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Opsonization

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Opsonization

An opsonin (from the Greek opsonin, 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 a binding enhancer 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 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.

IUPAC definition

Antibody in blood serum that attaches to invading microorganisms and
other antigens to make them more susceptible to the action of phagocytes.

Note: Opsonin molecules include antibodies: IgG and IgA, proteins of the
complement system: C3b, C4b, and iC3b, mannose-binding lectin (initiates
the formation of C3b), etc.[1]

Mechanism

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, the negative charge is masked. Take note that the negative charge of the target doesn't 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 (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. Secondly they activate the Complement pathway as part of innate immunity and lead to formation of C3b

Examples

Examples of opsonin molecules include:

The most important are IgG and C3b.[2][broken citation]

See also

References

External links

  • Medical Subject Headings (MeSH)


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