Table of Contents
Overview of Type I (Immediate) Allergies
Type I allergies, also called immediate-type hypersensitivity reactions, are IgE-mediated overreactions of the immune system against normally harmless environmental substances (allergens). The term “immediate type” refers to the fact that symptoms typically occur within seconds to minutes after contact with the allergen.
Typical examples of type I allergies are:
- Hay fever (allergic rhinitis) to pollen
- Allergic conjunctivitis (itchy, watery eyes)
- Allergic asthma
- Food allergies (e.g. nuts, eggs, shellfish)
- Insect venom allergies
- Some drug allergies
- Severe systemic reaction: anaphylaxis / anaphylactic shock
Type I allergies always develop in two phases:
- Sensitization phase (first contacts, usually no or few symptoms)
- Effector phase (renewed exposure, rapid symptoms)
Only after successful sensitization does an immediate allergic reaction occur.
Sensitization Phase: How the Allergy “Learns” the Allergen
In type I allergies, the body develops a special form of immune response to an allergen, which ends with the production of allergen-specific IgE antibodies. This process takes days to weeks and usually proceeds without dramatic symptoms.
Step 1: Allergen Entry and Uptake
- The allergen (e.g. pollen protein, food component, insect venom) enters the body through:
- Inhalation (nose, lungs)
- Ingestion (gastrointestinal tract)
- Skin contact
- Injection (insect sting, drugs)
- Specialized immune cells, often dendritic cells in the barrier tissues (skin, mucosa), take up the allergen, break it down and present fragments (peptides) to T lymphocytes.
Step 2: TH2 Response and Cytokines
Upon presentation, certain T helper cells (TH cells) differentiate into TH2 cells. TH2 cells secrete characteristic cytokines that drive the allergic response, especially:
- IL-4 and IL-13: Promote class switching of B cells to IgE
- IL-5: Supports the development and activation of eosinophils (cells important in later phases, especially in asthma and chronic allergic inflammation)
Step 3: Class Switching to IgE and Production of Allergen-Specific IgE
Activated B cells that recognize the same allergen receive help from TH2 cells and undergo class switch recombination to produce IgE antibodies instead of IgM or IgG.
- Result: Allergen-specific IgE is secreted into the blood and lymph.
- Concentrations can be measured in diagnostics (e.g. “specific IgE against birch pollen”).
Step 4: Binding of IgE to Mast Cells and Basophils
IgE does not simply circulate freely; it binds with high affinity to:
- Mast cells in tissues (especially in skin, respiratory mucosa, gastrointestinal mucosa)
- Basophilic granulocytes in the blood
These cells have specific receptors for the constant part of IgE:
- FcεRI (high-affinity Fc receptor for IgE)
Once IgE binds FcεRI, mast cells and basophils are said to be sensitized. They are now “armed” with IgE molecules that are specific to the allergen.
Important:
- In this state, the person usually shows no acute symptoms.
- The organism is, however, now predisposed – the next contact with the allergen can trigger an immediate allergic reaction.
Effector Phase: The Immediate Allergic Reaction
When the sensitized organism meets the same allergen again, the effector phase begins. This is the actually observable immediate reaction.
Step 1: Allergen Cross-Linking of IgE on Mast Cells
- The allergen binds simultaneously to two or more IgE molecules that are attached to FcεRI receptors on one mast cell or basophil.
- This cross-linking of IgE/FcεRI receptors is the trigger for cell activation.
Step 2: Mast Cell/Basophil Degranulation
Cross-linking leads, within seconds to minutes, to:
- Degranulation:
- Preformed mediators stored in secretory granules are discharged into the surrounding tissue and blood.
- New synthesis of mediators:
- Additional substances are formed and released over minutes to hours.
