First of all, this is a more advanced expansion on “You ate a peanut? Quick, block the airways!”, so I warn you now this may get a little complicated. For further reference, here is a table to show the differences between each Immunoglobulin (antibody) class, credit to http://www.scielo.br:
‘Allergic’ reactions, or hypersensitive reactions as they will be referred to for the rest of this post, are divided into the 4 main assortments: ‘Type I’, ‘Type II’, ‘Type III’ and finally ‘Type VI’; generally all allergy-based reactions fall into these groups. All of these involve immunoglobin antibodies (G/E), minus type IV, which works on a series of T-cells assisting to stimulate a cytotoxic response. The science behind the reaction is listed below, along with features that provoke the response, the underlying effectors’ mechanism, and the nature of the ailment caused.
Allergies are type I hypersensitive reactions: type I hypersensitive reactions result from the binding of the antigen to the immunoglobin E (to be referred to as IgE), already bound to its FC receptor (the cell receptor on mast cells); FCεRI receptors, typically associated with hypersensitive reactions, and whose surface receptors have an exceptionally high affinity to the IgE (A measure of the strength from which the molecules bind to, in this case, the receptor). The binding transmits a signal encoded by proteins within the mast cell to the nucleus, and this then leads swiftly onto the degranulation process of the mast cell, and its ultimate release of inflammatory mediators, causing potential anaphylactic symptoms when the mediators disperse. In the mast-cell based hypersensitive reaction, cross linkage of FCεRI by the antigens and immunoglobin causes mast cell activation and degranulation; primary mediators (e.g. Proteases, histamine and heparin) cause a standard inflammatory reaction, while secondary mediators -such as platelet allowing factor (or P.A.F for short)- have side effects which cause ‘heavier’ internal stimulation: the symptoms of Anaphylaxis. An example of type one would be the recipient inhaling flower pollen, these particulates are spotted by the IgE and grouped into clumps; which binds to the FCԑRI receptors (FC receptor). These then begins an inflammatory response, depending of the severity of the hypersensitive reaction.
Type II Hypersensitive reactions are due to small molecules that bond to the surface components of internal Human cells, producing modified cells that are seen as ‘foreign’ by the immune system. The immune system’s B-cell response produces immunoglobin G (to be referred to as IgG) via a MHC/HLA class I molecular stimulation (molecules bind to the B-cell’s receptor, causing the cell to release its immunoglobin G, and bind to the FC receptor on mast cells, beginning the release of primary inflammatory mediators). A MHC class I cell’s function is to display fragments of proteins -as a bacterial antigen- from within the cell to T-cells; healthy cells will be ignored, while cells containing foreign proteins will be attacked by the immune system, a process initiated by the Immune system once the T-cells recognise the protein. T-cells cause B-cells, whose only purpose is to create antibodies, to track down this foreign protein. These antibodies bond onto the modified complexes, causing their destruction via phagocytosis and complement activation (initiation of a series of reactions involving components of the Plasma [liquid in the blood], leading to the elimination of the cell now seen as a ‘pathogen’ modified complex). The body is attacking its own cells. A hypersensitive reaction to Penicillin is described as ‘Type II’, and such is the reason doctor’s will often ask (before being prescribed drugs) if the recipient is ‘allergic’ to any drugs, often led by “such as penicillin?”, as penicillin is prescribed often, and is one of the more popularized drugs to hold an sensitivity to.
Type III Hypersensitive reactions are due to tiny complexes formed by soluble antigens binding to the IgG/IgA made to combat them. Some of these complexes become deposited in the walls of blood vessels and alveoli of the lungs. This leads on to cause a response (generally inflammatory) that mainly damages tissue, impairing its function (impairing the lung’s function for example, the ability to breath). When other proteins from a non-human species are given to a human patient in medical issuing, or when mould spores are inhaled, type III is to be expected.
The molecules described as ‘effectors’ in type I, type II and type III are all antibodies (immunoglobin G/E/A). Type IV hypersensitive reactions, however, are cell-mediated instead, involving T-helper cells (CD4 Th1 cells): T-cells that –in this case– bind to the molecules on the antigen and acts as a receptor, in order to augment the T-cell’s response to the antigen; usually inflammatory.The helper T-cells response is usually due to the introduction of cytotoxic molecules that come into contact with the skin; these lipid soluble molecules (molecules that can easily access through cell membranes in the skin) covalently bond to human proteins, causing them to appear chemically modified. These chemically modified proteins degradate (the process involving the chemical breakdown of organic substances by living organisms) to reveal –to what the body sees as– foreign peptides (a chain of amino acids, packaged into a small[er] space). They bind to MHC/HLA class I molecules and stimulate a cytotoxic, destructive response caused by T-cells. The cytotoxic response causes inflammation, and is commonly associated with an ‘itch’ or ‘sting’, but usually nothing further, as where type-I/II/III can be found –more commonly- in fatal circumstances.
“Leaves of three? Leave it be!” – Old saying to avoid Poison Ivy.
Examples of a type IV hypersensitive reaction are both nettle and poison ivy stings, which inject chemicals such as the long-winded ‘pentadecacatechol’ into tissue, bypassing the skin as its lipid soluble nature allows it to diffuse through plasma membranes, consisting largely of phospholipids.
– Cole Holroyd, Sources:
The Immune System by Peter Parham,
|I||Antibodies (IgE), bond with the FC receptors on the mast cell. This causes mast cells to start the process of degranulation: eventually releasing their primary and secondary mediators, which cause symptoms.|
|II||Small, foreign molecules chemically modify cells. The body then views and recognises the cell as a pathogen, and proceeds to inflict the process of phagocytosis (destruction of the cell) upon it. This is commonly seen as the body ‘attacking’ its own cells.|
|III||Minute complexes formed by soluble antigens bind to the IgG designed to combat them. These complexes are then deposited in the walls of small blood vessels/alveoli in the lungs, that damages tissue and are the central cause of other internal symptoms (e.g. difficulty to breathe).|
|IV||Lipid soluble molecules bond to human proteins, causing them to appear chemically modified. They yield abnormal peptides, which binds to HLA/MHC class I molecules and cause a cytotoxic and ultimately destructive response from the immune system.|