Type I Hypersensitivity Reaction 

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  • A hypersensitivity reaction is an immunological response that causes host-harming excessive or inappropriate reactions.
  • It is a damaging immune response in which tissue damage is caused by excessive or inappropriate immune responses to the same antigen in a previously sensitised individual.
  • Hypersensitivity reactions may involve both the humoral and cell-mediated components of the immune response.
  • Hypersensitivity comprises two fundamental components. First priming dosage of antigen is required to activate the immune system, followed by a startling dose of the same antigen that results in harmful effects.
  • Based on the duration of the reactions and the processes that induce tissue damage, hypersensitivity has been widely categorised as either immediate or delayed.
  • In the former, the response occurs within minutes or hours after antigen exposure, but in the later, it takes days for symptoms to appear.
  • The Prince of Monaco was the first to observe the harmful effects of jellyfish on swimmers. Portier and Richet (1906) postulated that a poison was responsible for these symptoms and coined the term “anaphylaxis.”
  • Gell and Coombs (1963) categorised hypersensitive reactions into four groups depending on the length of time between antigen exposure and the onset of the reaction, as well as the immune system arm involved.
  • Types I, II, and III are antibody-mediated and are referred to as immediate hypersensitivity reactions, but type IV is cell-mediated (i.e., mediated by cell-mediated immunity) and is referred to as delayed hypersensitivity reactions.
  • The hypersensitive reaction of type V was previously described. It is known as a stimulatory-type reaction and is a variant of type II hypersensitivity.
TYPE I HYPERSENSITIVITY: PATHOGENESIS AND CLINICAL FINDINGS | Image Source: https://calgaryguide.ucalgary.ca/Type-I-Hypersensitivity:-Pathogenesis-and-clinical-findings/

Type I hypersensitivity

  • The typical name for a Type I hypersensitivity reaction is an allergic or acute hypersensitivity reaction.
  • This reaction is usually fast, happening within minutes of antigen contact, and invariably involves degranulation of basophils or mast cells mediated by IgE.
  • Type I reactions are also known as hypersensitivity reactions mediated by IgE. IgE is accountable for sensitising mast cells and giving antigen identification for rapid hypersensitivity responses.
  • Due to the existence of prepared mediators in mast cells, there is a small delay between antigen exposure and the development of clinical symptoms.
  • Consequently, the time required for these reactions to commence is small, so the onset of symptoms appears instantaneous.
  • There are two types of Type I reactions: anaphylaxis and atopy.


  • Anaphylaxis is an abrupt, sometimes fatal, systemic hypersensitivity reaction.
  • It happens when an antigen (allergen) attaches to IgE on the surface of mast cells, resulting in the release of several anaphylaxis mediators.
  • Upon antigen exposure, antigen-specific TH2 cells are activated, resulting in the activation of B cells to make IgE antibodies.
  • The IgE then binds with great affinity to the Fc region of mast cells and basophils. On reexposure to the allergen, IgE is activated and basophils and mast cells degranulate to release pharmacologically active mediators within minutes.
  • Binding of IgE to mast cells is also referred to as sensitization, as IgE-coated mast cells are prepared to be activated upon repeated antigen exposure.

Initiator cells in anaphylaxis

The allergen initiating a type I reaction is also known as the allergen. Typical allergies include: Plant pollen, proteins (e.g., foreign serum and vaccines).

  • Several food items (e.g., eggs, milk, seafood, and nuts).
  • Drugs (e.g., penicillin and local anaesthetics) (e.g., penicillin and local anesthetics).
  • insect-based goods (venom from bees, wasps, and ants),
  • Dust mites, mould spores.
  • Animal fur and dander.

Although the precise reason why these compounds behave as allergens is unknown, they share certain properties. Since these reactions are T-cell dependent, T-cell-independent antigens, such as polysaccharides, are incapable of inducing type I reactions.

Effector cells in anaphylaxis

In anaphylaxis, the effector cells are (a) mast cells, (b) basophils, and (c) eosinophils. All three of these cells contain cytoplasmic granules whose contents are the principal allergen-reaction mediators. Additionally, all three cell types create pro-inflammatory lipid mediators and cytokines.

