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:
- AB and Rh blood group reactions;
- autoimmune diseases such as:
- rheumatic fever where
antibodies result in joint and heart valve damage;
- idiopathic thrombocytopenia
purpura where antibodies result in the destruction of platelets;
- myasthenia gravis where
antibodies bind to the acetylcholine receptors on muscle cells causing
faulty enervation of muscles;
- Goodpasture's syndrome
where antibodies lead to destruction of cells in the kidney;
- multiple sclerosis where
antibodies are made against the oligodendroglial cells that make myelin,
the protein that forms the myelin sheath that insulates the nerve
fiber of neurons in the brain and spinal cord; and
- some drug reactions.
Type II hypersensitivity also
participates in early transplant rejections.
Gary E. Kaiser, Ph.D.
Professor of Microbiology
The Community College of Baltimore County, Catonsville Campus
This work is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work The Grapes of Staph at https://cwoer.ccbcmd.edu/science/microbiology/index_gos.html.
Last updated: Feb., 2020
Please send comments and inquiries to Dr.
Gary Kaiser