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CD100–plexin-B1/B2 interactions facilitate immune responses of natural killer (NK) cells. We propose a model that NK cells recognize hepatitis C virus (HCV)-infected hepatocytes via CD100–plexin-B1/B2 interactions and facilitate the NK killing activity in HCV infection. Interferon (IFN)-α-based therapy not only efficiently activates NK cells, but improves the activation between NK effectors and HCV-infected cells via increased CD100 and plexin-B1/B2 expressions.