Preformed Mediators (Released Immediately)
Important preformed mediators include:
- Histamine
- Dilates small blood vessels (vasodilation)
- Increases vascular permeability (fluid leakage into tissues)
- Stimulates nerve endings (itching)
- Constricts bronchial muscles (bronchospasm)
- Increases mucus production
- Heparin
- Anticoagulant effect, but in allergy primarily less central
- Proteases (e.g. tryptase, chymase)
- Can remodel tissue, contribute to inflammation and damage
Newly Synthesized Mediators
Within minutes to hours after activation, additional mediators are formed, for example:
- Leukotrienes (e.g. LTC₄, LTD₄, LTE₄)
- Very strong and long-acting bronchoconstriction
- Increase vascular permeability
- Promote mucus production
- Prostaglandins (e.g. PGD₂)
- Vasodilation, bronchoconstriction, recruitment of inflammatory cells
- Cytokines (e.g. IL-4, IL-5, IL-13, TNF-α)
- Strengthen and maintain the inflammatory reaction
- Recruit eosinophils and other cells
- Promote chronic allergic inflammation (e.g. in asthma)
Step 3: Clinical Symptoms of the Immediate Reaction
The combination of vasodilation, increased permeability, smooth muscle contraction and nerve stimulation leads to typical symptoms, which depend on:
- The entry route and location of the allergen
- The amount of allergen
- The distribution of sensitized mast cells
- The individual’s reactivity
Local Immediate Reactions
Some typical local manifestations:
- Skin:
- Redness (erythema)
- Swelling (wheal)
- Itching
- Urticaria (hives)
- Local angioedema (e.g. puffy eyelids, swollen lips)
- Respiratory tract:
- Sneezing, runny nose, nasal congestion (allergic rhinitis)
- Itchy, watery, red eyes (allergic conjunctivitis)
- Coughing, shortness of breath, wheezing (allergic asthma)
- Tightness in the chest
- Gastrointestinal tract (often in food allergy):
- Nausea, vomiting
- Abdominal pain, cramps
- Diarrhea
- At the insect sting site:
- Pronounced local swelling and redness
- Pain, itching
These symptoms often appear within minutes of exposure and can subside after minutes to a few hours, depending on severity and intervention.
Systemic Immediate Reactions: Anaphylaxis
If mediators are released massively and reach the whole organism, a systemic reaction may occur: anaphylaxis, the most severe form of type I allergy.
Typical features of anaphylaxis (not the full emergency treatment, which belongs in another chapter):
- Skin: generalized redness, hives, angioedema
- Respiratory tract: severe bronchospasm, throat tightness, hoarseness, difficulty breathing
- Circulation: drop in blood pressure, dizziness, consciousness disorders, shock
- Gastrointestinal tract: severe abdominal cramps, vomiting, diarrhea
Anaphylactic shock is a life-threatening emergency that requires immediate medical intervention.
Early and Late Phase of Type I Allergic Reactions
The immediate allergic reaction can be divided into:
- Early phase reaction (minutes)
- Late phase reaction (hours)
Early Phase Reaction
- Starts typically within seconds to 30 minutes after contact with the allergen.
- Dominated by:
- Mast cell/basophil degranulation
- Histamine and other rapidly released mediators
- Main symptoms:
- Itching
- Redness, wheals
- Bronchoconstriction
- Increased mucus production
This phase corresponds to what is classically called “immediate reaction”.
Late Phase Reaction
- Occurs 4–8 hours after allergen exposure; can last up to 24 hours or longer.
- Characterized by:
- Recruitment and activation of additional inflammatory cells, especially:
- Eosinophilic granulocytes
- TH2 cells
- Neutrophils
- Macrophages
- Release of cytokines, leukotrienes and other mediators from these cells
Clinical significance:
- Longer-lasting swelling and tissue damage
- Important for chronic allergic diseases, especially allergic asthma and atopic dermatitis, where repeated or persistent late-phase reactions contribute to structural changes (remodeling) in the tissue.
Typical Allergens in Type I Reactions
Many different substances can act as allergens in type I allergies. They are usually proteins or protein-bound molecules that can be recognized by the immune system.
