hypersensitivity(redirected from type II hypersensitivity)
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hypersensitivity,heightened response in a body tissue to an antigen or foreign substance. The body normally responds to an antigen by producing specific antibodiesantibody,
protein produced by the immune system (see immunity) in response to the presence in the body of antigens: foreign proteins or polysaccharides such as bacteria, bacterial toxins, viruses, or other cells or proteins.
..... Click the link for more information. against it. The antibodies impart immunityimmunity,
ability of an organism to resist disease by identifying and destroying foreign substances or organisms. Although all animals have some immune capabilities, little is known about nonmammalian immunity.
..... Click the link for more information. for any later exposure to that antigen. When exposure takes place under certain physiological conditions, or in allergic individuals with abnormal immune systems, a heightened immune response results that causes cell damage. Histamines, substances released from damaged cells, cause dilation of small blood vessels, tissue inflammation, and constriction of the bronchi of the lungs. Anaphylaxisanaphylaxis
, hypersensitive state that may develop after introduction of a foreign protein or other antigen into the body tissues. When an anaphylactic state exists, a second dose of the same protein (commonly an antibiotic such as penicillin, or certain insect venoms) will
..... Click the link for more information. is the immediate, sometimes fatal hypersensitivity reaction to drugs or serum to which an individual has been previously sensitized. Serum sicknessserum sickness,
hypersensitive response that occurs after injection of a large amount of foreign protein. The condition is named for the serum taken from horses or other animals immunized against a particular disease, e.g., tetanus or diphtheria.
..... Click the link for more information. is a similar but milder hypersensitivity to serum proteins or drugs that occurs several weeks after injection of foreign material. Delayed reaction allergies occur when cells of the immune system, the lymphocytes, that have previously been sensitized react to antigenic substance. The lymphocytes slowly infiltrate an area, such as skin exposed to poison ivy toxin and cause tissue damage. Anaphylaxis, serum sickness, and delayed sensitivity may occur in otherwise normal, nonallergic individuals as well as allergics, as a response to substances that are highly sensitizing. Individuals with allergic, or atopic, hypersensitivity form special weak types of antibodies, that cause local tissue damage and such symptoms as hiveshives
(urticaria), rash consisting of blotches or localized swellings (wheals) of the skin, caused by an allergic reaction (see allergy). The swelling is caused by distention of the skin capillaries and escape of serum and white cells into the skin and tissues.
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seasonal allergy causing inflammation of the mucous membranes of the nose and eyes. It is characterized by itching about the eyes and nose, sneezing, a profuse watery nasal discharge, and tearing of the eyes.
..... Click the link for more information. , and asthmaasthma
, chronic inflammatory respiratory disease characterized by periodic attacks of wheezing, shortness of breath, and a tight feeling in the chest. A cough producing sticky mucus is symptomatic.
..... Click the link for more information. . Antihistaminesantihistamine
, any one of a group of compounds having various chemical structures and characterized by the ability to antagonize the effects of histamine. Their principal use in medicine is in the control of allergies such as hay fever and hives.
..... Click the link for more information. are drugs that prevent histamine from acting on blood vessels, bronchioles, and other organs. Acute reactions, such as anaphylaxis, are treated by giving epinephrineepinephrine
, hormone important to the body's metabolism, also known as adrenaline. Epinephrine, a catecholamine, together with norepinephrine, is secreted principally by the medulla of the adrenal gland.
..... Click the link for more information. and other sympathomimetic drugs. Steroids such as cortisonecortisone
, steroid hormone whose main physiological effect is on carbohydrate metabolism. It is synthesized from cholesterol in the outer layer, or cortex, of the adrenal gland under the stimulation of adrenocorticotropic hormone (ACTH).
..... Click the link for more information. are also given to suppress inflammation and depress the immune system. In some cases, hypersensitized individuals receive injections of gradually increasing quantities of the antigenic material to which they are sensitive, in order to avoid or lessen their hypersensitivity to that particular substance.
