Allergy Season – Type 1 Hypersensitivity

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Allergy Season – Type 1 Hypersensitivity

Our Chief Science Officer, Jacky van Driel gives an overview of Type 1 Hypersensitivity.

I am sure you have by now heard so many of your friends, colleagues, or family members complaining about “hay fever”, it’s that time of the year again! There is so much to say about allergies and hypersensitivity reactions in general. This short article focuses on the mechanisms behind “spring allergies” to give the reader an insight into what actually goes on in the body and leads to the common symptoms the unfortunate sufferers experience.

Luckily, modern medicine can help with relieving these symptoms, even though sufferers cannot be cured, as the cause of these reactions is genetic. We are focusing on Type 1 Hypersensitivity reactions here. This will lead us to discuss Type 4 hypersensitivity reactions in a follow-up article, as this is something more commonly encountered in the hairdressing world, think ACD (allergic contact dermatitis), ICD (irritant contact dermatitis), rhinitis, asthma, and anaphylaxis. Hairdressers are exposed to a wide variety of hazardous substances in the workplace and are therefore at a higher risk of developing dermatological and respiratory problems. That is for another article.

Spring time is beautiful, finally some sunshine and warmth, but also a lot of allergens floating in the air resulting in allergic reactions in some individuals.

“Allergy” comes from the Greek “alos” meaning “other” and “ergon” meaning “reactivity” in Latin. So, allergies are reactions to molecules from outside the body, that most people do not react to.

What are allergens?

Antigens* that cause allergic reactions are called allergens, so allergens are substances (antigens) that are usually harmless but are capable of triggering a response from the immune system which may result in an allergic reaction. This is because the immune system perceives them as a threat and initiates an abnormally strong reaction to fight them off. This ends up causing more damage than good.

There is a variety of allergens we are exposed to such as pollen (common culprit for the spring time hay fever), dust mite excretions, dander, mould, drugs and medications, urushiol (found in poison ivy, and poison oak), stings from wasps, fire ants and bees can also cause allergies in sensitive people. Perfumes, soaps and latex are other common allergens.

For foods, some people are sensitive to tree nuts (i.e.: walnuts, macadamia nuts, pistachios, cashews, pecans, pine nuts, etc), peanuts (a legume), seafood and shellfish. Others have intolerances* and/or allergies to such foods as dairy products, wheat and soy and their derivatives, and food additives such as sulphites (chemical flavouring and colouring in foods).

Some people are more sensitive to allergens than others, these are atopic individuals. Their immune system overreacts when in contact with an allergen. They have a genetic predisposition to hypersensitivity, and a trigger (such as an allergen) will initiate the hypersensitivity reaction.

There are four different types of hypersensitivity: type 1, type 2, type 3 and type 4.

Type 1 hypersensitivity is the most prominent one in the spring and is often called IgE-mediated hypersensitivity, because it relies on immunoglobulin E (IgE antibody), which is a specific type of antibody (others are IgA, IgG, IgM and IgD).

The reaction happens really fast (immediate hypersensitivity), usually in a matter of minutes. Most hypersensitivity (allergic) reactions are actually of Type 1.

Type 1 hypersensitivity reactions happen in three phases:

  1. First exposure: This is the allergy-induced phase.
  2. Subsequent exposure. This is the allergy stimulation
  3. The effector phase: when a reaction actually occurs.

As previously mentioned, people who experience Type 1 Hypersensitivity reactions usually have a genetic predisposition to reacting to allergens. This is because they have certain genes that cause their T-Helper cells* to be more sensitive to certain antigens, so allergies tend to run in families as the production of these T-Helper cells is genetically linked.

Examples of Type 1 Hypersensitivity include: allergic asthma, allergic conjunctivitis, allergic rhinitis (“hay fever”), anaphylaxis, urticaria (“hives”), eosinophilia, atopic dermatitis (eczema), and angio-oedema.

With hay fever for example, the allergen in question is pollen (from trees, weeds, grasses, etc). This is what happens:

  • Phase 1: initial exposure – sensitisation phase.
  1. The allergen comes into contact with the skin, mucosal epithelium of the eyes, or the respiratory system when breathed in. Let’s say the person breathes in some ragweed pollen. If the individual has T-Helper cells that can bind to a specific molecule on the pollen, it makes that molecule an allergen.
  2. The allergen gets picked up by immune cells found in the membranes of the airways such as (dendritic) Langerhans cells or macrophages. These dendritic cells then migrate to the lymph nodes (regardless if the person is allergic or not).
  3. Dendritic and macrophage cells are antigen-presenting cells, as they carry the antigen to the lymph nodes and present it to the T cells there. Those T-Helper cells are said to be “naïve” as they haven’t encountered these antigens before, although they are built to fight them.
  4. If the person is allergic, the antigen-presenting cells also express co-stimulatory molecules. The co-stimulatory molecules are needed to mount an effective immune response.
  5. The naïve T-Helper cell involved in Type 1 hypersensitive reactions is a CD4+ naïve T-Helper cell. It binds to the antigens and to the co-stimulatory molecule, and it becomes “primed” and changes to a different sort of T-Helper cell. This is called differentiation.

In Type 1 reactions, it usually differentiates to a Type 2 T-Helper cell (TH2).

This differentiation is initiated by some molecules called cytokines*. The specific types of cytokines at play here are interleukins 4 (IL-4), 5 (IL-5) and 10 (IL-10).

  1. The TH2 cells release more cytokines (IL-4 and IL-3). These make the B cells undergo antibody class switching, so the B lymphocytes switch from making IgM antibodies to making allergen-specific IgE antibodies (this is also called isotype switching), which are excreted into the serum.
  2. TH2 cells also produce IL-5, which stimulates the production and activation of eosinophils (a type of granulated white blood cell)
  3. These ragweed-specific IgE antibodies have a high affinity for some receptors on effector cells (mast cells and basophils: types of white blood cells – granulocytes). These receptors are FcɛRI (F -C – epsilon receptors) and the IgE antibodies attach themselves to the surface of the mast cells and basophils.

These IgE antibodies are also called cytotropic antibodies because they can bind to cell surfaces.

  1. The eosinophils, mast cells and basophils are now ready for action.

Phase 2: subsequent exposure – allergy-stimulation phase.

  • The same person breathes in the ragweed pollen again (a few days, weeks or months later). The bound IgE is cross-linked by the re-introduced allergen (cross-linking usually happens when more than one allergen binds to receptors on the IgE molecule)

Phase 3: the effector phase.

There is an early phase reaction and late phase reaction to this stage.

  • Early phase reaction:
  1. The mast cells, using their code of antibodies, bind to the antigen. If two or more antigens bind to the mast cells, a cross-link is formed.
  2. A series of cell signalling events then takes place, which lead to degranulation of mast cells, which release a large number of mediators, which are pro-inflammatory molecules. These mediators cause the effects that are usually seen in an allergic reaction involving the skin, respiratory tract, circulation, or gastrointestinal tract.

The release of inflammatory mediators happens within minutes after activation, and this causes the early-phase or acute reaction.

  1. There are three main groups of inflammatory mediators: preformed mediators, newly synthesised mediators and cytokines. Preformed and newly synthesized mediators are the main components of the acute allergic reaction.

The preformed mediators include: histamine, serine proteases, tryptase, carboxylase A, and proteoglycans. Histamine is the principal and most important mediator. Mast cells and eosinophils release a lot of histamine.

Histamine binds the H1 receptors and cause the smooth muscles around the bronchi to contract, which makes the airways smaller and restricts breathing. It also causes blood vessel dilation and increased permeability of the blood vessels walls (fluid leaks out more easily into the interstitial spaces between the cells, causing swelling and hives).