Some typical allergen groups:
- Inhalation allergens:
- Pollen (e.g. birch, grass, ragweed)
- House dust mite components
- Animal dander (e.g. cat, dog, horse)
- Mold spores
- Food allergens:
- Nuts (e.g. peanuts, hazelnuts, walnuts)
- Eggs
- Milk proteins
- Fish, shellfish
- Certain fruits or vegetables (often cross-reactive with pollen)
- Insect venom allergens:
- Bee venom
- Wasp venom
- Drug allergens:
- Certain antibiotics (e.g. penicillins)
- Some anesthetics and other drugs
Important:
- Whether a person becomes allergic depends not only on the allergen but also on genetic predisposition and environmental influences.
- Some individuals tend to develop multiple type I allergies (atopy).
Distinction from Other Types of Hypersensitivity
Type I allergy is only one form of hypersensitivity. It is characterized by:
- Mediators: IgE, mast cells, basophils, histamine, leukotrienes
- Onset: seconds to minutes (immediate)
- Typical symptoms: hay fever, urticaria, anaphylaxis
Other hypersensitivity types (II, III, IV) proceed via other mechanisms and have different time courses (often hours to days) and are therefore not classified as type I allergies.
Diagnostics of Type I Allergies (Principles)
The detailed methods belong in a dedicated diagnostics context, but the basic idea is:
- Detection of sensitization: Is there allergen-specific IgE?
- Detection of clinical reactivity: Does contact with the allergen trigger symptoms?
Common approaches:
- Skin tests:
- Prick test: Small amounts of allergen are introduced into the superficial skin; redness and wheal formation as an immediate reaction indicate sensitization.
- Laboratory tests:
- Measurement of specific IgE in the blood against defined allergens.
- Provocation tests:
- Under medical supervision: Controlled exposure of the suspected organ (nose, eyes, bronchi, gastrointestinal tract) to the allergen to assess reaction.
Important:
- A positive sensitization test (e.g. elevated specific IgE) alone is not sufficient for the diagnosis of a clinical allergy. The medical history (symptoms on exposure) is crucial.
Principles of Prevention and Treatment (Overview)
Specific therapy details are covered more thoroughly in chapters on prophylaxis and therapy. For type I allergies, the central approaches are:
- Allergen avoidance (elimination, reduction):
- Example: Avoiding certain foods, minimizing contact with animal dander, adapting living environment for house dust mite allergy.
- Symptomatic drug therapy:
- Antihistamines: Block histamine receptors (e.g. for hay fever, urticaria).
- Glucocorticoids: Anti-inflammatory, e.g. as nasal sprays, inhalers, ointments.
- Bronchodilators: Inhaled drugs to expand narrowed bronchi in asthma.
- In emergencies (e.g. anaphylaxis): Adrenaline (epinephrine), volume infusions and other emergency medications (only medically administered).
- Causal therapy: Specific immunotherapy (hyposensitization, allergy shots):
- Controlled, gradually increasing administration of the allergen to change the immune response and reduce IgE-mediated reactivity.
- Especially established for pollen, insect venom, some other inhalation allergens.
- Emergency preparedness for high-risk patients:
- Carrying an emergency kit (e.g. adrenaline auto-injector, antihistamine, corticosteroid) for known risk of severe reactions such as insect venom allergy or certain food allergies.
Summary
Type I allergies (immediate type) are characterized by:
- Sensitization phase:
- Allergen-specific TH2 response
- Class switching of B cells to IgE
- Binding of IgE to mast cells and basophils
- Effector phase upon renewed contact:
- Allergen cross-links IgE on mast cells/basophils
- Rapid degranulation and release of histamine and other mediators
- Typical symptoms within minutes: itching, redness, swelling, bronchoconstriction, up to anaphylactic shock
This form of allergy is very common and ranges from mild local symptoms to life-threatening systemic reactions. Understanding the underlying mechanisms is the basis for targeted prevention, diagnostics and therapy.