Type I hypersensitivity (immediate, IgE) !

Process

An allergy: the body has made IgE against something harmless, and on the next contact mast cells burst open within minutes and release histamine.

Updated 2026-11-01

See it in 3D: Skin · Trachea

What it is

Type I hypersensitivity is the immediate allergic reaction. A first exposure primes Th2 cells, which push B cells to switch to IgE; that IgE sits on high-affinity receptors of mast cells and basophils. On re-exposure the allergen cross-links the IgE and the cells release preformed and newly made mediators within minutes. It ranges from a runny nose to anaphylaxis, the life-threatening multisystem form.

Step by step

First contact: dendritic cells present the allergen and naive CD4 T cells become Th2 cells.
Th2 cytokines IL-4 and IL-13 switch B cells to IgE; IL-5 recruits and activates eosinophils.
IgE binds FcεRI on mast cells and basophils: the person is now sensitized, with no symptoms yet.
Re-exposure: the allergen bridges two IgE molecules and the cell degranulates within minutes.
Early phase: histamine and tryptase cause vasodilation, leaky vessels, itching and smooth muscle spasm.
Late phase (hours later): leukotrienes, prostaglandins, cytokines and eosinophils sustain the inflammation.

Markers

IgE
FcεRI
Histamine
Tryptase
Leukotrienes
IL-4
IL-5
IL-13

Clinical notes

Anaphylaxis: sudden skin or mucosal signs (hives, swollen lips or tongue) plus breathing trouble, low blood pressure or persistent vomiting; after a known exposure, low blood pressure alone is enough.
Epinephrine given intramuscularly is the first-line treatment; antihistamines and corticosteroids are add-ons that do not replace it and do not reverse airway or circulatory collapse.
A second wave (biphasic reaction) can come hours after the first one settles, which is why patients are observed after treatment.
Common triggers: foods (peanut, tree nuts, shellfish, milk, egg), insect venom, drugs, latex and contrast media.
Atopic diseases (allergic asthma, allergic rhinitis, atopic dermatitis) are type I and tend to cluster in the same person and family.

In the lab

Skin prick test: a wheal and flare within minutes shows allergen-specific IgE on skin mast cells.
Serum allergen-specific IgE; total IgE and blood eosinophils are often high.
Serum tryptase drawn soon after a reaction supports anaphylaxis, but a normal value does not rule it out.

Test yourself

Think of the answer, then tap the question to see it.

Which cytokine drives the B-cell class switch to IgE?

IL-4 (with IL-13), made by Th2 cells. IL-5, from the same cells, recruits and activates eosinophils.

Which drug class is first-line in anaphylaxis, and why are antihistamines not enough?

Epinephrine, given intramuscularly. It raises blood pressure and opens the airway; antihistamines only ease itch and hives and do not reverse shock or bronchospasm.

Which blood test helps confirm that a reaction was anaphylaxis?

Serum tryptase drawn soon after the event. It comes from mast cells and stays high for a few hours, but a normal result does not exclude anaphylaxis.

Why must a person have met an allergen before to react to it in a type I reaction?

Because the first contact is needed to make specific IgE and load it onto mast cells. The reaction happens on later contacts, when allergen cross-links that IgE.

Add to my cards (4)

See it in 3D

The structures of Durgical's 3D anatomy where it is found.

← All of immunology

Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.

Sources: Atopy (StatPearls Publishing (NCBI Bookshelf), 2024); Anaphylaxis (StatPearls Publishing (NCBI Bookshelf), 2023); Anaphylaxis: MedlinePlus Medical Encyclopedia (MedlinePlus, U.S. National Library of Medicine, 2026).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.