![]() Membrane Attack Complex (Terminal Complement Complex C5b-9)Ĭomplement triggers the following immune functions: In the early 20th century, this controversy was resolved when it became understood that complement can act in combination with specific antibodies, or on its own in a non-specific way. Ehrlich believed that each antigen-specific amboceptor has its own specific complement, whereas Bordet believed that there is only one type of complement. Ehrlich, therefore, named this heat-labile component "complement", because it is something in the blood that "complements" the cells of the immune system. Those receptors, which we now call " antibodies", were called by Ehrlich "amboceptors" to emphasise their bifunctional binding capacity: They recognise and bind to a specific antigen, but they also recognise and bind to the heat-labile antimicrobial component of fresh serum. Upon immunization with an antigen, more of these receptors are formed, and they are then shed from the cells to circulate in the blood. According to this theory, the immune system consists of cells that have specific receptors on their surface to recognize antigens. In 1899, Paul Ehrlich renamed the heat-sensitive component "complement." Įhrlich introduced the term "complement" as part of his larger theory of the immune system. The heat-stable component was responsible for immunity against specific microorganisms, whereas the heat-sensitive component was responsible for the non-specific antimicrobial activity conferred by all normal sera. Jules Bordet, a young Belgian scientist in Paris at the Pasteur Institute, concluded that this principle has two components, one that maintained a "sensitizing" effect after being heated and one (alexin) whose toxic effect was lost after being heated. Nevertheless, the heat-inactivated serum, when injected into guinea pigs exposed to the cholera bacteria, maintained its ability to protect the animals from illness. Heating the serum destroyed its killing activity. By 1894, several laboratories had demonstrated that serum from guinea pigs that had recovered from cholera killed the cholera bacterium in vitro. In 1891, Hans Ernst August Buchner, noting the same property of blood in his experiments, named the killing property "alexin", which means "to ward off" in Greek. ![]() The killing activity disappeared when he heated the blood. In 1888, George Nuttall found that sheep blood serum had mild killing activity against the bacterium that causes anthrax. The alternative pathway accounts for the majority of terminal pathway activation and so therapeutic efforts in disease have revolved around its inhibition. Three biochemical pathways activate the complement system: the classical complement pathway, the alternative complement pathway, and the lectin pathway. They account for about 10% of the globulin fraction of blood serum. About 50 proteins and protein fragments make up the complement system, including serum proteins, and cell membrane receptors. The end result of this complement activation or complement fixation cascade is stimulation of phagocytes to clear foreign and damaged material, inflammation to attract additional phagocytes, and activation of the cell-killing membrane attack complex. 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 complement system consists of a number of small proteins that are synthesized by the liver, and circulate in the blood as inactive precursors. The complement system can, however, be recruited and brought into action by antibodies generated by the adaptive immune system. It is part of the innate immune system, which is not adaptable and does not change during an individual's lifetime. The complement system, also known as complement cascade, is a part of the immune system that enhances (complements) 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.
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