NK (natural killer) cells are lymphoid, often granular, cells that are an important component of natural immunity, along with the complement system and phagocytic activity. NK cells are defined as cells of the innate immune response. Recent studies, however, demonstrate that specific subsets of mouse NK cells can develop specific immunological “memory” to a variety of antigens. NK cells do not require prior contact with foreign (i.e. viral or tumor) antigens and are not MHC-restricted. NK cells are involved in antibody- -dependent cell-mediated cytotoxicity (ADCC) and are thus able to destroy target cells coated with antibodies. NK cells express strong cytotoxicity against neoplastic and virus-infected cells after the activation of the perforin/granzyme system. They express stimulatory and inhibitory receptors on cell surface that recognize self-MHC proteins and regulate their activation. Mice NK cells express a large number of receptors, such as Ly49 receptors, which can inhibit the activity of MHC class I molecules. This short review shows an important role of NK cells as the effector arms of the immune system.
Tetraspanins are a superfamily of surface membrane proteins characterized by their four transmembrane domains. They associate laterally with their partner proteins or with each other, and form large integrated signaling complexes or tetraspanin enriched microdomains (TEMs). Consequently, those proteins are involved in the coordination of many biological processes, including cell adhesion, migration and proliferation. Tetraspanins also play a prominent role in the pathogenesis of viral infectious diseases. Viruses can exploit tetraspanins for the modulation of the host immune response and/or for subsequent immune evasion. Thus tetraspanins are attractive novel antiviral therapeutic targets, which may provides a novel strategy to inhibit critical processes of viral infection. This review summarizes the involvement of tetraspanins in viral life cycles, including adsorption, entry, viral trafficking, fusion events and viral release.
This work describes the role of membrane bridges in the spread of ectromelia virus (ECTV) Moscow strain (ECTV-MOS) in vitro in BALB/3T3 and Vero cells. In this research, immunofluorescence techniques were used: cells were fixed, stained for the presence of viral antigens, F-actin, and DNA, and viewed under a fluorescence microscope. In both cell lines, ECTV-MOS infection induces production of two types of actin-rich protrusions: tiny actin tails or long filopodia-like structures. It appears that both types contribute to the spread of ECTV-MOS particles and may be classified as membrane bridges.