THE ADAPTIVE IMMUNE SYSTEM

V. HYPERSENSITIVITY

B. Immediate Hypersensitivity

2. Type II (Antibody-Dependent Cytotoxicity)

Fundamental Statements for this Learning Object:

1. During type II (antibody-dependent cytotoxicity) hypersensitivity, either IgG or IgM is made against normal self antigens as a result of a failure in immune tolerance, or a foreign antigen resembling some molecule on the surface of host cells enters the body and IgG or IgM made against that antigen then cross reacts with the host cell surface.
2. The binding of these antibodies to the surface of host cells then leads to opsonization of the host cells, membrane attack complex (MAC) lysis of the cells, and antibody-dependent cellular cytotoxicity (ADCC) destruction of the host cells.
3. Examples include AB and Rh blood group reactions and autoimmune diseases such as rheumatic fever, acute glomerulonephritis, myasthenia gravis, and multiple sclerosis.

 

LEARNING OBJECTIVES FOR THIS SECTION


When the immune systems cause harm to the body, it is referred to as a hypersensitivity (def). There are two categories of adaptive hypersensitivities: immediate hypersensitivity and delayed hypersensitivity. Immediate hypersensitivities (def) refer to humoral immunity (antigen/antibody reactions) causing harm; delayed hypersensitivities (def) refer to cell-mediated immunity (cytotoxic T-lymphocytes. macrophages, and cytokines) leading to harm.

There are 3 types of immediate hypersensitivities that depend on the interaction of antigens (def) with antibodies (def): Type I, Type II, Type III, and Type V. In this section we will look at Type II immediate hypersensitivities.


 

2. Type II (Antibody-dependent cytotoxicity) (def)

Mechanism: Either IgG or IgM is made against normal self antigens as a result of a failure in immune tolerance (def), or a foreign antigen resembling some molecule on the surface of host cells enters the body and IgG or IgM made against that antigen then cross reacts with the host cell surface. The binding of these antibodies to the surface of host cells then leads to:

a. Opsonization (def) of the host cells whereby phagocytes stick to host cells by way of IgG, C3b, or C4b and discharge their lysosomes (see Fig. 1 and Fig. 2);

b. Activation of the classical complement pathway causing MAC lysis (def) of the cells (see Fig. 3 and Fig. 4); and

c. ADCC (def) destruction of the host cells whereby NK cells (def) attach to the Fc portion (def) of the antibodies. The NK cell then release pore-forming proteins called perforins and proteolytic enzymes called granzymes. Granzymes pass through the pores and activate the enzymes that lead to apoptosis (def) of the infected cell by means of destruction of its structural cytoskeleton proteins and by chromosomal degradation. (see Fig. 5 , Fig. 5A, and Fig. 6).

 

Examples include:

Type II hypersensitivity also participates in early transplant rejections.

 


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