Receptor Crosslinkage

IgE-mediated degranulation begins when an allergen crosslinks IgE that is bound (fixed) to the Fc receptor on the surface of a mast cell or basophil. In itself, the binding of IgE to FceRI apparently has no effect on a target cell. It is only after allergen crosslinks the fixed IgE-receptor complex that degranulation proceeds. The importance of crosslinkage is indicated by the inability of monovalent allergens, which cannot crosslink the fixed IgE, to trigger degranulation.

Experiments have revealed that the essential step in degranulation is crosslinkage of two or more FceRI mole-cules—with or without bound IgE. Although crosslinkage is normally effected by the interaction of fixed IgE with divalent or multivalent allergen, it also can be effected by a variety of experimental means that bypass the need for allergen and in some cases even for IgE (Figure 16-5).

(a) Allergen crosslinkage of cell-bound IgE

Allergen

IgE Fc receptor

(a) Allergen crosslinkage of cell-bound IgE

Allergen

Mast cell

(b) Antibody crosslinkage of IgE

Anti-isotype Ab

(b) Antibody crosslinkage of IgE

Idiotype Antiidiotype Interaction

Anti-idiotype Ab

FIGURE 16-5

Anti-idiotype Ab

(c) Chemical crosslinkage of IgE

Crosslinking chemical

(c) Chemical crosslinkage of IgE

Crosslinking chemical

(d) Crosslinkage of IgE receptors by anti-receptor antibody

(d) Crosslinkage of IgE receptors by anti-receptor antibody

Anti-receptor Ab

Anti-receptor Ab

(e) Enhanced Ca2+ influx by ionophore that increases membrane permeability to Ca2+

(e) Enhanced Ca2+ influx by ionophore that increases membrane permeability to Ca2+

Ca2+ Ionophore |

Ca2+ Ionophore |

FIGURE 16-5

Schematic diagrams of mechanisms that can trigger degranulation of mast cells. Note that mechanisms (b) and (c) do not require allergen; mechanisms (d) and (e) require neither allergen nor IgE; and mechanism (e) does not even require receptor crosslinkage.

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