Type I hypersensitivity triggers an extreme or unnecessary immune response against certain allergens in our body. You can understand allergen as types of toxic or foreign antigen that is capable of inducing a hyper-immune response. Among the four types of hypersensitivity, type I is the most immediate one. This is because it generates a very swift response after coming in contact with some specific allergen.
Individuals that exhibit this type 1 hypersensitivity usually possess a genetic predisposition to this. Their oversensitivity against unknown molecules is due to some set of genes causing T helper cells to become hyperactive against certain molecules.
What is Hypersensitivity?
The body’s immune machinery constantly works to maintain our healthy being. Moreover, it protects us from pathogenic organisms like bacteria, viruses, and fungi that try to invade and harm our bodies.
However, this system can malfunction and might act a bit too sensitive to everything. Hypersensitivity refers to this same condition where someone’s defence system starts reacting in such a way that it ends up damaging and harming the body instead of protecting it. This basically occurs when our immune mechanisms fail to distinguish between self and foreign substances. Thereby, they eventually start attacking the self-antigens also.
The only difference between a normal person and a hypersensitive person is that the allergens do not produce a harsh immune response in normal individuals. Generally, hypersensitive responses cause tolerable harm to the body, but in critical cases, it can be fatal.
Content: Type 1 Hypersensitivity
- Type 1 Hypersensitivity Reactions
- Hypersensitivity Type 1 Symptoms
- Hypersensitivity Type 1 Mechanism
- Treatment of Type 1 hypersensitivity
Type 1 Hypersensitivity Reactions
There are two stages of this hypersensitivity:
- Sensitization
- Effect Stage
Sensitization Stage
It is the very much initial phase, where the individual doesn’t manifest any symptoms even after encountering the allergen. During the initial encounter, two types of white blood cells are involved – mast cells and basophils. In addition to that, immunoglobulin E (Ig E) also remain involved.
After encountering the antigen, our immune system starts producing IgE antibodies that bind to the cell surface of mast cells and basophils. The generated antibodies are highly sensitive and specific to a particular allergen. When the person encounters the same allergen again, these same antibodies serve the role of antigen detectors.
Effect Stage
This is the stage where the person experiences second exposure to the allergen. As the body already recognizes the antigen from its first exposure, it immediately produces an immune response. Due to rapid response, the person starts manifesting allergic symptoms.
The rapid immune response occurs because Ig E antibodies attached to basophils and mast cells bind to the allergen. This binding immediately initiates degranulation in white blood cells. During the process of degranulation, the involved WBCs release granules containing inflammatory elements such as histamine, heparin, and serotonin that result in allergic symptoms.
Hypersensitivity Type 1 Symptoms
- Rashes, Red marks or patches
- Runny nose
- Watery eyes
- Hives
- Coughing, Wheezing & Breathlessness
- Oedema
- Nausea & Vomiting
- Itching
- Rhinitis
- Cramps
- Unconsciousness
Hypersensitivity Type 1 Mechanism
Suppose a person is allergic or hypersensitive to ragweed pollens. So when he inhales some ragweed pollens, they act as allergic antigens inside his body.
First Exposure: Sensitization
First of all, this antigen which is nothing but ragweed pollen, gets picked up by our immune cells that are present on the membranes along the air passage. These immune cells hanging around in our body are actually antigen-presenting cells (APC). Their main function is to carry the antigens to the lymph nodes and present them to the T helper cells living there. Dendritic cells and macrophages are the most common ACPs.
So, as discussed earlier, ACPs grab and carry the antigen to the lymph nodes. This is the very much initial process that happens regardless the person is allergic or not. In case the person is allergic, the ACPs also release costimulatory molecules, which is necessary to mount an effective immune response.
Before the T helper cells encounter the antigen, we refer to it as naïve T helper cells. This implies that even if it was built to recognize a certain type of antigen, it hasn’t seen them before.
As soon as the T helper cell gets its hands-on antigen, it binds to it as well as to the secreted costimulatory molecule. This particular reaction causes the priming of T helper cells, which causes the conversion of naïve T helper into different sorts of T helper cells.
Also, there are various small proteins named interleukins that remain floating in the body and help in this conversion process. Some of the important interleukins are IL 4, IL 5, & IL 10.
The already excited T helper cells secrete their own bit of IL 4, which causes the class switching of B cells. As a result, the B cells switch their production from making Ig M to making Ig E antibodies which are highly specific to the attacking allergen. T helper cells also secrete IL 5, which induces the production and activation of eosinophils (a granulocyte). It is a type of white blood cell that degranulates, thereby releasing a set of toxic elements that damage invading cells as well as nearby hosts.
Working of Ig E
The produced Ig E are very specific and has a high affinity for the FC ε receptor that is present in mast cells. Mast cells are another type of granulocyte, so the Ig E rapidly attaches itself to the surface of mast cells.
Since the Ig E antibodies adhere to the surface of cells. Therefore we also refer to them as cytotropic antibodies. At this stage where the mast cells are geared up and ready for action. Here, the sensitization phase finishes completely.
Second Exposure: Effect Stage
The geared-up mast cells bind to the allergic antigen using its coat of antibodies. Actually, the cross-linking of IgE antibodies requires two or more bound antigens. They signal the mast cells to start degranulation. The process of degranulation releases a group of pro-inflammatory elements called mediators. Ultimately, these mediators cause allergic reactions.
One of the most common pro-inflammatory mediators is histamine which binds to H1 receptors. This binding causes the contraction of smooth muscles around the bronchi. Due to this, the airway gets smaller, and breathing becomes difficult.
Anaphylaxis
Systemic inflammation causes low blood pressure and air blockage because of the tongue and throat swelling. This serious condition where multiple systemic reactions occur due to histamine is termed Anaphylaxis. This might become fatal if the person is not instantly treated with epinephrine.
In addition to that, it also causes blood vessel dilation and increases the permeability of the walls of blood vessels. Gradually the blood flows to the affected area increases, and the fluid more easily leaks out of the blood vessel walls. This leaked fluid enters into the interstitium (the spaces between the cells), causing Oedema (swelling) and Urticaria (hives).
Early Phase Reaction
Other than histamine, the mast cells also release some more pro-inflammatory mediators to activate proteases and eosinophils. The effect of these mediators is called “early phase reactions”, and they occur within a few minutes of 2nd exposure.
Late Phase Reaction
After the early phase, there is a late phase reaction which takes place after 8-12 hours of 2nd exposure. In his phase, more quantity of immune cells (mainly granulocytes) are recruited at the infection site where the invading antigen is located. This basically occurs in response to cytokines and pro-inflammatory molecules that are produced during the early phase.
Treatment of Type 1 hypersensitivity
There are a variety of medications used for the treatment of type 1 hypersensitivity.
- Antihistamines: They block the effect of histamine, which reduces the permeability of vascular tissues and constrictions of bronchi.
- Corticosteroids: They help in the reduction of inflammatory response.
- Epinephrine: Mainly used in severe anaphylactic reactions. It basically constricts the blood vessels and stops anaphylactic shocks.
- Steroids: In some severe cases, doctors often recommend steroids.
In severe conditions, it is most important to take medical attention as it can become lethal and sometimes can get better than becoming worse again.
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