Recognition of immunogenic cell death by myeloid cells promotes inflammation
Hemidesmus indicus induces immunogenic death in human colorectal cancer cells
Endoplasmic reticulum stress leads to partial caspase-8 activation and exocytosis of calreticulin to the surface of the cell before apoptosis. As the cancer cells expose phosphatidylserine, they secrete ATP. Moreover, as the cancer cells undergo secondary necrosis and disrupt their plasma membrane, they release HMGB1. Calreticulin serves as an engulfment signal for dendritic cells. ATP acts on purinergic P2RX7 receptors on the surface of dendritic cells to stimulate the NLRP3 inflammasome, which via the activation of caspase-1 allows for the proteolytic maturation and secretion of IL-1beta. HMGB1 acts on TLR4 on dendritic cells to stimulate the production of proIL-1beta, as well as optimal tumor antigen processing. Additional, yet unknown signals emanating from dying cells induce dendritic cell maturation leading to the expression of suitable co-stimuli such as CD80 and CD86.
Immunogenic Cell Death Primes DC
see also:
Apoptosis
Ferroptosis