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Tumour necrosis factor (TNF) plays a central role in chronic inflammatory diseases, and TNF inhibitors rapidly reduce tissue inflammation and clinical symptoms. Notably, TNF blockade often improves disease outcomes without eliminating autoreactive lymphocytes or autoantibody production, suggesting that TNF acts upstream of multiple inflammatory processes rather than directly determining antigen specificity.
Which TNF‑mediated process most directly explains its key role in sustaining autoimmune pathology?