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The complement system is a crucial component of the innate immune system, enhancing the ability of antibodies and phagocytic cells to clear microbes, damaged cells, and pathogens from an organism. It plays a significant role in inducing acute inflammation, killing microbes, and removing apoptotic host cells. Interestingly, the complement system also has implications for muscle movement and function, particularly in the context of post-exercise response and muscle disorders. For instance, complement fragments C3a and C5a have been found to increase smooth muscle contraction and play a role in muscle regeneration. Additionally, complement activation has been linked to muscle weakness in certain muscle disorders, such as myasthenia gravis.
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What You'll Learn
- The complement system is a part of the innate immune system
- It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells
- Complement fragments C3a and C5a are anaphylatoxins that mediate inflammation
- Complement activation is observed post-exposure to physical stress stimuli
- Complement therapies are used to treat myasthenia gravis
The complement system is a part of the innate immune system
The complement system, also known as the complement cascade, is a crucial component of the innate immune system. It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane. The term "complement" was introduced by Paul Ehrlich in 1899 as part of his theory of the immune system. Ehrlich observed that upon immunization with an antigen, certain receptors on the surface of immune cells, now known as antibodies, increase in number and circulate in the blood. These antibodies can recognise and bind to specific antigens and complement the cells of the immune system.
The complement system consists of a series of small, inactive, liver-synthesised protein precursors circulating in the blood. These proteins are activated by various triggers, such as the presence of pathogens or damaged cells, leading to a cascade of proteolytic cleavages. The classical pathway, one of the three main pathways of complement activation, is typically triggered by antigen-antibody complexes. However, the alternative pathway can be activated by foreign material, pathogens, or damaged cells, even in the absence of antibodies.
The activation of the complement system results in the stimulation of phagocytes, which clear foreign and damaged material through a process called opsonisation. It also promotes inflammation to attract additional phagocytes and initiate an immune response. Additionally, the complement system contributes to the destruction of microbes and the attack of pathogen cell membranes. This system is so effective that even bacteria and viruses have adapted ways to escape complement activation and utilise the host's complement receptors to infect cells.
The complement cascade has been observed in species earlier than vertebrates, such as the protostome horseshoe crab, indicating that this defence mechanism has ancient evolutionary origins. The study of the complement system and its role in innate immunity has provided valuable insights into the complex relationship between the immune system and diseases, including autoimmune disorders, tumours, and neurodegenerative conditions.
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It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells
The complement system, also known as the complement cascade, is a crucial part of the innate immune system. It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism. The complement system consists of a series of proteins that result in the destruction of microbes. It is composed of about 50 serum and membrane proteins with tightly regulated proteolytic activation cascades that result in the production of effector molecules with multiple biological functions.
The complement system has three pathways of activation: the classical pathway, the alternative pathway, and the lectin pathway. The classical pathway is triggered by the activation of the C1-complex, which occurs when C1q binds to IgM or IgG complexed with antigens. The alternative pathway can be activated by spontaneous complement component 3 (C3) hydrolysis, foreign material, pathogens, or damaged cells. The lectin pathway, which is homologous to the classical pathway, is activated by the binding of mannose-binding lectin (MBL) to mannose residues on the pathogen surface.
In all three pathways, C3-convertase cleaves and activates component C3, creating C3a and C3b, which leads to a cascade of further cleavage and activation events. C3b binds to the surface of pathogens, leading to greater internalization by phagocytic cells through opsonization. The complement system also promotes inflammation, which attracts additional phagocytes, and activates the cell-killing membrane attack.
The complement system plays a crucial role in host defense by mediating inflammation through the interaction of C3a and C5a with their respective receptors. This results in increased vascular permeability, smooth muscle contraction, and the recruitment and activation of immune cells. Additionally, the complement system contributes to the activation of the adaptive immune response through the mobilization and activation of antigen-presenting cells (APCs).
The activation of complement can also lead to the production of a strong antibody response. B cells, with antigen receptors specific for a given pathogen, receive an augmented signal when the pathogen is coated with C3dg, a breakdown product of C3b. This demonstrates how the complement system, an innate humoral immune response, can contribute to activating the adaptive humoral immunity.
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Complement fragments C3a and C5a are anaphylatoxins that mediate inflammation
The complement system, also known as the complement cascade, is a crucial part of the innate immune system. It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack pathogens' cell membranes. The complement system consists of about 35–50 small, inactive, liver-synthesised protein precursors circulating in the blood.
