An opsonin (from the Greek opsōneîn, to prepare for eating) is any molecule that enhances phagocytosis by marking an antigen for an immune response (i.e., causes the phagocyte to "relish" the marked cell). However, the term is usually used in reference to molecules that act as binding enhancers for the process of phagocytosis, especially antibodies, which coat the negatively charged molecules on the membrane. Molecules that activate the complement system are also considered opsonins. Phagocytic cells do not have an Fc receptor for immunoglobulin M (IgM), making IgM ineffective in assisting phagocytosis. However, IgM is extremely efficient at activating complement and is, therefore, considered an opsonin. Opsonins can also refer to molecules that target a cell for destruction through the action of natural killer (NK) cells.
Opson in ancient Greece referred to the delicious side-dish of any meal, versus the sitos, or the staple of the meal. Opsonisation is thus the molecular mechanism whereby microbes are chemically modified to be made more "delicious" for inflammatory phagocytosis.
Both the membrane of a phagocytosing cell and its target have a negative charge (Zeta potential), making it difficult for the two cells to come close together. Once the opsonins attach to the target, however, the negative charge is masked. However, the negative charge of the target does not disappear. The opsonin simply overrides the charge, making it easier for white blood cells (phagocytic cells) to carry out phagocytosis. During the process of opsonization from the Greek word for "to make tasty" (also, opsonisation), antigens are bound by antibody or complement molecules. Phagocytic cells express receptors, CR1 and Fc receptors, that bind opsonin molecules, C3b and antibody, respectively. With the antigen coated in these molecules, binding of the antigen to the phagocyte is greatly enhanced. In fact, most phagocytic binding cannot occur without opsonization of the antigen. Furthermore, opsonization of the antigen and subsequent binding to an activated phagocyte will cause increased expression of complement receptors on neighboring phagocytes.
Mannose-binding lectins contribute in two ways. First, they coat the microbes as opsonins and enhance neutrophil reactivity against them. Second, they activate the lectin pathway of the complement pathway as part of innate immunity and lead to formation of C3b.
Examples of opsonin molecules include:
- Antibodies: IgG and IgM (IgM does not opsonize directly, but does assist in complement fixation and subsequent opsonization by C3b). This is a part of the classical complement pathway.
- Complement proteins: C3b, C4b, and iC3b
- As a part of the alternative complement pathway, the activation of a complement cascade converts C3 to C3b, a component that can serve as an opsonin when bound to the target surface. It is after C3b has bound to the capsular surface that bacteria can be recognized by phagocyte receptors and increase phagocytosis.
- Circulating proteins: Mannose-binding lectin and C-reactive protein.
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- Immunology at MCG 1/phagocyt
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