![]() 1 It was subsequently discovered that MAC could also be formed in response to cell-bound mannose-binding lectin (the lectin pathway) or C3 tickover (the alternative pathway). These recent insights into the mechanisms of action of MAC provide an updated framework to therapeutic approaches that can target MAC assembly, signaling, and proinflammatory effects in various complement-mediated diseases.Ĭomplement membrane attack complex (MAC) was first identified as an effector of the immune system in which certain classes of antibodies trigger assembly of a pore-forming complex that inserts into the lipid bilayer of the plasma membrane (the classic pathway), complementing the ability of antibodies to kill cells. MAC-activated cells have been found to express proinflammatory proteins-often through NF-κB–dependent transcription, assemble inflammasomes, enabling processing, and facilitate secretion of IL-1β and IL-18, as well as other signaling pathways. ![]() In addition, new mechanisms of MAC-mediated signaling and its contribution to disease pathogenesis have recently come to light. New discoveries into the structure and biophysical properties of MAC revealed heterogeneous MAC precursors and conformations that provide insights into MAC function. In the absence of lysis, MAC may induce intracellular signaling and cell activation, responses implicated in a variety of autoimmune, inflammatory, and transplant disease settings. Nucleated cells resist MAC-mediated cytolysis by expression of inhibitors that block MAC assembly or by rapid removal of MAC through endocytosis or shedding. The complement membrane attack complex (MAC) is classically known as a cytolytic effector of innate and adaptive immunity that forms pores in the plasma membrane of pathogens or targeted cells, leading to osmolysis.
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