THE ADAPTIVE IMMUNE SYSTEM
B. Immediate Hypersensitivity
2. Type II (Antibody-Dependent Cytotoxicity)
The overall purpose of this Learning Object is to learn the mechanism behind Type II hypersensitivity, several examples, and their general treatments.
LEARNING OBJECTIVES FOR THIS SECTION
Adaptive (acquired) immunity refers to antigen-specific defense mechanisms that take several days to become protective and are designed to remove a specific antigen (def). This is the immunity one develops throughout life. There are two major branches of the adaptive immune responses: humoral immunity and cell-mediated immunity.
1. humoral immunity (def): humoral immunity involves the production of antibody molecules in response to an antigen (def) and is mediated by B-lymphocytes.
2. cell-mediated immunity (def): Cell-mediated immunity involves the production of cytotoxic T-lymphocytes, activated macrophages, activated NK cells, and cytokines in response to an antigen (def) and is mediated by T-lymphocytes.
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.
In this section we will look at Type II immediate hypersensitivities.
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.
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) destructionof 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).
Type II hypersensitivity also participates in early transplant rejections.
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Updated: Nov., 2008
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