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Natural killer cell
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==Function== [[File:Nk cell.jpg|thumb|Natural Killer cells]] The majority of [[lymphocyte]]s, a [[leucocyte]] subgroup, are [[B cell|B]] or [[T cell]]s but approximately 15% of the lymphocyte population lack B or T cell receptors; these are NK cells.<ref name="MaleD2007" /> The latter develop in the [[bone marrow]] and have a half-life of approximately 7 days.<ref name="SompayracL2008" /> Most NK cells are found in the [[blood]], [[spleen]] or [[liver]] and enter tissues at sites of [[inflammation]] following [[infection]]. There are two NK cell subgroups dependent on the expression of either [[CD16]] (FcγRIII) or [[CD56]] [[cell surface receptors]].<ref name="Robson2014" /> NK cells play a major role in eliminating virally infected cells. Following infection, [[Virus|viruses]] block cell synthesis of [[major histocompatibility complex]] class I (MHCI) molecules.<ref name="MaleD2007" /> Presentation of MHC class I molecules at an infected cell’s surface is used by [[Cytotoxicity|cytotoxic]] T cells (Tc cells) to target and destroy the cell. By preventing MHC class I presentation, viruses ensure the cell is unrecognised and escapes elimination by Tc cells: this is where NK cells prove vitally important in the body’s immune response.<ref name="MaleD2007" /> NK cells express specialized receptors – [[killer inhibitory receptors]] (KIRs) – which can identify MHC class I molecules. Following recognition of the MHC class I molecule, the KIR inhibits NK cell cytotoxic activity and destruction of the target.<ref name="MaleD2007" /> Virally infected cells, lacking the surface expression of MHC class I molecules, can be targeted and eliminated by NK cells. NK cells can also target virally infected cells via expression of the [[IgG]] receptor CD16. This receptor binds antibodies attached to viral molecules on infected cell surfaces in a process called [[antibody-dependent cell mediated cytotoxicity]] (ADCC).<ref name="MaleD2007" /> '''NK Cell Cytotoxic Mechanisms''' NK cells can terminate an infected cell via several mechanisms including: *Direct cell-to-cell contact *Cytokine synthesis and release<ref name="MaleD2007" /> As [[Large Granular Lymphocytes]] (LGLs), NK cells utilize their granular structure to kill infected cells. On fusing with virally infected cells’ [[plasma membranes]], granules release their contents into the cell<ref name="MaleD2007" />. These contents include the [[protein]] [[perforin]], which perforates the infected cell's membrane, enabling entry of specialized ‘suicide’ [[Enzyme|enzymes]], including [[granzyme B]], into the virally infected cell; these initiate apoptosis (programmed cell death).<ref name="MaleD2007" /><ref name="SompayracL2008" /> Granzymes can also damage the infected cell directly and play a vital role in virally infected cell destruction. Apoptosis can also be triggered via the attachment of [[Fas ligands]] (FasL) on the NK cell surface to Fas proteins on the target cell, activating apoptosis-inducing signalling.<ref name="SompayracL2008" /> NK cells express two receptor types: *Activating *Inhibitory [[Activating receptors]] induce NK cells to eliminate infected cells, while [[inhibitory receptors]] block killing mechanisms<ref name="SompayracL2008" />. Resting NK cells synthesize [[Cytokine|cytokines]] and are capable of destroying virally infected cells but activated NK cells produce higher numbers of cytokines and are more efficient at eliminating infected cells<ref name="SompayracL2008" />. '''Factors Leading to NK cell Activation''' Several elements can produce NK cell activation, including: *The detection of [[Lipopolysaccharides|lipopolysaccharide]] (LPS, a bacterial cell wall constituent) *The release of various cytokines, e.g. [[Interferon alpha|IFN-α]] and [[Interferon beta|IFN-β]], when cells are infected with viruses LPS is bound by NK cell surface receptors, inducing responses including IFN-γ synthesis, which can prepare [[Macrophage|macrophages]] for activation. Following activation, macrophages synthesize TNF ([[Tumor necrosis factor|tumour necrosis factor]]), which binds a macrophage’s own surface receptors<ref name="SompayracL2008" />. This initiates [[interleukin 12|IL-12]] (interleukin-12) activation. The combination of TNF and IL-12 expression induces increased NK cell synthesis of [[Interferon gamma|IFN-γ]] leading to more macrophage priming, an example of an enhanced immune response via a positive feedback loop<ref name="SompayracL2008" />. TNF synthesis by macrophages also upregulates [[interleukin 2|IL-2]] expression on NK cell surfaces, NK cells respond to their own IL-2 synthesis and undergo rapid division<ref name="SompayracL2008" />.
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