Heightened reactivity to antigens (molecules capable of stimulating an immune response). Many different examples of hypersensitivity have been recognized in animals and humans. These are often referred to collectively as allergies, and clinically may take such forms as asthma, hives, hay fever, anaphylactic reactions to certain foods or insect venoms, some forms of eczema and kidney diseases, and skin reactions to poison ivy antigens and many other substances. See Antigen
Because molecules foreign to the body are often antigenic, the various forms of hypersensitivity are most commonly induced either by exposure to foreign antigens derived from microorganisms during infections, or by contact with certain noninfectious agents (some plant pollens, some drugs, and certain simple chemicals such as components of poison ivy). However, under certain circumstances, molecules of the body itself can induce an immune response. In these cases, hypersensitivity reactions can be directed against antigens of the body's own organs or tissues. Whether foreign or derived from the body itself, antigenic substances often produce little or no tissue reaction in unsensitized individuals. But once hypersensitivity develops, additional exposure to antigen can give rise to clinically obvious symptoms (hives, sneezing, runny nose), tissue damage, or even (in certain extreme cases) death. See Autoimmunity
The development of hypersensitivity in animals or humans may be divided into two phases. During the first phase, induction of hypersensitivity, exposure of the organism to antigen results in (1) recognition of the antigen by cells of the immune system; (2) proliferation (multiplication) of the types of immune cells that recognize and respond to that antigen; and (3) long-term storage of the information required to recognize and respond to the antigen in immune “memory” cells. Although a variety of cell types assist in these processes, all of the three functions are primarily dependent on various types of lymphocytes.
Once the state of hypersensitivity has been induced, reexposure of the organism to the antigen that induced the response usually leads to the second phase, expression of a hypersensitivity reaction. Hypersensitivity reactions historically have been classified according to two characteristics: the delay between the exposure of a previously sensitized (hypersensitive) individual to antigen and the development of a clinically recognizable reaction; and the types of cells and humoral substances thought to be responsible for the induction and expression of the reaction. According to this scheme, classical delayed hypersensitivity reactions differ from other forms of hypersensitivity in first becoming clinically prominent in sensitized individuals approximately 1 day after exposure to the specific antigen against which the individual expresses hypersensitivity; and depending for their expression on the activity of certain lymphocytes (thymic-dependent lymphocytes, or T cells) rather than soluble antibodies. By contrast, immediate hypersensitivity reactions may develop within seconds or minutes of exposure to specific antigen, and require the participation of antibodies. See Antibody
In addition to its association with certain infections, delayed hypersensitivity has been implicated in a variety of noninfectious disease processes. These include the annoying reactions induced in some individuals by contact with certain plants (for example, poison ivy), detergents, or drugs, as well as certain of the immune responses resulting in the rejection of transplanted tissues such as skin, kidneys, and hearts. In many of these processes, the immunological reactions are thought largely to reflect the activity of T lymphocytes (as in classical delayed hypersensitivity), whereas in others soluble antibodies may also have a role. See Cellular immunology, Transplantation biology
Immediate hypersensitivity reactions, collectively known as allergies, occur usually within minutes or up to a few hours after inhalation, ingestion, or injection of an antigen. Such reactions may be severe, even life-threatening, such as anaphylactic shock and asthma, or relatively minor but uncomfortable, such as hay fever or urticaria (hives). They may be of short duration—hours for anaphylaxis—or prolonged for several days or even weeks, as in immune complex-induced vasculitis. See Allergy
Hypersensitivities have been classified into four main types with different mechanisms: type I, anaphylaxis or atopy; type II, cytotoxic or cytolytic; type III, immune complex or Arthus reaction; and type IV, delayed or cellular-immune; the last type has been described above.
In type I the antigen is recognized immunologically upon first exposure and initiates antibody formation, usually of immunoglobulin E (IgE) or IgG class. IgE-mediated allergy, known as atopy, has a strong hereditary component, and occurs commonly in humans and dogs, while IgG-mediated anaphylaxis can occur in most vertebrates. The antibodies (IgE or IgG) attach or fix to target cells, such as tissue mast cells and blood basophils. Upon subsequent exposure to the antigen, the target cell–fixed antibodies react with antigen to cause degranulation and release of chemical mediators, such as histamine. See Histamine, Immunoglobulin
In cytotoxic or cytolytic (type II) reactions, the antigen may be certain altered body cells themselves; they may be altered physically or by chemicals and drugs attached to the cells. These are usually circulating cells, such as red blood cells coated with penicillin, platelets coated with a drug, or white blood cells coated with sulfonamides. Altered cells are recognized by the body's immune system as foreign or altered self, and IgG or IgM antibodies are formed which react with the altered cells and activate the serum complement enzymatic cascade that culminates in the lysis of the altered cells. Thus, cytotoxic hypersensitivity leads to anemia, bleeding due to low platelet levels, and increased infections from loss of white blood cells (agranulocytosis).
In immune complex or Arthus (Type III) reaction, neither antibody nor antigen is fixed to cells. Rather, they combine in various ratios in blood and tissues. If they are in the proper ratio, they form microprecipitates, or immune complexes, in capillaries and venules. The immune complexes activate complement to form chemoattractants for neutrophils and monocytes. Microprecipitates and phagocytosing neutrophils block the small vessels, resulting in a typical Arthus reaction—lack of blood to the tissue and subsequent tissue necrosis and death.