Professional Documents
Culture Documents
Hypersensitivity reactions occur when the immune system responds in an exaggerated fashion to foreign antigens such as pollen or food proteins.
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.
Read on
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 Kcells 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.
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.
Read more at Suite101: Hypersensitivity Reactions: The Exaggerated Immune Response in Autoimmune Disease http://www.suite101.com/content/hypersensitivity-reactionsa69024#ixzz0y5hsHzGB