FADD deficiency sensitized more efficiently for TNFR1-mediated necroptosis than caspase-8 deficiency pointing to a caspase-8 independent inhibitory activity of FADD on TNF-induced necroptosis.
Mixed bone marrow chimeric mice demonstrate that caspase-8 deficiency does not confer preferential expansion of synovial macrophage and dendritic cell populations, nor do caspase-8-deficient synovial populations succumb to RIPK3-mediated necroptotic death.
Studies of patients with autoimmune lymphoproliferative syndrome (ALPS) or caspase-8 deficiency state (CEDS) demonstrated the ability of gene expression microarray analyses and small interfering RNAs (siRNA) to establish the physiologically important roles of NRAS, caspase-10, and caspase-8 for normal lymphocyte apoptosis and activation.
Thus, caspase-8 deficiency in humans is compatible with normal development and shows that caspase-8 has a postnatal role in immune activation of naive lymphocytes.
Thus, caspase-8 deficiency in humans is compatible with normal development and shows that caspase-8 has a postnatal role in immune activation of naive lymphocytes.