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Tumour-necrosis factors are cytokines that are secreted by immune cell such as monocytes and lymphocytes. Tumour-necrosis factors can cause cell death or T cell activation and proliferation by binding to their receptors as a homotrimer or heterotrimer.
MLKL is regarded as an executor of the necroptotic inflammatory cell death pathway. Here authors show, by introducing a mutation into mouse MLKL representing a frequently occurring human single nucleotide polymorphism, that MLKL mutations could critically alter the inflammatory response and the clearance of Salmonella from organs upon infection.
New research shows that induction of ferroptosis can deplete synovial fibroblasts that are activated in rheumatoid arthritis, and that co-treatment with a TNF inhibitor enhances this depletion.
Intestinal ILC3s produce the epidermal growth factor family mediator HB-EGF, which protects the intestinal barrier against TNF-induced epithelial cell death.
