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C5
C5 Full Name
complement component 5
C5 Introduction
Complement component C5 is a central protein in the human innate immune system—specifically within the complement system—playing a pivotal and integrative role in immune defense and the regulation of inflammation. As a key downstream molecule in the complement cascade, C5 converges signals from all upstream activation pathways—the classical, lectin, and alternative pathways—and initiates the terminal biological effects of the system. The activation of C5 is a decisive event in the complement pathway, catalyzed by specific C5 convertases. This process marks the starting point for the complement system's ultimate effector functions and represents a tightly regulated biochemical reaction, ensuring that the immune system can precisely eliminate pathogens and abnormal cells while avoiding damage to healthy host tissues.
Figure 1. C5a complement activation pathways. (Source: Giorgio C, et al. 2021)
The core biological functions of C5 are mediated through two active fragments generated upon its cleavage: C5a and C5b. C5a is a small peptide fragment, yet it is one of the most potent endogenous pro-inflammatory mediators and anaphylatoxins in the human body. It efficiently recruits and activates immune cells such as neutrophils and macrophages, guiding them to rapidly accumulate at sites of infection or injury, thereby initiating and amplifying local inflammatory responses. In contrast, the larger C5b fragment is responsible for launching the terminal lytic pathway of the complement system. Once generated, C5b immediately binds to cell membranes and sequentially recruits components C6, C7, C8, and multiple C9 molecules, assembling a large transmembrane pore-like structure known as the Membrane Attack Complex (MAC). This pore can insert directly into the membrane of pathogens (e.g., bacteria) or target cells, disrupting osmotic balance and ultimately leading to leakage of cellular contents and cell lysis—one of the most direct and effective means by which the complement system eliminates invaders.
When the complement system, particularly the C5 step, becomes overactivated or inappropriately triggered, it can lead to sustained attack on host tissues, resulting in serious autoimmune or inflammatory disorders. For instance, in paroxysmal nocturnal hemoglobinuria (PNH), deficiency of complement regulatory proteins on red blood cell surfaces leads to persistent MAC-mediated attack, causing chronic intravascular hemolysis. In certain autoimmune neurological diseases, such as anti-acetylcholine receptor (AChR) antibody-positive generalized myasthenia gravis (gMG) and anti-aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD), autoantibodies trigger the complement cascade at the neuromuscular junction or on astrocytes in the central nervous system. Here, C5 activation and MAC formation are key pathological steps leading to neurological damage.
Alternate Names for C5
C5; complement component 5; C5D; C5a; C5b; ECLZB; CPAMD4; complement C5; prepro-C5; C5a anaphylatoxin; anaphylatoxin C5a analog; C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4;
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