"Types of Hypersensitivity" is a perfect example of a paper on the immune system. Hypersensitivity Hypersensitivity can be defined as a harmful, exaggerated response of the immune system towards a certain antigen. Hypersensitivity had been discovered by the end of the 19th century; however, the different types and extents of it were discovered in 1963 by Patrick Gell and Robin Coombs. This Gell and Coombs classification divided hypersensitivity into 4 types of reactions and based them on antibody and cell-mediated mechanisms (Coico and Sunshine, 2009). Even though type I, II, and III are all caused by antibodies, there is a striking difference between type I and the other two. Type I Hypersensitivity (anaphylactic): This is an immediate response caused by factors called allergens.
Exposure to allergens leads to the production of IgE antibodies. IgE antibodies may sometimes bind with certain substances such as mast cells or basophils over the Fc portion. Type II Hypersensitivity (cytotoxic): This occurs when an antibody binds to a cellular target of fixed tissue antigen as in erythroblastosis fetalis. Type III Hypersensitivity (immune complex): Result of antibodies binding to self or foreign antigens Type IV Hypersensitivity (delayed-type): This phenomenon is different from the rest and is caused by the T lymphocytes against antigens usually causing inflammatory responses. Table1.
Mechanism and examples of hypersensitivity Mechanism Examples IgE Anaphylaxis, eczema, asthma, hay fever, food allergies. Cytotoxic Ab HDN and HTR by ABO and Rh incompatibility respectively Immune complexes Serum sickness, rheumatoid arthritis, Arthus phenomenon Cell-Mediated Contact dermatitis and Kochs phenomenon Hypersensitivity by antibodies Vs Hypersensitivity by T lymphocytes Reactions by antibodies are fairly fast and happen within 8 hours of infliction while hypersensitivity by T lymphocytes if delayed, which is why it is also termed DTH Delayed-Type Hypersensitivity (Samuelsson, 1983).
An example of Type IV hypersensitivity is Tuberculin which maxes out in a period of 24-72 hours. Although hypersensitivity type I-III can be isolated to allergies, type IV has also been reported to be involved in Diabetes Mellitus as well as transplant rejection. Where type IV poses a rather serious threat, type I hypersensitivity local reactions such as in the lungs or on the skin. In type IV cytokines are released by Th1 cells, this activates macrophages or T lymphocytes cause direct damage (Meager, 1991).
However, in type I-III Ag, Ab or Ag-Ab complexes are directed against cell surfaces to mediate the destruction of antigens. Type I-III hypersensitivity is caused by antigens which are exogenous, soluble, or on the cell surface whereas type IV hypersensitivity is caused over the tissues and organs and thus has a rather serious and exaggerated effect on the human body. Where the first three types are mostly treated with anti allergies or some doctor prescribed remedies, type IV may have fatal effects even by causing situations that might not even be related to allergies or hypersensitivity. Each type of hypersensitivity causes different clinical syndromes such as histamine causes intense bronchial smooth muscle contraction, increased nasal, bronchial and gastric secretion, and increases bronchial permeability (Takino, Takino, and Takino, 1989).
Type IV hypersensitivity however causes rather serious clinical syndromes which s sometimes because of exotoxins production (House and Descotes, 2007). Reactions There are different types of reactions caused by type IV which include: Superga-induced disease: SuperAg molecules activate a large number of T cells creating a bridge that results in the activation of numerous cytokines (Chignard, 1996). CD3 mAb-Induced Cytokine Release: When patients are treated with anti-CD3 it can cause a massive release of T cells and cytokines resulting in a reaction that is usually not fatal and may be treated with corticosteroids. TNF-alpha and Shock: TNF-alpha causes decreased cardiovascular resistance and cardiac output as well as capillary leakage. Endotoxin Shock: This is the spread of bacteria in the blood usually caused by endotoxin producing gram-negative bacilli and is also called septic shock.
It is one of the most usual causes of death in ICUs.
• Boyd, W., and others, (1946). Fundamentals of immunology. Fundamentals of Immunology..
• Castells, M. (2011). Anaphylaxis and hypersensitivity reactions. 1st ed. New York: Humana Press.
• Chignard, M. (1996). Cytokines and adhesion molecules in lung inflammation. 1st ed. New York: New York Academy of Sciences.
• Coico, R. and Sunshine, G. (2009). Immunology. 1st ed. Hoboken, N.J.: Wiley-Blackwell.
• David, J. (1966). Delayed hypersensitivity in vitro: its mediation by cell-free substances formed by lymphoid cell-antigen interaction. Proceedings of the National Academy of Sciences of the United States of America, 56(1), p.72.
• House, R. and Descotes, J. (2007). Cytokines in human health. 1st ed. Totowa, N.J.: Humana Press.
• Meager, A. (1991). Cytokines. 1st ed. Englewood Cliffs, N.J.: Prentice-Hall.
• Pathmicro.med.sc.edu, (2014). Hypersensitivity reactions. [online] Available at: http://pathmicro.med.sc.edu/ghaffar/hyper00.htm [Accessed 10 Jul. 2014].
• Samuelsson, B. (1983). Leukotrienes: mediators of immediate hypersensitivity reactions and inflammation. Science, 220(4597), pp.568--575.
• Takino, M., Takino, Y. and Takino, T. (1989). Respiratory hypersensitivity. 1st ed. Pentland.