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Blood Cell Destruction in Type 2 Hypersensitivity

Opsonization
  • Coats cells in antibodies, leads to phagocytosis and/or complement activation.
— IgG binding of cell-bound antigens initiates the complement cascade, which generates active proteins. — Some of these proteins, including C3b, are deposited on the cell surface.
  • Thus, neutrophils can recognize the opsonized cell via two mechanisms:
— Its high-affinity Fc receptor can bind with the Fc region of the IgG antibody. — Its C3b receptor can bind with the deposited complement on the cell’s surface.
  • In both cases, binding promotes phagocytosis of the host cell.
Opsonization Examples:
  • Transfusion reactions can occur when donor cell antigens are bound by host IgG antibodies.
— If complement protein C1 binds also those antibodies, the complement cascade ultimately produces a Membrane Attack Complex (MAC); the MAC allows massive water influx into the cell, causing its lysis.
  • Hemolytic disease of the fetus and newborn: maternal anti-Rh+ antibodies attack fetal Rh+ red blood cells.
— The maternal antibodies were produced in response to prior pregnancy with a Rh+ fetus; upon subsequent exposure to a another Rh+ fetus, the maternal antibodies readily react.
  • Autoimmune blood cell destruction occurs when one’s own blood cells are targeted:
— Anemia can result when red blood cells are destroyed. — Agranulocytosis, when granulocytes, such as neutrophil, are targeted. — Thrombocytopenia, when platelets are removed.
  • Drug hapten reactions occur when haptens adhere directly to the cell surface.
— When IgG antibodies bind the hapten, the complement system is activated and phagocytosis occurs. Penicillin is an example of a drug that can cause type II hypersensitivity reactions.