Complement Antigen Technology
Hypersensitivity or Immune Reactions
IgM is a primary response to any antigen but lasts only 90 days from exposure, and is, therefore, difficult to measure because many problems are chronic.
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.
I hold a unique, patented process that elevates testing to a new level by measuring not only IgG but also immune complexes (Type II and III) simultaneously.
Immunology recognizes the following Gell/Coombs classifications of hypersensitivity reactions.
Type I is an IgE antibody-mediated reaction commonly called an immediate hypersensitivity. This allergic reaction occurs in less than two hours after being exposed or ingesting an antigen. 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 reaction occurs from two hours to several days after 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 conditions.
Type III immune complex is also a delayed hypersensitivity, because the reaction occurs days to weeks post exposure. 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. Exposure results in production of IgG, which, in turn, forms 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 reaction occurs days to weeks post exposure. The most serious delayed hypersensitivity is granulomatous tissue rejection, which occurs when macrophages ingest but cannot degrade an antigen, 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 is a common example of Type IV reactions.