Differentiate between Type II and Type III hypersensitivities.

Differentiate between Type II and Type III hypersensitivities.

• A. Type II uses immune complexes; Type III involves cell-bound antibodies
• B. Type II involves antibodies bound to cells causing lysis; Type III involves immune complexes that deposit
• C. Type II is T cell mediated
• D. Type II and III are the same

Answer: (B)

The difference here is between antibody-driven cytotoxic reactions against cell surfaces and immune complex–driven tissue inflammation. In the Type II, antibodies (usually IgG or IgM) bind directly to antigens on the surface of cells or on extracellular matrix components. This binding flags the cell for destruction or dysfunction through mechanisms like complement activation, opsonization with phagocytosis, or antibody-dependent cellular cytotoxicity. This is why you see things like autoimmune hemolytic anemia or Goodpasture syndrome, where the target is a cell-bound or surface-associated antigen. In the Type III response, the problem is soluble antigen–antibody complexes that form in the circulation and then deposit in tissues such as blood vessels, kidneys, or joints. These immune complexes activate complement and recruit neutrophils, leading to inflammation and tissue injury in those sites. Serum sickness and certain manifestations of lupus are classic examples. So the statement that Type II involves antibodies bound to cells causing lysis, while Type III involves immune complexes that deposit in tissues, captures the fundamental distinction. The other options mix up which mechanism applies to which type, or incorrectly label Type II as T cell–mediated or say the two are the same.

The difference here is between antibody-driven cytotoxic reactions against cell surfaces and immune complex–driven tissue inflammation.

In the Type II, antibodies (usually IgG or IgM) bind directly to antigens on the surface of cells or on extracellular matrix components. This binding flags the cell for destruction or dysfunction through mechanisms like complement activation, opsonization with phagocytosis, or antibody-dependent cellular cytotoxicity. This is why you see things like autoimmune hemolytic anemia or Goodpasture syndrome, where the target is a cell-bound or surface-associated antigen.

In the Type III response, the problem is soluble antigen–antibody complexes that form in the circulation and then deposit in tissues such as blood vessels, kidneys, or joints. These immune complexes activate complement and recruit neutrophils, leading to inflammation and tissue injury in those sites. Serum sickness and certain manifestations of lupus are classic examples.

So the statement that Type II involves antibodies bound to cells causing lysis, while Type III involves immune complexes that deposit in tissues, captures the fundamental distinction. The other options mix up which mechanism applies to which type, or incorrectly label Type II as T cell–mediated or say the two are the same.