Mast cells

  • Anaphylaxis is mediated mostly by mast cells. These cells are found throughout connective tissue, particularly near blood and lymphatic vessels.
  • Degranulation of mast cells is mediated by IgE when an allergen promotes cross-linking of membrane-bound IgE.
  • Monovalent molecules, which are incapable of causing cross-linking, are incapable of causing degranulation, demonstrating the significance of cross-linking in the process.


  • It is the most significant anaphylaxis mediator.
  • It is found in a prepared condition in mast cell granules and basophil granules.
  • It induces vasodilation, increased capillary permeability, and contraction of smooth muscle.
  • It is the main mediator of allergic rhinitis, urticaria, and angioedema.
  • Antihistamines that inhibit histamine receptors are relatively helpful for allergic rhinitis but ineffective for asthma.

Slow-reacting substances of anaphylaxis

  • Leukocytes manufacture these substances.
  • These are composed of several leukotrienes, which do not exist in a preformed state but are created during anaphylactic reactions.
  • Antihistamines do not suppress the primary mediators of bronchoconstriction in asthma, which are leukotrienes.
  • They promote enhanced vascular permeability and contraction of smooth muscle.


  • Preformed serotonin is present in mast cells and platelets.
  • It produces vasoconstriction, increased capillary permeability, and contraction of smooth muscle.

Eosinophilic chemotactic factors of anaphylaxis

  • It is found in granules of mast cells in a prepared condition. It draws eosinophils to the action site.
  • However, the involvement of eosinophils in type I hypersensitivity reactions is unclear.
  • It is believed to lessen the intensity of type I hypersensitivity by releasing the enzymes that breakdown histamine and SRS-A, histaminase and arylsulfatase.

Prostaglandins and thromboxanes

  • Prostaglandins cause bronchoconstriction in addition to capillary dilation and enhanced permeability.
  • Thromboxanes cause platelet aggregation.
  • All of these mediators are rapidly deactivated by enzymatic processes, and are therefore only active for a few minutes following their release.

Phases of anaphylaxis

The range of type I hypersensitivity-related alterations can be categorised into acute and late phases.

1. Immediate phase

  • Within minutes of reexposure to the same antigen, degranulation and the release of pharmacologically active mediators characterise this phase.
  • Histamine is the primary biogenic amine that generates fast vascular and smooth muscle responses, including vascular leakage, vasodilation, and bronchoconstriction.
  • It is responsible for the “wheal and flare” reaction seen in cutaneous anaphylaxis as well as the increased peristalsis and bronchospasm caused by ingested allergens and asthma, respectively.
  • Other lipid mediators, such as prostaglandins (PGD2) and leukotrienes (LTC4), which are produced from arachidonic acid via the cyclooxygenase pathway and lipoxygenase system, respectively, also result in comparable effects.
  • At inflammatory sites, prostaglandins and leukotrienes promote bronchoconstriction, neutrophil chemotaxis, and neutrophil aggregation.

2. Late phase

  • This phase develops 4–6 hours following the onset of the immediate phase and lasts 1–2 days.
  • It is characterised by neutrophils, macrophages, eosinophils, and lymphocytes infiltrating the response site.
  • This results in an exacerbation of the different inflammatory symptoms seen in the early response, such as bronchoconstriction and vasodilation.
  • After degranulation, the cells remain alive and continue to produce other chemicals that are released later, creating the late phase of type I responses.
  • The mediators cannot be detected until several hours after the initial reaction.
  • Important mediators during the late phase include slow-reacting substances of anaphylaxis (SRS-A) including 
    • several leukotrienes (e.g., LTC4, LTD4, and LTE4).
    • The platelet aggregation factor
    • cytokines released by mast cells.

Clinical manifestations of anaphylaxis

  • Anaphylaxis is an abrupt, sometimes fatal reaction that typically affects many organs.
  • The onset of symptoms relies on the degree of hypersensitivity, as well as the amount, diffusion, and place of antigen exposure.
  • Multiple organ systems, including the skin (pruritus, flushing, urticaria, and angioedema), respiratory tract (bronchospasm and laryngeal edoema), and cardiovascular system, are typically impacted (hypotension and cardiac arrhythmias).
  • The most common causes of death within the first two hours include laryngeal edoema, intractable bronchospasm, hypotensive shock, and cardiac arrhythmias.

