Hypersensitivity Flashcards
(11 cards)
Hypersensitivity
An over-reaction of adaptive immune system to innocuous antigens, self-antigens, or transplants, leading to tissue damage or disease.
Involves sensitisation on first exposure & pathological reactions on repeated exposure.
Four types: types I–III are antibody-mediated, while type IV is T cell-mediated.
Type I hypersensitivity
Triggered by IgE binding to allergens.
Triggers mast cell degranulation.
Basophils & eosinophils amplify IgE response → secrete IL-4 & IL-13, promote Th2 responses, & ↑ IgE production.
Causes rapid allergic responses → anaphylaxis, asthma, hay fever.
How do mast cells contribute to hypersensitivity?
Release preformed inflammatory mediators like histamine, cytokines, & lipid mediators.
Histamine & lipid mediators cause: ