Komplementtikaskadin

Komplementtikaskadin, or the complement cascade, refers to a series of biochemical reactions in the immune system that play a crucial role in enhancing the ability to clear microbes and damaged cells from an organism, promoting inflammation, and attacking the pathogen’s cell membrane. This process primarily involves a group of proteins known as complement proteins, which are found in the blood serum and are part of the innate immune system.

The cascade is typically initiated by one of three pathways: the classical pathway, the lectin pathway, and the alternative pathway. The classical pathway is triggered by antibodies binding to antigens on the surface of pathogens, while the lectin pathway is activated by mannose-binding lectin or other mannose-binding proteins recognizing carbohydrate patterns on microbial surfaces. The alternative pathway, on the other hand, is spontaneously activated by microbial surfaces, which lack the regulatory proteins found on host cells.

Once activated, the cascade proceeds through a series of sequential reactions, leading to the formation of the membrane attack complex (MAC). This complex creates pores in the microbial cell membrane, causing cell lysis and death. Additionally, complement proteins contribute to opsonization, marking pathogens for phagocytosis by immune cells, and promote inflammation through the release of anaphylatoxins, such as C3a and C5a.

Regulation of the complement system is essential to prevent excessive activation, which could lead to tissue damage. Proteins like factor H, factor I, and decay-accelerating factors (DAFs) help control the cascade by inhibiting its progression or promoting its termination. Dysregulation of the complement system has been linked to various diseases, including autoimmune disorders, inflammatory conditions, and certain infections. Research into the complement cascade continues to provide insights into immune function and potential therapeutic targets for immune-mediated diseases.