Anaphylactoid reaction

This resembles an anaphylactic reaction clinically, but varies from it in other ways. First, it is not mediated by IgE. Second, the inciting substances (drugs or iodinated contrast media, for example) directly stimulate basophils and mast cells to release mediators without the involvement of IgE.

Management and prevention of anaphylaxis

Desensitization is a successful method for preventing systemic anaphylaxis. Desensitization is of two types: acute and chronic.

Acute desensitization

  • Acute desensitisation involves the delivery of modest doses of the antigen to which the individual is allergic, at 15-minute intervals. 
  • The antigen–IgE combination is generated in minute quantities; hence, not enough mediators are released to cause a significant reaction. 
  • However, this effect is short-lived due to the continuing manufacturing of IgE, which causes the hypersensitive reaction to recur.

Chronic desensitization

  • Chronic desensitisation entails the delivery of an antigen to which a person is allergic over a period of weeks. 
  • This induces the creation of IgA and IgG antibodies that inhibit antigen from attaching to mast cells, so avoiding the allergic reaction. 
  • Administration of medications to suppress mediator action, maintenance of airways, and support of respiratory and cardiac functions are the cornerstones of treating anaphylactic reactions.


  • Coca (1923) initially proposed the term atopy to describe family hypersensitivities that arise spontaneously in humans.
  • Atopy is a local, repeated, and nonfatal symptom of an acute hypersensitivity reaction.
  • This reaction is associated with a high IgE level and a high degree of familial predisposition.
  • It is restricted to a particular tissue, typically involving epithelial surfaces at the site of antigen introduction.
  • It is mediated by the homocytotropic IgE antibodies (i.e., species specific). Only human IgE can attach to mast cell surfaces.
  • Atopy is typically manifested by asthma, rhinitis, urticaria, and atopic dermatitis. Among atopic reactions, bronchial asthma is the most prevalent.
  • Certain mutations in genes encoding the alpha chain of the IL-4 receptor are related with atopy.
  • These alterations enhance the efficacy of IL-4, resulting in an increase in the manufacture of IgE by B cells.
  • In reaction to allergens, atopic individuals create large quantities of IgE, whereas normal individuals do not. This is dependent on an individual’s propensity to develop a TH2 response, as only TH2-derived cytokines trigger the heavy-chain isotype switch to IgE class in B cells.
  • Stimulation of heavy chain isotype flipping to the IgE class may be regulated by a number of variables, including inherited genes, the form of antigens, and antigen exposure history.
  • Atopic hypersensitivity cannot be transmitted by lymphoid cells, but can be transmitted by serum. In the past, this observation was used to diagnose passive cutaneous anaphylaxis by the Prausnitz–Kustner reaction. Radioallergosorbent test (RAST), enzyme linked immunosorbent assay (ELISA), and passive agglutination tests are commonly used to detect IgE in the serum in order to diagnose atopy.

Prausnitz–Kustner reaction

  • This is due to the unique affinity of IgE antibodies for skin cells. In this experiment, Kustner, who suffered from an allergy to specific cooked fish, provided a sample of his serum.
  • Prausnitz received an intradermal injection of the same serum, followed by an intradermal injection of a small amount of cooked fish at the same place 24 hours later.
  • This caused a wheal and inflammation at the injection site within minutes.
  • Due to the risk of transmitting certain bloodborne viral illnesses, such as hepatitis B, hepatitis C, and HIV, the test is no longer performed.

Steps of Type I hypersensitivity reaction

Two antigen doses are required for the development of allergy or anaphylaxis. The first dose is known as the sensitising dose, whereas the second dose is known as the stunning dose.

1. Production of IgE antibody

  • When antigen (allergen) enters the host, antibody production occurs.
  • Antigen-presenting cells (APCs) initially process and present allergen to CD4 T cells.
  • The division of activated CD4 t cells into T helper cells and memory cells. T helper generates IL4.
  • In the presence of APC and IL4, B cells simultaneously attach to antigen and become activated.
  • The division of activated B lymphocytes into plasma cells and memory cells.
  • Up to this point, the mechanism resembles the usual humoral immune response. Plasma cells produce IgE antibody instead of Ig M or IgG during Type I hypersensitivity, as opposed to Ig M or IgG during normal immune response.

