A mechanism of innate immunity in which the liver markedly increases its synthesis of certain immune proteins, the acute-phase proteins, in response to infection. This change in protein output by liver cells is triggered by tumour necrosis factor α‎ (TNF-α‎), interleukin-1 (IL-1), and IL-6, which are released by macrophages following their activation as a result of contact with bacteria or other pathogens. The main acute-phase proteins are C-reactive protein and mannose-binding lectin. These behave like antibodies but are nonspecific and bind to a much broader range of targets. Their binding sites attach to surface components of bacteria and fungi, making them more susceptible to ingestion by phagocytic cells (see opsonization); they also activate the complement system of immune proteins, which initiates destruction of the targeted cell.