Type II Hypersensitivity Reaction

Excerpt

Type II hypersensitivity reactions are antibody-mediated processes in which IgG or IgM antibodies target antigens on the cell surfaces or within the extracellular matrix. This antibody-antigen interaction initiates pathological mechanisms that lead to cell lysis, impaired cellular function, or tissue injury. The resulting tissue damage occurs through 3 primary mechanisms: opsonization with complement- and Fc receptor–mediated phagocytosis, complement- and Fc receptor–driven inflammation, and antibody-mediated disruption of normal cell signaling or function.

Common causes of type II hypersensitivity reactions include drugs such as anticonvulsants, sulfonamides, penicillin, thiazides, and heparin, as well as blood transfusions, group A Streptococcus infections, receptor autoantibodies in patients with Graves' disease and myasthenia gravis, and maternal sensitization to blood group antigens. The clinical manifestations are directly related to the underlying condition, ranging from acute cytopenias, hemolytic transfusion reactions, and hemolytic disease of the newborn to organ-specific injury, such as glomerulonephritis in anti-glomerular basement membrane (anti-GBM) disease or blistering skin disorders like pemphigus vulgaris. Treatment typically involves discontinuation of the offending agent, immunosuppressive therapy with corticosteroids or other agents, IVIG, or plasmapheresis in severe cases. Potential complications include chronic relapsing disease, treatment-related toxicities, organ failure, and life-threatening events such as pulmonary hemorrhage or intracranial bleeding, underscoring the need for timely recognition, accurate diagnosis, and coordinated interprofessional management.