Immunology
Summary
Lesson Outline
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FAQs
The Complement Cascade, a part of the immune system, plays a crucial role in host defense against infections. It's a complex series of enzymatic reactions involving protein cleavage, during which inactived complement proteins are systematically split apart, or cleaved, effectively "activating" them. They work to enhance the ability of the immune system to clear microbes and damaged cells, promote inflammation, and attack the pathogen's plasma membrane through the formation of a Membrane Attack Complex (MAC).
There are three Complement Activation Pathways: Classical, Alternate and Lectin pathways. Each pathway is initiated by different stimuli, but all eventually lead to the cleavage and activation of C3, a complement protein. Once C3 is activated, the pathways converge, leading to opsonization of pathogens, inflammation, and even lysis of pathogens through the formation of the Membrane Attack Complex. The classical pathway is triggered by antibody-antigen interactions, while the lectin pathway recognizes microbial polysaccharides. The alternate pathway can be initiated spontaneously or by components of microorganisms.
Opsonization is a process in which pathogens are marked for destruction by the immune system. The Complement system contributes to opsonizaton when activated Complement proteins bind to the surface of pathogens, marking them for destruction. These 'tags' signal cells of the immune system like macrophages to engulf and destroy the pathogen. This function of the Complement system aids in effectively clearing pathogens from the body.
C3 cleavage is a pivotal step in the Complement Cascade. The cleavage of the C3 protein yields two active fragments, C3a and C3b. C3b is involved in opsonization, enhancing the ability of phagocytic cells to engulf bacteria. Additionally, C3b contributes to the formation of C5 convertase, an enzyme vital to the initiation of the terminal pathway of the complement system, culminating in the formation of the Membrane Attack Complex. Meanwhile, C3a is an anaphylatoxin that triggers inflammation.
The Membrane Attack Complex (MAC) is a key player in combating infections. It forms when complement proteins assemble on the membrane surface of pathogenic cells, creating a pore that disrupts the cell membrane integrity. This leads to the lysis and eventual death of the pathogen. The MAC is therefore considered one of the terminal effector functions of the Complement system, directly contributing to the elimination of pathogens from the body.