2. Sensitization

  • On the surface of tissue mast cells and blood basophils is a receptor for the Fc region of IgE antibody. The IgE antibody therefore attaches to the FcRI on mast cells and basophils.
  • This binding of IgE to mast cell and basophil is referred to as Sensitization, and mast cells and basophils are said to be sensitised.

3. Shocking dose of antigen

  • When the same antigen (allergen) enters the same host for the second time, the antigen binds to the Fab region of IgE molecules on the surface of mast cells and basophils.

4. Degranulation of mast cell

  • The cross-linking of antigen (allergen) to IgE antibody results in the destruction of mast cells and basophils, resulting in the release of many pharmacologically active substances, including histamine, heparin, serotonin, cytokines, leucotriene, prostaglandin, etc.

5. Anaphylatic reaction

  • These active chemical mediators operate on the surrounding tissue to produce diverse allergy symptoms, including vasodylation, smooth muscle contraction, mucus formation, and sneezing, among others.
  • Depending on the allergen, an allergic reaction can be either localised or systemic.

Mechanism of Activation and Degranulation of mast cell

The intracellular signalling pathways that ultimately result in mast cell degranulation involve the cooperation of multiple protein and lipid kinase and phosphatase, as well as cytoskeleton rearrangement. Mast cell activation and degranulation can be broken down into three metabolic processes.

  1. Phosphorylation
  2. Methylation
  3. Adenylation
Mechanism of Activation and Degranulation of mast cell
Mechanism of Activation and Degranulation of mast cell

1. Phosphorylation

  • The activation of protein tyrosine kinase by relying on FcERI-bounded antibody (PTK).
  • Then, PTK phosphorylates phospholipase C, which transforms phosphatidylinositol 4,5 bisphosphate (PIP2) into diacetylglycerol (DAG) and inositol triphosphate (IP3).
  • IP3 is an effective mobilise that induces pore formation and release. Ca++ ions stimulate protein kinase c via DAG (PKC).

2. Methylation

  • Cross-linkage of FcERI triggers an enzyme that transforms phosphatidyl serine (PS) into phosphatidylethanolamine (PE).
  • The enzymes phopholipid methyl transferase I and II eventually methylate PE to produce phosphotidyl choline (PC) (PMT I and PMT II).
  • The accumulation of PC on the external surface of the plasma membrane increases membrane fluidity and enhances the development of the Ca++ channel, via which Ca++ ions enter.
  • Ca++ ion and PTK stimulate the activation of Mitoegn-activated protein kinase (MAPK).
  • MAPK activates phopolipase A2, which promotes the conversion of phosphotidyl cholone (PC) to Lyso PC and arachidonic acid.
  • The conversion of arachidonic acid into the powerful mediators leckotrines and prostaglandin D2
  • Activated MAPK also stimulates cytokine release by boosting cytokine gene transcription.

3. Adenylation

  • FcERI cross-linkage also activates the membrane adenylate cyclase enzyme, resulting in a 15-second transient increase in cAMP.
  • A subsequent decrease in cAMP, mediated by protein kinase, is required for mast cell degranulation.
  • cAMP-dependent protein kinase phosphorylates the granule membrane protein, altering the granules’ permeability to water and Ca++ ions and causing granule swelling.
  • As a result, swelling of granules and formation of the Soluble N-ethylmaleimid attachment receptor (SNARE) protein complex facilitates membrane fusion and the release of pharmacological chemical products, which are responsible for allergic symptoms.
Mechanism of Activation and Degranulation of mast cell
Mechanism of Activation and Degranulation of mast cell

Clinical manifestation

Clinical manifestations range from life-threatening conditions like systemic anaphylaxis and severe asthma to localised reactions like hay fever and eczema.

