Our previous reports showed that DcR3.Fc modulates the differentiation of the macrophages toward M2-like phenotype and suppresses the secretion of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), and interferon-alpha (IFN-α) after viral infections and stimulation of the lipopolysaccharides (LPS) (8, 9). Here, IL6 is linked to viral infectious disease.