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Sylwia Borys, Ronza Khozmi, Wiesława Kranc, Artur Bryja, Marta Dyszkiewicz-Konwińska, Michal Jeseta and Bartosz Kempisty
Cell death plays an important role in maintaining the homeostasis of multicellular organisms. It can occur in a controlled manner by apoptosis or autophagy. Cell death which occurs regardless of regulatory factors include necrosis, mitotic catastrophe or oncosis.
Apoptosis and necrosis are cellular process that leads to cell death. However their mechanisms are different, although factors triggering them can be similar. Necrosis and apoptosis have many different characteristics in terms of biochemistry and morphology.
There are two main pathways of apoptosis induction signal: receptor - dependent and mitochondrial. The outsider apoptotic pathway is induced by external factors stimulating membrane receptors having an intracellular domain called death domain.
Mitochondrial apoptotic pathway is activated by increased concentration of reactive oxygen species (ROS), DNA damage, disorders electrolyte transport and an increase in the concentration of the calcium ions in the cytoplasm. In response to stress-factors, mitochondrial channels are opened, so that is released into the cytoplasm cytochrome C. This work is aimed at an overall description of exchanged processes.
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The immune checkpoints, such as cytotoxic T-lymphocyte-associated antigen 4, programmedcelldeath protein and programmedcelldeath protein ligand 1, were the normal self-regulatory pathways to control T-cell activities in human body. In tumor microenvironment, these molecules were overexpressed to inhibit the normal T-cell function and survival, leading to an escape from the destruction from immune system. The immune checkpoint inhibitors (ICPis) block this mechanism and restore the T-cell immunity to achieve tumor destructions. However, the
Dragana Jovanović, Marina Roksandić-Milenković, Jelena Kotur-Stevuljević, Vesna Ćeriman, Ivana Vukanić, Natalija Samardžić, Spasoje Popević, Branislav Ilić, Milija Gajić, Marioara Simon, Ioan Simon, Vesna Spasojević-Kalimanovska, Milica Belić, Damjan Mirkov, Zorica Šumarac and Vladislav Milenković
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-stimulatory and co-inhibitory signals, which normally regulates immune response and prevents autoimmunity, is deranged by the cancer cell to escape immune surveillance ( 1 - 2 ).
Among co-inhibitory signals, immune checkpoints represent immunological breaks that repress activating effects in order to avoid unchecked self-destruction of normal tissues ( 3 ). Cytotoxic T lymphocyte Antigen 4 (CTLA-4) and ProgrammedCellDeath protein 1 (PD-1) are the two main inhibitory checkpoint pathways involved. CTLA-4 exerts its effects when it is expressed on the surface of CD4+ and CD8
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