A. Systemic anaphylaxis

It is a shock-like and frequently fatal condition that is typically caused by allergens injected directly into the bloodstream or absorbed through the skin. The symptoms include:

  • Labored breathing
  • Drop in blood pressure
  • Smooth muscle contraction
  • Bronchiole constriction
  • Suffocation

B. Localized hypersensitivity

It is restricted to specific target tissues or organs and frequently involves the epithelial surface at the allergen entry point. The tendency to manifests hypersensitivity reaction is inherited and is called atopy. Atopic allergy encompasses a vast array of IgE-mediated disorders, including:

  • Hey fever (allergic rhinitis)
  • Asthma (allergic or intrinsic)
  • Food allergy
  • Atopic dermatitis (eczema)

Diagnosis Type 1 hypersensitivity reaction

  • A thorough patient history and educated estimates may be used to identify the allergy.
  • Ag skin testing with a comprehensive panel. This is accomplished through subcutaneous Ag injection or a patch test to determine wheal and flare response.
    • Subcutaneous administration of the antigen results in the release of prepared mediators that increase vascular permeability, local edoema, and irritation.
    • The late phase reaction is frequently neglected, and typically manifests as a painful lump on the skin that is not irritating.
    • IgE level: IgE levels in the majority of patients may be elevated.
    • This is a radioallergosorbent test that identifies allergen-specific IgE. It is an expensive test that is inferior to skin tests.
    • Eosinophil Count:-Eosinophilia in the blood may be present in allergic disorders.

Treatment / Management of Type I Hypersensitivity

The sort of treatment administered to a patient with type I hypersensitivity varies on the patient’s symptoms and the reaction’s cause.

A. Anaphylaxis

  • Anaphylaxis necessitates urgent treatment, as its onset is typically quick and it can be fatal.
  • If feasible, the offending agent should be eliminated immediately, and patients should be placed in a supine position with their lower extremities elevated, unless there is a substantial blockage or airway inflammation.
  • If there is significant stridor or severe respiratory distress, intubation may be required immediately.
  • If the patient has a history of allergic reactions, they will be given prescriptions for emergency self-treatment, including an epinephrine IM autoinjector or 1:1,000 solution, bronchodilators, antihistamines, and/or corticosteroids.
  • Epinephrine intramuscular (IM) injection is the recommended first-line treatment that should be delivered without delay, followed by the use of the following adjuvant therapies:


  • Epinephrine exerts agonist actions on alpha-1, beta-1, and beta-2 adrenergic receptors. Consequently, it can promote vasoconstriction and peripheral vascular resistance while decreasing airway or mucosal edoema. The beta effects result in an increase in inotropy, chronotropy, vasodilation, and a decrease in the release of inflammatory mediators from mast cells and basophils.
  • The epinephrine dosage is depending on body weight and may be repeated every 5 to 15 minutes. Studies have revealed that a second dose is necessary in approximately 35% of cases.
  • When possible, infants weighing less than 10 kg should be given an exact dose based on their weight (rather than an approximation). The 0.1 mg dose may be administered via autoinjector or by drawing up 0.1 mL of the 1 mg/mL solution if drawing up an accurate dose is anticipated to cause a considerable delay in a patient with severe symptoms or who is rapidly deteriorating. In the absence of the 0.1 mg autoinjector, the 0.15 mg autoinjector may be utilised.
  • For weights between 10 and 25 kg, 0.15 mg of IM epinephrine is administered into the anterior-lateral thigh.
  • For weights greater than 25 kilogrammes, 0.3 mg of IM epinephrine is injected into the anterior-lateral thigh.
  • The dose of epinephrine solution (1 per 1,000) is 0.01 mg/kg per dose, with a maximum of 0.5 mg/dose.
  • Additionally, epinephrine can be delivered via slow continuous infusion, endotracheal, and intra-osseous routes. It is recommended that blood pressure and heart rate be monitored during administration.


  • Albuterol is often administered as a metered-dose inhaler (MDI), dry powder inhaler (DPI), or nebulized solution when the patient does not respond to epinephrine for the treatment of bronchospasm.
  • Albuterol MDI or DPI dosing (90 mcg/actuation): Adults should provide 2 to 3 inhalations as needed for symptom alleviation; during severe exacerbations, up to 8 inhalations every 20 minutes may be required. Although the paediatric dose is 4 to 8 puffs every 20 minutes for up to 3 doses, data for kids 4 years is limited.
  • Albuterol nebulization solution: (2.5 to 5 mg as needed) The nebulized solution can also be administered continuously to critically ill adult and paediatric patients at a rate of 10 to 14 mg per hour.

