Host-pathogen interactions are complex associations which evolve over long co-evolutionary histories. Pathogens exhibit different mechanisms to gain advantage over their host. Mimicry of host factors is an influential tool in subverting host mechanisms to ensure pathogenesis. This chapter discusses such molecular mimicry exhibited during viral infections. Understanding the evolutionary relationships, shared identity and functional impact of the virus encoded mimics is critical. With a particular emphasis on viral mimics and their association with cancer and autoimmune diseases, this chapter highlights the importance of molecular mimicry in virus biology.

• Klíčová slova
• Autoimmune diseases, Cancer, Host-pathogen interaction, Infectious diseases, Virus,
• MeSH
• autoimunitní nemoci metabolismus   virologie   imunologie   MeSH
• endokrinní systém metabolismus   MeSH
• interakce hostitele a patogenu MeSH
• lidé MeSH
• molekulární mimikry * MeSH
• nádory metabolismus   virologie   MeSH
• virové nemoci metabolismus   virologie   imunologie   MeSH
• viry metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Natural killer (NK) cells are a family of lymphocytes with a natural ability to kill infected, harmed, or malignantly transformed cells. As these cells are part of the innate immunity, the cytotoxic mechanisms are activated upon recognizing specific patterns without prior antigen sensitization. This recognition is crucial for NK cell function in the maintenance of homeostasis and immunosurveillance. NK cells not only act directly toward malignant cells but also participate in the complex immune response by producing cytokines or cross-talk with other immune cells. Cancer may be seen as a break of all immune defenses when malignant cells escape the immunity and invade surrounding tissues creating a microenvironment supporting tumor progression. This process may be reverted by intervening immune response with immunotherapy, which may restore immune recognition. NK cells are important effector cells for immunotherapy. They may be used for adoptive cell transfer, genetically modified with chimeric antigen receptors, or triggered with appropriate antibodies and other antibody-fragment-based recombinant therapeutic proteins tailored specifically for NK cell engagement. NK cell receptors, responsible for target recognition and activation of cytotoxic response, could also be targeted in immunotherapy, for example, by various bi-, tri-, or multi-specific fusion proteins designed to bridge the gap between tumor markers present on target cells and activation receptors expressed on NK cells. However, this kind of immunoactive therapeutics may be developed only with a deep functional and structural knowledge of NK cell receptor: ligand interactions. This review describes the recent developments in the fascinating protein-engineering field of NK cell immunotherapeutics.

• Klíčová slova
• ADCC, Adoptive cell transfer, BiKE, CAR NK cells, NK cell immunosurveillance, NK cells, Natural killer cell engagers, Therapeutic fusion proteins, TriKE, mAbs,
• MeSH
• antitumorózní látky * MeSH
• buňky NK patologie   MeSH
• chimerické antigenní receptory * terapeutické užití   MeSH
• imunologické faktory MeSH
• imunoterapie adoptivní MeSH
• imunoterapie MeSH
• lidé MeSH
• nádorové mikroprostředí MeSH
• nádory * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antitumorózní látky * MeSH
• chimerické antigenní receptory * MeSH
• imunologické faktory MeSH

Numbers of pathogenic bacteria can induce apoptosis in human host cells and modulate the cellular pathways responsible for inducing or inhibiting apoptosis. These pathogens are significantly recognized by host proteins and provoke the multitude of several signaling pathways and alter the cellular apoptotic stimuli. This process leads the bacterial entry into the mammalian cells and evokes a variety of responses like phagocytosis, release of mitochondrial cytochrome c, secretion of bacterial effectors, release of both apoptotic and inflammatory cytokines, and the triggering of apoptosis. Several mechanisms are involved in bacteria-induced apoptosis including, initiation of the endogenous death machinery, pore-forming proteins, and secretion of superantigens. Either small molecules or proteins may act as a binding partner responsible for forming the protein complexes and regulate enzymatic activity via protein-protein interactions. The bacteria induce apoptosis, attack the human cell and gain control over various types of cells and tissue. Since these processes are intricate in the defense mechanisms of host organisms against pathogenic bacteria and play an important function in host-pathogen interactions. In this chapter, we focus on the various bacterial-induced apoptosis mechanisms in host cells and discuss the important proteins and bacterial effectors that trigger the host cell apoptosis. The structural characterization of bacterial effector proteins and their interaction with human host cells are also considered.

• Klíčová slova
• Apoptosis, Bcl-2, CagA, Caspase, Cytochrome c, Hemolysin, Nf-kB, Pathogenic bacteria, TLR,
• MeSH
• apoptóza imunologie   MeSH
• Bacteria * imunologie   patogenita   MeSH
• bakteriální infekce imunologie   MeSH
• bakteriální proteiny * chemie   imunologie   MeSH
• faktory virulence * chemie   imunologie   MeSH
• lidé MeSH
• vztahy mezi strukturou a aktivitou MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• bakteriální proteiny * MeSH
• faktory virulence * MeSH