioral changes. Furthermore, the pathological and immune profiles were examined by immunostaining, ELISA, Q-PCR, and IP. In vitro assays were designed to examine DcR3-mediated innate cytokine profile alteration and the potential protective mechanism. Results: We reported that DcR3 ameliorates hippocampus-dependent memory deficits and reduces amyloid plaque deposition in APP transgenic mouse. The protective mechanism of DcR3 mediates through interacting with heparan sulfate proteoglycans and activating IL-4(+) YM1(+) M2a-like microglia that reduces A beta-induced proinflammatory cytokines and promotes phagocytosis ability of microglia. Conclusion: The neuroprotective effect of DcR3 is mediated via modulating microglia activation into anti-inflammatory M2a phenotype, and upregulating DcR3 expression in the brain may be a potential therapeutic approach for AD.