A number of organoselenium compounds have been described as anti-inflammatory, antioxidant, glutathione peroxidase-like agents and inhibitors of prostaglandin synthesis. Here we report that bis [2-(N-phenyl-carboxamido)]phenyl diselenide, 2-phenyl-1,2-benzisoselenazol-3(2H)-one (Ebselen) and related compounds are inducers of interferon gamma (IFN-gamma) and tumor necrosis factor (TNF) in human peripheral blood leukocytes. The IFN and TNF response was rapid, occurring within 20 h, and high--up to 1000 and 2000 units ml-1--and was clearly related to the dosage and the structure of the compounds. The action of the compounds and phytohemagglutinin was synergistic. The IFN gamma and TNF production was reduced after removing adherent cells. Although the mode of action of the compounds is not known, they appear to interact directly or indirectly with both adherent and non-adherent leukocytes, and stimulate the synthesis of a set of different cytokines including factors controlling the cell proliferation. Therefore, organoselenides may be regarded as the biological response modifiers.
Transforming growth factor-beta (TGF-beta) at concentration of 10 ng/ml inhibited the development of the interferon-alpha- (IFN-alpha) or IFN-gamma-induced antiviral state in quiescent human embryonic fibroblasts. The action of the cytokines was dose-related; TGF-beta had no direct effect on the replication of either vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMCV) used as the challenge viruses in the IFN assays. We suggest that despite the fact that TGF-beta acts mainly as a "negative" growth factor, its interactions with IFNs in the antiviral assays resemble known effects of the typical "positive" peptide growth factors.
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