Sage Test Technology

Hypersensitivity Reactions

Sage Medical Laboratory research has shown IgM is a primary response to any antigen but lasts only 90 days, and is, therefore, difficult to measure because food allergies are a chronic problem. IgA is a mucosal antibody and its elevation is a protective/adaptive response. IgG alone, and with complement, are the main maladaptive pathways in foods, food additives, and dyes. Sage holds a unique patent-pending process that elevates delayed food allergy testing to a new level by measuring not only IgG but also immune complexes simultaneously. The Gell/Coombs classifications of hypersensitivity reactions are types I, II, III, and IV.

Type I is an IgE antibody-mediated reaction commonly called an immediate hypersensitivity. This maladaptive allergic reaction occurs in less than two hours post allergen exposure or ingestion. Most immediate reactions are so fast that individuals can easily identify the cause of their reactions, (i.e., eating strawberries and breaking out with hives).

Type II is also antibody-mediated (IgG, IgM,) and is commonly called delayed hypersensitivity because the allergic reaction occurs from two hours to several days post allergen exposure. Type II hypersensitivity occurs when antibodies bind to either self-antigens or foreign antigens, and leads to phagocytosis, killer cell activity or complement- mediated lysis. IgG activates complement leading to formation of the membrane-attack-complex and cell lysis, whereas IgA does not activate complement. IgM, while activating complement lasts only for 60-90 days and usually cannot be measured in chronic delayed allergies.

Type III immune complex is also a delayed hypersensitivity, because the allergic reaction occurs days to weeks post allergen exposure or indigestion. Type III hypersensitivity develops when immune complexes, usually IgG, are formed in large quantities and cannot be cleared adequately by the reticuloendothelial system via the CR1 receptor site. Allergen exposure results in production of IgG, which, in turn, binds to the allergen, forming immune complexes in blood. Immune complexes activate complement, resulting in covalent binding of C3b to IgG forming immune complex-C3b. Immune complexes are deposited at various sites throughout the body. Damage ensues when immune complexes deposit at a site and further activate the complement, producing inflammatory cytokines. This causes leukocytes to release protease, mast cells and vasoactive amines that damage blood vessels, which escalates the inflammatory process.

Type IV is the cell mediated form of delayed hypersensitivity. The allergic reaction occurs days to weeks post allergen exposure. The most serious delayed hypersensitivity is granulomatous tissue rejection, which occurs when macrophages ingest but cannot degrade an allergen, resulting in persistent macrophage stimulation. Stimulated macrophages elaborate cytokines that cause the macrophage itself and other cell types to concentrate in the area of injury. T-cells are then stimulated by cytokines, which activate complement and induce immune complex formation. Transplant rejection and nickel skin allergies are common examples of Type IV.

Sage Test Technology - Sage ELISA vs. IgG, IgG4 ELISA, or IgE tests Sage Test Technology - Sage ELISA vs. IgG, IgG4 ELISA, or IgE tests