The Hypersensitive Immune Response
In hypersensitivity, the immune system is ineffective, erratically targeting innocent proteins. Hypersensitivity is caused by a defect in the immune system's functional properties similar to the defect seen in acquired and other immune deficiency syndromes.
However, in hypersensitivity reactions, the immune system overreacts. In immune deficiency syndromes, the immune system under-reacts.
Hypersensitivity in Autoimmune Disease
Hypersensitivity reactions are common in people with autoimmune diseases. Some hypersensitivity reactions are also known to trigger autoimmune disease development and exacerbate symptoms in individuals with autoimmune disorders. Furthermore, individuals with autoimmune disease are more likely to experience one or more different types of hypersensitivity reactions. The specific environmental substances someone will react to and the severity of these reactions are under the control of immune system and organ-specific genes.
Types of Hypersensitivity Reactions
- Type I or Immediate hypersensitivity
- Type II or Cytotoxic (capable of destroying cells) hypersensitivity
- Type III or Immune complex hypersensitivity
- Type IV or Delayed hypersensitivity
Each subtype plays a role in autoimmune disease, with the type of reaction triggering the type of disorder that occurs. For instance, in immune complex reactions, complexes of antigens and antibodies lodge into kidney tissue, which leads to kidney damage.
Type I Hypersensitivity
In type I hypersensitivity reactions, the reaction is immediate and related to the production of immunoglobulin E. Immunoglobulin E, upon entering the blood circulations, latches on to mast cells, which produce histamine. Histamine then induces allergy-associated symptoms. Examples include reactions to penicillin, insect bites and molds.
Common symptoms include hives, itching (urticaria) and swelling of the larynx. Individuals with hypersensitivity to specific allergens may develop anaphylactic reactions when they're exposed to significant amounts of these allergens. Reactions may be more intense during times of stress or during exercise. While type I hypersensitivity reactions don't cause autoimmune diseases directly, they stimulate the immune system. Chronic immune stimulation, over time, impairs its effectiveness. For instance, about 42 percent of patients with autoimmune thyroid disease are likely to have type I hypersensitivity reactions compared to 32 percent of normal subjects. When Type I hypersensitivity reactions occur, symptoms in autoimmune disease flare or worsen. For instance, studies show that when IgE levels rise due to pollen allergies, symptoms in Graves’ disease worsen, with higher IgE levels correlating with more severe disease states.
Type II Hypersensitivity
Type II hypersensitivity or cytotoxic hypersensitivity is caused by antibody-mediated reactions. When the immune system reacts to antigens it produces various immunoglobulins or antibodies, usually long-lasting immunoglobulin G (IgG) antibodies. In type II hypersensitivity reactions K-cells rather than mast cells are involved and complement production increases. These changes injure tissue cells. Autoimmune diseases mediated by type II hypersensitivity reactions include pemphigus, autoimmune hemolytic anemia (AIHA) and Goodpasture's syndrome.
In pemphigus, IgG antibodies react with intracellular substances found between the skin's epidermal cells. In AIHA, protein antigens elicit the production of antibodies that destroy red blood cells. In Goodpasture's syndrome, which primarily causes glomerulonephritis, IgG antibodies destroy the kidney's basement membrane cells.
Type III Hypersensitivity
Type III or complex hypersensitivity is characterized by circulating autoantibodies that are linked to targeted antigens. These immune complexes can lodge between tissue cells and interfere with the function of the affected organ. Immune complexes are responsible for lupus nephritis in several autoimmune conditions, including systemic lupus erythematosus.
Type IV Hypersensitivity
Type IV hypersensitivity reactions are delayed reactions in which the immune system's response to specific antigens is slow, typically occurring 1-2 days after the antigenic exposure. An example is the delayed rash that can occur 2 days after receiving an inoculation of tuberculin in the tuberculosis skin test.
Resource:
Mary L Turgeon, Immunology & Serology in Laboratory Medicine, 2003
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