[2] ICD or immunogenic apoptosis is a form of cell death resulting in a regulated activation of the immune response.
Endoplasmic reticulum (ER) stress is generally recognised as a causative agent for ICD, with high production of reactive oxygen species (ROS).
Type I inducers cause stress to the ER only as collateral damage, mainly targeting DNA or chromatin maintenance apparatus or membrane components.
Calreticulin (CRT), one of the DAMP molecules which is normally in the lumen of the endoplasmic reticulum, is translocated after the induction of immunogenic death to the surface of dying cell.
Other important surface exposed DAMPs are heat-shock proteins (HSPs), namely HSP70 and HSP90, which under stress condition also translocate to the plasma membrane.
[2] HMGB1 is considered to be a marker of late ICD and its release to the extracellular space seems to be required for the optimal presentation of antigens by dendritic cells.
ATP released during immunogenic cell death functions as a "find-me" signal for phagocytes when secreted and induces their attraction to the site of ICD.
The concept of using ICD in antitumor therapy has started taking shape with the identification of some inducers mentioned above, which have a potential as anti-tumor vaccination strategies.
[2][1] Pyroptosis is a distinct type of regulated cell death, exhibiting a necrotic morphology and cellular content spilling.
[11] Cytosolic presence of bacterial metabolites or structures, termed pathogen associated molecular patterns (PAMPs), initiates the pyroptotic response.
Detection of such PAMPs by some members of Nod-like receptor family (NLRs), absent in melanoma 2 (AIM2) or pyrin leads to the assembly of an inflammasome structure and caspase 1 activation.
Lipid peroxidation can be inhibited in the cell by glutathione peroxidase 4 (GPX4), making the balance of these enzymes a central regulator of ferroptosis.
The precise mechanisms leading to the formation of permeability-transition pore complexes, which assemble between the inner and outer mitochondrial membranes, are still unknown.
This cell death is initiated by the DNA damage response components, mainly poly(ADP-ribose) polymerase 1(PARP1).
[2] This type of cell death has been linked to some pathologies, such as some cardiovascular and renal disorders, diabetes, cerebral ischemia, and neurodegeneration.
NET formation is generally induced in response to microbial infections, but pathologically also in sterile conditions of some inflammatory diseases.
ROS inside the cell trigger release of elastase (ELANE) and myeloperoxidase (MPO), their translocation to the nucleus and cytoskeleton remodeling.