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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.
Human TNF is required for respiratory-burst-dependent immunity to Mycobacterium tuberculosis in macrophages but seems to be largely redundant physiologically.
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.