Lecture notes
Allergies in immunology
- Module
- Immunology
- Institution
- Bournemouth University Talbot Campus (BUTC)
Lecture notes detailing allergies, and their immunological backstory
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Lecture 17 – AllergiesImmune system must respond to dangerous pathogens but not harmless antigens.
Allergies such as hay fever (allergic rhinitis), atopic eczema, asthma.
Allergy/Hypersensitivity – almost interchangeable terms for an over-reaction to a (usually harmless)
antigen which causes damage to the host.
Allergen – any antigen that causes an allergy.
Atopy – a tendency to allergic reactions in an individual.
Person is said to be atopic Exposure through inhalation, on skin, consumption of food etc
Some Features of Allergens
- Often multiple epitopes (enables cross-linking of receptors)
- Often enzymes – cause damage/facilitate entry into cells
- Often contain/are PAMPs
- Often exposure is at a low concentration – favours TH2 response (CD4+ T cells secreting IL-4
which leads to IgE)
4 Types of Hypersensitivity Reaction
I= allergic anaphylaxis and atopy.
II= antibody.
III= immune complex.
IV= delayed.
Type I has the most common allergies.
Type I hypersensitivity
- Driven by IgE Remember that B cells differentiate into plasma cells which secrete high levels
of antibodies (immunoglobulins).
- Antibodies can be IgA, IgG, IgD, IgE or IgM.
In health, IgE is a response to a large parasite.
In atopic individuals IgE is produced in response to a harmless allergen.
Allergic reaction does not occur the first time an allergen is encountered.
, This first contact sensitises the immune system.
The second encounter leads to the signs and symptoms.
In the type 1 hypersensitivity reaction, IgE is bound to the FC epsilon RI receptor, is stable for weeks.
Anaphylatoxins- C3a, C4a, C5a can bind complement receptors and causes granule release.
Mast Cell [Basophil] Activation
Degranulation- release of vesicle contents.
Histamine:
- Muscle contraction (bronchospasm).
- Vascular leakage.
- Vasodilation.
- Mucus production.
- Acid production by the stomach.
- Stimulates secretory glands.
Synthesis of inflammatory cytokines.
Production of eicosanoids.
2 Phases to the Type I Hypersensitivity Reaction
Immediate phase:
- Starts within 30 minutes. Ends y 60 minutes.
- Mainly histamine and other granule components.
Late phase:
- 2-8 hours, lasts hours.
- Arachidonic acid pathway and cytokines.
Mediators of Type I Hypersensitivity
- Leukotrienes are potent bronchoconstrictors.
- They also induce vascular leakage and mucus production.
Cytokines of Type I Hypersensitivity
Produced by many ell types:
- Il-4= induces TH2 cells, promotes production of IgE.
- IL-5= recruit’s eosinophils.
- IL-8= recruit’s neutrophils.
- TNF-alpha= pyrogen and very inflammatory leading to shock.
These contribute to the late phase reaction.
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