12.4C: Type II (Cytotoxic) Reactions

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In type II (cytotoxic) hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces.

Learning Objectives

Describe Type II hypersensitivity reactions

Key Points

The antigens recognized in this way may either be intrinsic (“self” antigen, innately part of the patient’s cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen).
Mediators of acute inflammation are generated at the site where a foreign antigen is recognized and membrane attack complexes cause cell lysis and death.
In antibody -dependent cell-mediated cytotoxicity (ADCC), cells exhibiting the foreign antigen are tagged with antibodies ( IgG or IgM) and they are then recognised by natural killer (NK) cells and macrophages which in turn kill these tagged cells.

Key Terms

macrophages: A type of white blood cell that targets foreign material, including bacteria and viruses.
dendritic cells: Dendritic cells are immune cells that function to process antigen material and present it on the surface of other cells of the immune system. They act as messengers between innate and adaptive immunity.
cytotoxic hypersensitivity: In type II hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces.

In type II hypersensitivity (or cytotoxic hypersensitivity), the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces. The antigens recognized in this way may either be intrinsic (“self” antigen, innately part of the patient’s cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.

Figure: **Complement death**: A complement protein attacking an invader.

An example of type II hypersensitivity is the reaction to penicillin wherein the drug can bind to red blood cells, causing them to be recognized as different; B cell proliferation will take place and antibodies to the drug are produced. IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation to eliminate cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day. The membrane attack complex (MAC; ) is typically formed on the surface of pathogenic bacterial cells as a result of the activation of the alternative pathway and the classical pathway of the complement system, and it is one of the effector proteins of the immune system. The membrane-attack complex (MAC) forms transmembrane channels. These channels disrupt the phospholipid bilayer of target cells, leading to cell lysis and death.

Another form of type II hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged cells.

Autoimmune diseases resemble type II-IV hypersensitivity reactions. They differ from hypersensitivity reactions in that the antigens driving the immune process are self-antigens rather than non-self as in hypersensitivity reactions. Below are some examples of Type II hypersensitivity-like autoimmunity.