C3a and C5a also play a role in the regeneration of bone, cardiac muscle, and skeletal muscle, as well as stem cell engraftment. They are involved in complement activation, immune defence, and immune regulation. In all pathways of complement activation, the pivotal step is the conversion of the component C3 to C3b and C3a, which is responsible for eliminating pathogens and opsonization. C3a and C5a contribute to the initiation of the adaptive immune response by activating mast cells, recruiting antibodies, complement, and phagocytic cells, and increasing fluid in the tissue.
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Complement activation is observed post-exposure to physical stress stimuli
The complement system, also known as the complement cascade, is an enzyme cascade that is part of the innate immune system. It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack pathogens' cell membranes. The system consists of over 30 proteins that are either soluble in the blood or membrane-associated.
The complement system was first discovered in the 1890s when it was found to aid or "complement" the killing of bacteria by antibodies in serum. The term "complement" was introduced by Ehrlich as part of his theory of the immune system. According to this theory, the immune system consists of cells with specific receptors that recognise antigens. When an antigen is introduced, more receptors are formed and shed into the blood, where they bind to the antigen and a heat-labile antimicrobial component of fresh serum. This heat-labile component was named "complement" by Ehrlich because it complements the cells of the immune system.
The complement system can be activated through three pathways: the classical pathway, the alternative pathway, and the mannose-binding lectin pathway. The classical pathway is triggered by the activation of the C1-complex, which occurs when C1q binds to IgM or IgG complexed with antigens. The alternative pathway can be activated by spontaneous C3 hydrolysis, foreign material, pathogens, or damaged cells. The mannose-binding lectin pathway can be activated by C3 hydrolysis or antigens without the presence of antibodies.
Complement activation has been observed post-exposure to physical stress stimuli. While the precise molecular processes underlying this activation remain to be fully understood, some possible mechanisms have been proposed. These mechanisms are mainly based on metabolic shifts that occur within the microenvironment of skeletal muscle and adipose tissue. For example, lactate, an organic ion, accumulates in the cytoplasm of muscle cells during increased muscle use due to repetitive contractions. This leads to the release of glucose during glycogenolysis, which then enters the glycolytic pathway. Animal models have also demonstrated the complement's involvement in the early stages of increased muscle use and its role in modulating the immune system's response to muscle damage.
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Complement therapies are used to treat myasthenia gravis
The complement system, also known as the complement cascade, is a crucial component of the innate immune system. It enhances the ability of antibodies and phagocytic cells to clear microbes, damaged cells, and pathogens from an organism. The term "complement" was first introduced by Ehrlich as part of his theory of the immune system.
Myasthenia gravis (MG) is an autoimmune disease where specific antibodies lead to endplate dysfunction, particularly affecting the muscles. It is estimated that 80-85% of patients have antibodies directed against the acetylcholine receptor (AChR) on the post-synaptic membrane. The disease is characterised by weakness and fatigability of ocular, bulbar, and skeletal muscles.
Complement therapies are being explored as a potential treatment for myasthenia gravis. Anti-complement drugs have shown promise in treating AChR-positive MG patients by inhibiting the complement cascade and reducing the formation of the membrane attack complex (MAC). Eculizumab, for example, has been approved for the treatment of AChR antibody-positive gMG. However, the high costs of these drugs limit their usage. Other complement inhibitors targeting C5 are currently in phase III studies.
The development of complement inhibitors has the potential to improve the quality of life of MG patients, especially those who do not respond adequately to available drugs or exhibit poor tolerance. However, it is important to note that complement inhibition alone may not lead to remission, and lifelong treatment may be necessary. Furthermore, there is a need to identify biomarkers that can predict the therapeutic response to complement-directed therapies better.
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Frequently asked questions
The complement system, also known as the complement cascade, is a part of the innate immune system. It enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane.
The complement system helps or "complements" the ability of antibodies and phagocytic cells to clear pathogens from an organism. It is triggered by the characteristic molecular patterns of carbohydrates and lipids found on certain pathogens.
The complement system consists of a number of small, inactive, liver-synthesized protein precursors circulating in the blood. When stimulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end result is a massive amplification of the response and the activation of the cell-killing membrane attack complex.
The term "complement" was coined by Paul Ehrlich in 1899. Ehrlich introduced the term as part of his larger theory of the immune system. He believed that each antigen-specific amboceptor has its own specific complement, while Bordet believed that there is only one type of complement.
