Describe Type II hypersensitivity mechanisms and give an example.

• A. Type II involves antibodies (IgG/IgM) directed at cell-surface or matrix antigens, triggering destruction or dysfunction (e.g., autoimmune hemolytic anemia, transfusion reactions).
• B. Type II involves immune complex deposition in tissues, activating complement.
• C. Type II is mediated by T cells only and involves delayed-type hypersensitivity.
• D. Type II is IgA-mediated mucosal immunity.

Answer: (A)

Type II hypersensitivity is driven by antibodies that bind to antigens on the surface of cells or in the extracellular matrix, leading to rapid dysfunction or destruction of those targets. The antibodies involved are typically IgG or IgM. When they bind, they can activate complement, which promotes cell lysis and phagocytosis; they can opsonize the target for destruction by phagocytes; they can mediate antibody-dependent cellular cytotoxicity; and in some cases they block or overstimulate receptors, altering normal cellular function.

A classic illustration is autoimmune hemolytic anemia, where antibodies target red blood cell surface antigens and cause destruction of RBCs. Transfusion reactions are another outcome when antibodies against donor cell antigens trigger rapid destruction of transfused cells. Other real-world examples include Goodpasture syndrome (antibodies against basement membranes in kidney and lung) and pemphigus (antibodies against desmosomes in skin), which all fit the pattern of antibodies causing direct effects on cells or matrices rather than relying on immune complex deposition.

This differs from other hypersensitivity types: immune complex–mediated reactions involve deposition of antibody–antigen complexes in tissues, not direct targeting of cells; T-cell–mediated delayed-type hypersensitivity relies on T lymphocytes rather than antibodies; and IgA-mediated mucosal immunity involves a different antibody class and immune setting.