In the case of a toxin molecule in the blood, the simple binding of an antibody to the toxin molecule is probably all that is required to remove the problem. But with microbes, an antibody by itself can't be expect to remove the microbe. Also required are "hit-men" to deal with the microbe after the antibody provides the identification.
Earlier, in the context of innate immunity, we encountered the concept of an opsonin. But by far the most effective opsonins are antibodies of the type IgG and IgM. Once the antibody binds to its antigen on a microbe, the Fc region of the antibody can now bind to an Fc receptor on a neutrophil. Phagocytosis then rapidly follows.
Phagocytosis by itself may not be enough to kill the microbes. It is macrophages that deal with longer term, chronic infections. For example, some phagocytized pathogens are difficult for macrophages to kill and require that the macrophages become "activated". In this supercharged state, the lysosomes are more likely to fuse with the phagosome and release a more potent mix into the phagolysosome. CD4+ Tcells of the type TH1 provide this function. They bind to the macrophage via their T cell receptor and release INF-gamma.
The figure to the right is from the earlier page on the complement system. Recall that the complement system can be activated either in innate immunity or via antibodies bound to microbes. The antibodies can be either IgG or IgM, especially the pentameric form.
Which one of the following best describes how a TH1 cell identifies a macrophage to activate?
a. By binding to the macrophage using molecules of innate immunity
b. By its T cell receptor binding to peptide antigen displayed on MHC II molecules
c. By its T cell receptor binding to peptide antigen displayed on MHC I molecules
d. By binding to the macrophage with C3b attached.
e. By the macrophage using a Fc receptor to bind to IgG.
Eosinophils have an Fc receptor for IgE. After IgE binds to the cuticle of a helminth worm, the Fc receptor on an eosinophil can bind to the Fc region on the IgE.
Mast cells are found throughout the body and especially under epithelia. They are jam-packed with large secretion vesicles filled with inflammatory paracrines, including much histamine. On their membranes, the mast cells have Fc receptors for IgE. Observe below how IgE binds to these receptors. When the multivalent antigen appears again, it causes the the Fc receptors to cluster. As a result, the receptors phosphorylate each other through the action of a type of protein kinase called tyrosine kinase. This leads to exocytosis of the vesicles and synthesis of prostaglandins and leukotrienes.
