Autoimmune hemolytic anemia involving IgG corresponds to which hypersensitivity type?

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Multiple Choice

Autoimmune hemolytic anemia involving IgG corresponds to which hypersensitivity type?

Explanation:
This question tests recognizing how antibody-mediated destruction of cells fits into hypersensitivity types. When IgG is directed against antigens on the surface of red blood cells, the immune response causes cytotoxic destruction of those cells. This is the hallmark of a Type II hypersensitivity reaction. Mechanistically, IgG binding to RBC surface proteins marks the cells for attack by effector systems. The spleen’s macrophages can recognize the Fc portion of IgG-coated red cells and phagocytose them (opsonization), leading to extravascular hemolysis. Complement activation can also occur, contributing to cell lysis, sometimes within blood vessels (intravascular hemolysis). The key point is that the immune attack targets cell-surface antigens with antibodies, rather than forming soluble immune complexes or involving T-cell–mediated delayed responses. In contrast, Type I involves IgE-mediated allergic reactions, Type III involves immune complex deposition causing tissue injury, and Type IV is a T-cell–mediated delayed-type reaction. Since the destruction is driven by antibodies binding to cell surfaces and triggering effector mechanisms, it fits Type II hypersensitivity.

This question tests recognizing how antibody-mediated destruction of cells fits into hypersensitivity types. When IgG is directed against antigens on the surface of red blood cells, the immune response causes cytotoxic destruction of those cells. This is the hallmark of a Type II hypersensitivity reaction.

Mechanistically, IgG binding to RBC surface proteins marks the cells for attack by effector systems. The spleen’s macrophages can recognize the Fc portion of IgG-coated red cells and phagocytose them (opsonization), leading to extravascular hemolysis. Complement activation can also occur, contributing to cell lysis, sometimes within blood vessels (intravascular hemolysis). The key point is that the immune attack targets cell-surface antigens with antibodies, rather than forming soluble immune complexes or involving T-cell–mediated delayed responses.

In contrast, Type I involves IgE-mediated allergic reactions, Type III involves immune complex deposition causing tissue injury, and Type IV is a T-cell–mediated delayed-type reaction. Since the destruction is driven by antibodies binding to cell surfaces and triggering effector mechanisms, it fits Type II hypersensitivity.

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