Fig. 1

NK cells execute multiple tasks in innate immunity, they are i) responsible for direct defence of the host organism by checking for and eliminating stressed or transformed autologous cells with low MHC I levels, ii) execute ADCC in case of virus infected cells by binding IgG to FcγRIII (CD16) receptor, or iii) eliminate microbes by recognition of conserved structures with different PRRs. On the other side NK cells influence maturation and activation of other immune cells and e.g. can kill immature DCs or M0 and M2 macrophages and thus selectively let activated APCs present antigens to T cells in a controlled manner. Activated T cells can also be killed by NK cell-mediated lysis. NK cells therefore directly manipulate the adaptive immune response by influencing antigen presentation and quantity of other immune cells. Immune cross talk often implies bidirectional activation, which leads, like activating signalling in direct host defence, to enhanced proliferation, cytokine production, and cytotoxicity by increased expression of granzymes, perforin, and granulysin. Numerous cytokines can so be released by NK cells, primarily IFN-γ, TNF-α, and GM-CSF, but also many ILs and various inflammatory chemokines, which attract and traffic e.g. T cells, DCs, monocytes, eosinophils, basophils, or neutrophils. ADCC, antibody-dependent cell-mediated cytotoxicity; CCL, C-C motif ligand; CTL, cytotoxic T lymphocyte; CXCL, C-X-C motif ligand; DNAM-1, DNAX accessory molecule-1; FASL, fragment apoptosis stimulating ligand; GM-CSF, granulocyte macrophage colony-stimulating factor; IFN, interferon; IL, interleukin; MHC I, major histocompatibility complex I; MIP1, macrophage inflammatory protein 1; NK cells, natural killer cells; NKG2D, natural-killer group 2, member D; NKp30/46, natural killer cell p30/46-related protein; NLR, nucleotide oligomerization domain (NOD)-like receptor; PAMP, pathogen-associated molecular pattern; PRR, pattern recognition receptor; RLR, RNA helicase retinoic inducible gene I (RIG-I)-like receptor; TCR, T cell receptor; TLR, Toll-like receptor; TNF, tumour necrosis factor; TRAIL, TNF-related apoptosis-inducing ligand; XCL, X-C motif ligand