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Our immune system has developed a complex set of tools to protect our bodies from harm, and facilitate repair. Under certain circumstances, however, these tools may respond inappropriately.

 

An inappropriate immune response response can be of two types: reacting to a substance that’s not a threat, or an excessive reaction that continues after the threat has been neutralised and may go on to damage healthy cells. These types of reactions are known as hypersensitivity.

 

Allergies are a type of hypersensitivity (type 1, to be specific), and they’re all too common. They include pollen allergies (which cause a runny nose), contact allergies (which cause a skin rash) or even severe food allergies (which can lead to constriction of the windpipe, suffocation and even death).

 

Regardless of the way it physically presents itself, the underlying process to any allergic reaction is basically the same.

 

Let’s use pollen as an example (since it can be highly allergenic to some individuals). When these individuals are first exposed to the allergen in pollen, their body mistakenly recognises it as a pathogen.

 

As a response, it produces plasma cells (which are a part of our adaptive immune system). Plasma cells always secrete antibodies that are specifically designed for a particular pathogen’s structure, and even now release antibodies specifically designed for the allergen that’s present in pollen.

 

Something changes in an allergic response, though: these antibodies aren’t the same as the ones generally released during an immune response. When exposed to an allergen, plasma cells secrete a special type of antibody called IgE antibodies.

 

What’s the difference? Instead of immediately triggering an immune response the way other antibodies do, IgE antibodies instead move through our body, until they latch on to receptors found on the surface of two types of specialised immune cells: mast cells and basophils.

 

These cells contain granules that are filled with various chemicals, including histamine: a chemical mediator that triggers a cascade of effects in the local area.

 

By binding to mast cells and basophils, the IgE antibodies now make these specialised cells ‘sensitised’ to pollen. No one experiences the symptoms of an allergy during this sensitisation process- but the next time the sensitised mast cells and basophils encounter pollen, they trigger an allergic reaction.

 

This time, the IgE molecules bound to a single mast cell’s surface (two IgE molecules per mast cell, to be specific) attach themselves to a molecule of the allergen, creating a cross linkage. This cross-linking causes the granules in the mast cell to move to the cells’ surface and release their histamine and other components into the surrounding tissue.

 

In the case of a pollen allergy, the mast cells in our nostrils are the first point of contact between the allergen and our immune system.

 

The histamine that they release acts on other cells in the nasal cavity. They trigger the production of mucous (a runny nose), constrict smooth muscle (leading to congestion) and recruit other cells of the immune system.

 

(Antihistamine drugs work by binding to the histamine receptors, thereby blocking histamine’s ability to bind to them and trigger these effects).

 

Within a minute of the IgE receptor cross-linking, mast cells also begin forming pro-inflammatory compounds from an omega 6 fatty acid called arachadonic acid. These compounds are as much as 1000 times more potent at constricting our respiratory tract’s muscles, and are also far more effective at stimulating mucous secretion. (Some of them are also believed to be responsible for the breathlessness and mucous build-up seen in asthmatics.)

 

Allergic reactions are mediated by many factors, all of which aren’t completely understood. These include –

 

Genetics:
Our genetics can influence our susceptibility to allergies. If both parents are allergic, there is a 50% chance that a child will be also allergic. If only one parent is allergic, there is a 30% chance that the child will manifest some kind of hypersensitivity.

 

The dose of the allergen:
IgE antibodies are believed to be triggered when an individual is repeatedly exposed to low doses of a foreign substance. However, high doses of the same substance can cause a shift towards the production of a different type of antibody (called IgG), which does not cause allergies.

 

The proportion of various immune cells:
Having high proportions of a type of immune cell called Th2 cells can predispose an individual to the production of IgE antibodies. This would make them more likely to have an allergic reaction.

 

 

 

 

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