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Hypersensitivity disease

The human immune response protects the host by maintaining homeostasis. The immune system is activated as a result of exposure to antigen, allergen, infection and/or neoplasm, resulting in the alteration of homeostasis. In some instances, an immune response generated against a foreign invader is harmful to the host itself, which is referred to as hypersensitivity disease and has been divided into five subtypes  [Pg.127]

Type I Reactions These reactions result from the production of IgE they are also termed immediate hypersensitivity disease. These are allergic reactions that [Pg.127]

Immunopharmacology, DOI 10.1007/978-0-387-77976-8.6, Springer Science+Business Media, LLC 2008 [Pg.127]

Type II Reactions These reactions result from the recognition of cells to which antigens (extrinsic or intrinsic) are bound by macrophages or dendritic cells, [Pg.128]

Type III Reactions These reactions involve the presence of antigen-antibody complexes, particularly those formed as a result of the production of autoantibodies. These complexes deposit in various tissues and involve inflammatory cells as well as complement, resulting in tissue damage due to the production of proteolytic enzymes by polymorphonuclear leukocytes and macrophages. A number of autoimmune diseases result from these reactions. Some clinical examples include systemic lupus erythematosus, rheumatoid arthritis, immune complex glomerulonephritis, Arthus reaction and serum sickness. [Pg.129]


Glucocorticoids (GC) produced endogenously in response to stress alter both innate and antigen-driven immunity. Cortisol (hydrocortisone) is the predominant GC in humans and most other species, whereas corticosterone is the most plentiful in mice and rats. Both natural and synthetic GC are used to reduce inflammation, manage autoimmune and hypersensitivity diseases, and treat certain neoplastic diseases. Certain inflammatory cytokines, including IL-1, IL-6 and TNFa stimulate (directly and indirectly) GC synthesis and release, a feedback mechanism to control inflammation. [Pg.777]

Delledonne, M., Murgia, I., Ederle, D., Sbicego, P.F., Biondani, A., Polverari, A. and Lamb, C., 2002, Reactive oxygen intermediates modulate nitric oxide signaling in the plant hypersensitive disease-resistance response. Plant Physiol. Biochem. 40 605-610. [Pg.226]

Hypersensitivity Diseases Research, The Upjohn Company, Kalamazoo, MI 49001-0199, USA Dr A. B. Jones... [Pg.1024]

Pepys, J. (1969). Hypersensitivity disease of the lungs due to fungi and other organic dusts. Monogr. Allergy 4, 1-145. [Pg.205]

Allergic to everything Allergic toxemia Autointoxication Candida hypersensitivity syndrome Cerebral allergy Chemical acquired immunodeficiency syndrome Chemical hypersensitivity disease Chemical multiple sensitivity Chemical-induced immune dysregulation Ecological illness Environmental illness or disease Environmental somatization disorder... [Pg.272]

LEVINE, A., TENHAKEN, R., DIXON, R., LAMB, C., HjOj from the oxidative burst orchestrates the plant hypersensitive disease resistance response. Cell, 1994, 79, 583-593. [Pg.195]

Hypersensitivity diseases— Diseases characterized by allergic responses to animal antigens, often associated with indoor air quality conditions such as asthma and rhinitis. [Pg.488]

Allergic rhinitis is a type I hypersensitivity disease, and its pathogenesis occurs in three stages (1) sensitization, (2) reexposure or provocation resulting in the acute (early phase) allergic reaction, and (3) the late phase reaction and chronic inflammation. The pathogenesis of allergic rhinitis involves many different cell types, inflammatory mediators, cytokines, chemokines, and adhesion molecules. [Pg.300]


See other pages where Hypersensitivity disease is mentioned: [Pg.268]    [Pg.127]    [Pg.685]    [Pg.1399]    [Pg.35]    [Pg.258]    [Pg.649]    [Pg.92]    [Pg.31]    [Pg.457]    [Pg.266]    [Pg.403]   
See also in sourсe #XX -- [ Pg.127 , Pg.128 ]




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Hypersensitivity disease associations

Hypersensitization

Immediate hypersensitivity disease

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