Antihistamines: i.e., diphenhydramine (H1 antagonist), famotidine or ranitidine (H2 antagonists)

  • Antihistamines are considered second-line adjunctive therapy and can provide relief of symptoms such as hives or pruritis. However, antihistamines should not be used as monotherapy, as they do not mitigate upper or lower airway obstruction, shock, or hypotension. Although antihistamines are usually used in combination with both an H1 antagonist and an H2 antagonist in anaphylaxis, there is a lack of direct evidence to support their administration. Second-generation H1 antagonists have fewer sedative effects than first-generation agents, and as such, they may also be considered. Some studies suggest that when H2 antagonists are given intravenously (IV), they can increase hypotension.
  • Diphenhydramine IV dose: 25 to 50 mg per dose in adult patients and 1 to 2 mg/kg/dose in pediatrics (maximum 50 mg/dose); dose may be repeated every 6 hours.
  • Ranitidine oral (PO) or IV: 1 to 2 mg/kg per dose (maximum 75 to 150 mg of oral and IV in adults and a maximum of 50 mg/dose in pediatrics).
  • Famotidine IV: 20 mg diluted to 5 ml 0.9% normal saline and pushed over two minutes in adults and 0.25 mg/kg (maximum 20 mg per dose) in pediatrics. 


  • Due to their delayed start of effect, glucocorticoids do not have an acute role in the treatment of anaphylaxis, and there are no randomised, controlled trials that demonstrate the benefits of their use. However, the theoretical justification for its use is to reduce biphasic or prolonged anaphylactic reactions.
  • Methylprednisolone: 1 to 2 mg/kg/day (maximum of 125 mg per dosage) for one to two days without tapering.

Additional adjuvant therapy for anaphylaxis include supplementary oxygenation, intravenous fluids for volume replacement, glucagon or vasopressors for refractory hypotension, and/or atropine for bradycardia. Ideally, the following parameters should be evaluated continuously or regularly during and after anaphylaxis: blood pressure, respiratory status, oxygenation, urine output, cardiac function, and heart rate.

B. Urticaria/Angioedema

  • Treatment of urticaria is similar to anaphylaxis where the offending chemical is removed if identified, and then the patient is given an H1 antihistamine and glucocorticoids (see above for dose) (see above for dosing).
  • There is not a need for epinephrine unless there is suspicion for anaphylaxis.
  • Patients with chronic urticaria who are unresponsive to H1 antihistamines may benefit from omalizumab, which is a monoclonal antibody that blocks the binding of IgE to receptors on mast cells and basophils, or cyclosporine, which is an immunomodulator.

C. Allergic Asthma/Allergic Rhinitis/ Allergic Conjunctivitis/Allergic Dermatitis/Eczema/Wasp or bee venom/Drug Allergy/Food Allergy

  • For allergic diseases, avoidance of the offending agent is the initial step in treatment. Oral or topical H1 antihistamine and oral or inhalation glucocorticoids may be used for symptomatic management.
  • For allergic rhinitis, topical nasal or ocular decongestants can provide temporary relief of symptoms.
  • For allergic asthma, patients can be provided inhaled beta-agonists with or without inhaled corticosteroids based on phases of asthma therapy recommended by the National Heart, Lung, and Blood Institute.
  • Patients with considerable symptoms despite avoidance of the allergen and who have a lack of remission from adjunctive therapy can undergo allergen immunotherapy, such as desensitisation or hypo-sensitization (allergy injections).
  • The patient must have a verified IgE-mediated allergy (allergic: asthma, rhinitis, conjunctivitis, dermatitis, drug allergy) prior to beginning of immunotherapy.
  • The treatment is carried out in a clinical setting for the first doses, where particular allergens are supplied in a slow escalation of subclinical dosages.
  • The route of delivery is either via subcutaneous immunotherapy (SCIT), sublingual/sallow immunotherapy (SLIT), or mucosal route.
  • The purpose of desensitisation is to increase the synthesis of immunoglobulin G (IgG) antibodies on mast cells instead of IgE.
  • This procedure is called as isotype swapping and normally lasts for three years. Desensitization treatment is successful in about 67% of patients and is usually more useful in younger individuals and those who have a sensitivity to a monovalent allergen.
  • Patients need to be prescribed and instructed on the proper use of epinephrine autoinjectors prior to the commencement of immunotherapy.


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