delayed hypersensitivity(redirected from tuberculin-type hypersensitivity)
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a state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent; anaphylaxis and allergy are forms of hypersensitivity. The hypersensitivity states and resulting hypersensitivity reactions are usually subclassified by the Gell and Coombs classification. adj., adj hypersen´sitive.
contact hypersensitivity that produced by contact of the skin with a chemical substance having the properties of an antigen or hapten.
delayed hypersensitivity (DH) (delayed type hypersensitivity (DTH)) the type of hypersensitivity exemplified by the tuberculin reaction, which (as opposed to immediate hypersensitivity) takes 12 to 48 hours to develop and which can be transferred by lymphocytes but not by serum. Delayed hypersensitivity can be induced by most viral infections, many bacterial infections, all mycotic infections, and a few protozoal infections (leishmaniasis and toxoplasmosis). The scope of the term is sometimes expanded to cover all aspects of cell-mediated immunity including contact dermatitis, granulomatous reactions, and allograft rejection.
immediate hypersensitivity antibody-mediated hypersensitivity occurring within minutes when a sensitized individual is exposed to antigen; clinical manifestations include systemic anaphylaxis and atopic allergy (allergic rhinitis, asthma, dermatitis, urticaria, and angioedema). The first exposure to the antigen induces the production of IgE antibodies (cytotropic antibodies, reagin) that bind to receptors on mast cells and basophils. Subsequent exposure to the antigen triggers production and release of a diverse array of mediators of hypersensitivity that act on other cells producing symptoms such as bronchospasm, edema, mucous secretion, and inflammation.
hypersensitivity reaction the exaggerated or inappropriate immune response occurring in hypersensitivity, in response to a substance either foreign or perceived as foreign and resulting in local or general tissue damage. Such reactions are usually classified as types I–IV on the basis of the Gell and Coombs classification.
1. Synonym(s): cell-mediated immunity
2. Synonym(s): delayed reaction
3. a cell-mediated response that occurs in immune people peaking at 24-48 hours after challenge with the same antigen used in an initial challenge. The interaction of T-helper 1 (Th-1) lymphocytes with MHC class II positive antigen-presenting cells initiates the response. This interaction induces the Th-1s and macrophages at the site to secrete cytokines, which are the major factors in the reaction. Called tuberculin-type hypersensitivity.
the type of hypersensitivity which (as opposed to immediate hypersensitivity) takes 24 to 72 hours to develop and is mediated by T lymphocytes rather than by antibodies. Compare immediate hypersensitivity.
delayed hypersensitivityAn allergic reaction occurring two to three days after the antigen contact and mediated by CYTOKINE release from sensitized T cells (T LYMPHOCYTES).
allergic reactionsacute inflammatory skin hypersensitivity reaction (redness, tissue oedema, pruritus) induced by the histamine released from local mast cells in response to allergen contact in susceptible individuals (Table 1)
|Type I||Type II||Type III||Type IV||Type V|
|Antigen||Pollens, moulds, mites, drugs, foods, parasites||Cell surface moieties||Bacteria, fungi, parasites||Cell or tissue moieties||Cell surface receptors|
|Mediators||IgE and mast cells||IgG, IgM, complement||IgG, IgM, IgA, complement||T-cell-activated macrophages and lymphokines||IgG|
|Tests||Skin tests (wheal and flare)||Coombs' test|
Red cell agglutination
|Immune complexes||Skin test (erythema, induration)||Indirect immunofluorescence|
|Time to reaction||5–10 minutes||6–36 hours||4–12 hours||48–72 hours||Variable|
|Histology||Oedema, vasodilatation, mast cell deregulation, eosinophils||Target cell damage||Acute inflammation, neutrophils, vasculitis||Perivascular inflammation, mononuclear cells, granuloma, caseation and necrosis in TB||Normal or hypertrophy|
|Characteristic diseases||Extrinsic asthma, atopic eczema, allergic rhinitis, anaphylaxis||Haemolytic anaemia, transfusion reactions, HDN, Goodpasture's syndrome, addisonian pernicious anaemia, myasthenia gravis||Autoimmune disease (RA, SLE, glomerulonephritis)|
Low-grade persistent infection (viral hepatitis)
Environmental diseases (farmer's lung)
|Pulmonary TB, contact dermatitis, graft-versus-host disease, insect bites, Hansen's disease||Graves, disease, myasthenia gravis|
|Exchange transfusion, plasmapheresis, immunosuppressives||Corticosteroids, immunosuppressives, plasmapheresis||Immunosuppressives, cortico-steroids, antigen removal||Treatment of presenting disease|
Ig, immunoglobulin; TB, tuberculosis; HDN, haemolytic disease of the newborn; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.
n sensitivity regulated by T-lymphocytes that may take anywhere from 24–72 hours to develop.
de·layed hy·per·sen·si·ti·vi·ty(dē-lād hīpĕr-sensi-tivi-tē)
A cell-mediated response that occurs in immune people peaking at 24-48 hours after challenge with the same antigen used in an initial challenge.
prolonged beyond the time normally required.
see delayed hypersensitivity.
delayed neurotoxic effects
a characteristic effect of the neurotoxins in industrial triaryl phosphates.
individual cows appear to have a prolonged follicular phase in their estral cycle, usually about 48 hours.
delayed primary closure
the surgical closing of a wound several days after the injury because the wound was initially too contaminated to close. Union of the wound closed in this manner is called healing by third intention.
1. a state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent; allergy is a synonym for hypersensitivity. anaphylaxis is a form of hypersensitivity.
There are four basic types of hypersensitivity reactions: Type I (called also immediate hypersensitivity) involves cell-fixed antibody, mainly IgE attached to mast cells or basophils. Antigen binding causes the cell to release vasoactive factors. The basis for anaphylaxis and atopy. Type II causes cell destruction (cytotoxicity) by the action of immunoglobulin with complement or cytotoxic cells. Seen in red blood cell transfusion reactions and in alloimmune hemolytic anemia. See also antibody-dependent cellular cytotoxicity. Type III (called also immune-complex or subacute hypersensitivity) causes tissue damage and inflammation by the deposition of antigen-antibody complexes that activate complement and attract polymorphonuclear cells. Type IV (called also delayed hypersensitivity) involves sensitized T lymphocytes that react with cell bound or associated antigen and release lymphokines, causing mononuclear cell accumulation, tissue damage and inflammation, typically manifesting at least 24 hours after exposure to the antigen.
2. a state of increased responsivity to physical stimuli.
variant of polyarteritis nodosa; a disease of small blood vessels in humans; called also leukocytoclastic vasculitis.
types I, II and III hypersensitivity reactions. Called also immediate hypersensitivity.
immune responses to bacteria or bacterial products may contribute to the clinical features of some diseases, e.g. the anemia associated with salmonellosis, arthritis in erysipelas of pigs, intestinal lesions in Johne's disease, or be the principal cause as in staphylococcal hypersensitivity dermatitis in dogs.
a type IV reaction produced by contact of the skin with a low-molecular-weight chemical substance having the properties of a hapten in a sensitized individual; it includes allergic contact dermatitis.
cutaneous basophil hypersensitivity
a delayed inflammatory response characterized by large numbers of basophils.
type II hypersensitivity.
type IV reaction. A slowly developing cell-mediated immune response in which T helper 1 lymphocytes respond to specific antigen by releasing cytokines, some of which activate macrophages, as occurs in tuberculin reaction, graft rejection, some autoimmune diseases, etc.
may be either an immediate (antibody mediated) or delayed type (T lymphocyte mediated) reaction. See also drug eruption.
flea bite hypersensitivity
see flea allergy dermatitis.
hypersensitivity reaction to various dietary constituents has been the suspected cause of allergic dermatitis in most species, but conclusive evidence is often lacking. It may also result in diarrhea.
may contribute to the clinical features of cutaneous fungal infections, particularly kerion formation. It is also the basis for skin testing for systemic mycoses, e.g. histoplasmin and coccidioidin.
occurs, e.g. the self-cure phenomenon, and the allergic response of a sensitized animal to an invasion, e.g. of lungs, causes massive pulmonary edema.
antibody-mediated hypersensitivity, i.e. types I, II and III, characterized by a response that appears within minutes to hours, resulting either from a release of histamine and other mediators of hypersensitivity from IgE-sensitized mast cells, causing increased vascular permeability, edema and smooth muscle contraction (type I), from antibody-mediated lysis of red blood cells (type II), or from immune complex mediated pathology (type III).
immune complex hypersensitivity
type III hypersensitivity (above).
see acute bovine pulmonary emphysema-edema.
see hypersensitivity pneumonitis.
see bacterial hypersensitivity (above).
a theory that certain levels of allergens may be tolerated by some sensitized individuals without manifestations of disease, but a slight increase in the level precipitates clinical signs.
tuberculin type hypersensitivity
the classical T lymphocyte cell-mediated hypersensitivity associated with mycobacterium infection or immunization with antigens containing Freund's adjuvant.