Type II Hypersensitivity
Complement dependent reactions: Antibody is directed against antigen on cells (such as circulating red blood cells) or extracellular materials (basement membrane). The resulting Ag-Ab complexes activate complement (via the classic pathway), leading to cell lysis or extracellular tissue damage.
In the above diagram, a red blood cell has antigen fixed on its surface to which antibody attaches. The attached antibody sets off the complement cascade, which ends with the formation of the "membrane attack complex" of C5-9 which causes lysis of the cell. Other complement components may be generated, such as the opsonin C3b.
Diseases in this complement dependent category include:
Antibody-dependent cell-mediated cytotoxicity (ADCC): Low concentrations of IgG or IgE (in the case of parasites) coat target cells. Inflammatory cells such as NK (natural killer) cells, monocytes, and granulocytes then bind to the immunoglobulin Fc receptors and lyse, but do not phagocytize, the target cells.
In the diagram above, a macrophage with Fc receptors on its surface is able to recognize a target cell coated with antibody via the Fc receptor portion of the attached antibody. The macrophage can then demolish the targeted cell by elaboration of proteases.
Examples of ADCC include:
Antireceptor antibodies: IgG antibody is directed against receptors in target cells, resulting in complement-mediated destruction of the receptors.
In the diagram above, antibody is directed against acetylcholine receptors at the motor end plate of a muscle, blocking the receptors and diminishing the muscular response. This is the mechanism for muscle weakness in myasthenia gravis.
Diseases caused by this mechanism include: