Summary

* Humoral immunity is mediated by antibodies and is the effector arm of the adaptive immune system responsible for defense against extracellular microbes and microbial toxins. The antibodies that provide protection against infection may be produced by long-lived antibody-secreting cells generated by the first exposure to microbial antigen or by reactivation of memory B cells by the antigen.

* The effector functions of antibodies include neutralization of antigens, Fc receptor-dependent phagocytosis of opsonized particles, and activation of the complement system.

* Antibodies block, or neutralize, the infectivity of microbes by binding to the microbes and sterically hindering interactions of the microbes with cellular receptors. Antibodies similarly block the pathologic actions of toxins by preventing binding of the toxins to host cells.

* Antibody-coated (opsonized) particles are phago-cytosed by binding of the Fc portions of the antibodies to phagocyte Fc receptors. There are several types of Fc receptors specific for different subclasses of IgG and for IgA and IgE antibodies, and different Fc receptors bind the antibodies with varying affinities. Attachment of antigen-complexed Ig to phagocyte Fc receptors also delivers signals that stimulate the microbicidal activities of phagocytes.

* The complement system consists of serum and membrane proteins that interact in a highly regulated manner to produce biologically active protein products. The three major pathways of complement activation are the alternative pathway, which is activated on microbial surfaces in the absence of antibody; the classical pathway, which is activated by antigen-antibody complexes; and the lectin pathway, initiated by collectins binding to antigens. These pathways generate enzymes that cleave the C3 protein, and cleaved products of C3 become covalently attached to microbial surfaces

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