Different opsonin molecules perform different functions, including antibody mediated opsonization, complement protein mediated opsonization and circulating protein mediated opsonization.
Among these, antibody mediated opsonization is the process by which a pathogen is marked for ingestion and eliminated by a phagocyte.The Fab region of the antibody binds to the antigen, whereas the Fc region of the antibody binds to an Fc receptor on the phagocyte, facilitating phagocytosis. The antigen-antibody complex can also activate complement through the classical complement pathway. Phagocytic cells do not have an Fc receptor for immunoglobulin M (IgM), making IgM ineffective in assisting phagocytosis alone. However, IgM is extremely efficient at activating complement and is, therefore, considered an opsonin. IgG antibodies are also capable of binding immune effector cells via their Fc domain, triggering a release of lysis products from the bound immune effector cell (monocytes, neutrophils, eosinophils, and natural killer cells). This process, called antibody-dependent cellular cytotoxicity / ADCC, can cause inflammation of surrounding tissues and damage to healthy cells.
The complement system is a part of the innate immune response. C3b, C4b, and C1q are important complement proteins that mediate opsonization. As a part of the alternative complement pathway, the spontaneous activation of a complement cascade converts C3 to C3b, a component that can serve as an opsonin when bound to an antigen's surface. Antibodies can also activate complement via the classical pathway, resulting in deposition of C3b and C4b onto the antigen surface. After C3b has bound to the surface of an antigen, it can be recognized by phagocyte receptors that signal for phagocytosis. Complement receptor 1 is expressed on all phagocytes and recognizes a number of complement opsonins, including C3b and C4b which are both parts of C3-convertase.
Pentraxins, collectins, and ficolins are all circulating proteins that mediate opsonization. They are secreted Pattern recognition receptors (PRRs). These molecules coat the microbes as opsonins and enhance neutrophil reactivity against them through a number of mechanisms.
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