User:Adelanavratil/sandbox

= Mast Cell extracellular traps = As well as in neutrophils, formation of extracellular traps has been observed in mast cells.

A specific death of mast cells, so called MCETosis, in which rupture of plasmatic membrane, loose DNA in complex with histones, proteins, and cytoplasmic enzymes occurs, is similarly as NETosis an active process controlled by specific stimuli.

MCETs probably serve as an antimicrobial weapon if the cells itself fail in phagocytosis of the pathogens that are too spacious, e.g. clumped bacterias or fungi. Released DNA, histones, specific protease tryptase and antimicrobial proteins as cathelicidin LL-37 has its toxic role in killing or inhibiting the pathogens growth. This process can also be triggered by pharmaceutics like PMA or glucose oxidase which is leading to the ROS production. It turned out that MCETosis is also transcriptionally regulated by oxygen stress and hypoxia regulator HIF-1-alpha.

Both, NETosis and MCETosis, share previously described trap characteristics and differ in others. Significantly lower amount of mast cells (40%)  undergo „ETosis“ type of death under same stimuli and concentration of PMA than neutrophils (90%), which may reflect the high heterogeneity of mast cell population. Another difference is in composition of traps resulting from specific gene expression: elastase and myeloperoxidase is commonly found in NETs but in MCETs there has not been any expression found, mast cell-specific tryptase probably works as a substitution of these enzymes. When comparing the viability there has been demonstrated a survival in neutrophils after releasing NETs, but no such observation was described in mast cells.

Extracellular traps including MCETs are associated with e.g. psoriasis, where they are linked to IL-17/IL-23 axis.