  • The newly synthesized mediators from the mast cells include prostaglandins (PGD 2), platelet-activating factor and leukotrienes (LTC4, LTD4, and LTB4).
  • The cytokines are released by activated mast cells and include: IL-3, IL-4, IL-5, IL-6, IL-8, GM-CSF, and TNF (tumour necrotic factor). These cytokines recruit leukocytes such as eosinophils, neutrophils, and TH2 cells (chemotaxis*), which are then involved in the late phase reaction.

Late phase reaction:

  • This happens 8 to 12 hours after the second exposure, and involves more immune cells like TH2 cells, eosinophils, neutrophils and basophils.
  • These immune cells are recruited to the site where the allergen is located, because of the cytokines and pro-inflammatory molecules produced in the early phase reaction.

These include interleukins 4, 5, and 10 but also leukotrienes.

  • Leukotrienes are smaller molecules made out of fatty acids (metabolites of arachidonic acid) and facilitate communication between a local group of cells.

There are two leukotrienes of interest here: LTB4 and LTC4. They can cause smooth muscle contraction and damage to the epithelium like histamine, and they can also attract immune cells (chemotaxis) like neutrophils, mast cells and eosinophils to their location, even when the allergen is long gone.

Most people experience mild symptoms during a Type 1 hypersensitivity reaction, such as hives, eczema, allergic rhinitis (inflammation of the nose), and mild asthma, but some people have quite a severe reaction when exposed to a large dose of allergen (as with seafood or peanuts). This reaction is called anaphylaxis and can be life-threatening. The increased vascular permeability, along with the constriction of the airways can be so severe as to cut off the oxygen supply to the brain.

Treatment for Type 1 hypersensitivity can be:

  • Antihistamines to block the effects of histamine, which reduces vascular permeability and broncho-constriction.
  • Corticosteroids which reduce the inflammatory response.
  • Epinephrine which is sometimes given during a severe reaction in the form of an intramuscular injections through an epi-pen or intravenous injection. It can help constrict blood vessels and help prevent anaphylactic shock.

When the reaction is severe, it’s best to seek medical help (call an ambulance) as it can be fatal. Sometimes it seems to get better before it actually gets worse.

So, if you are sensitive to pollen and other allergens, it might be a good idea to be prepared and carry some antihistamine pills with you, natural tears eye drops (for hydration) and steroid nose spray. Of course, consult with your doctor first and don’t overdose on the antihistamine pills!

Some definitions:

*an antigen is a large complex substance which the body does not recognise as “self”, and therefore mounts an attack (usually in the form of antibodies) against.

*intolerances usually result in less severe reactions (often limited to digestive issues) compared to allergies which cause the involvement of the immune system and can affect several organs in the body. Allergic reactions tend to me more severe.

*T-Helper cells are a category of T lymphocytes in immune responses. Lymphocytes are a type of leukocytes (white blood cells).

There are 3 different types of lymphocytes: Natural Killer Cells (involved in innate immunity) , B-Lymphocytes and T-lymphocytes. T-cells provide cell-mediated immunity.

*cytokines are small proteins or glycoproteins involved in cells communication in the body. They are secreted by white blood cells (and other types of cells as well) in the body in response to a number of stimuli. They bind to specific receptors on target cells membranes and trigger signal-transduction pathways. This alters gene expression in the target cells.

“cyto” means “cell” and “kino” means “movement”. So, cytokines are cell signalling molecules which help cell to cell communication in an immune response. They also stimulate the movement of cells to the site of trauma.

*chemotaxis is the movement of white blood cells from the lumen of blood vessels to the affected (damaged) area. It is mediated by chemotactic factors (mediators, cytokines, fibrin, bacterial components, etc) that diffuse from the area of tissue damage. The granulocytes and monocytes which respond move down a concentration gradient (from an area of higher concentration to an area of lower concentration, much like diffusion)

 

Jacky van Driel-Nguene

Trichologist, Cystine Trichology Clinic

Amsterdam, Netherlands.

Website: www.cystine.nl

Instagram handle: @cystinehaircare

Facebook: https://www.facebook.com/Cystine-651067518247786/

2018-06-11T20:36:02+00:00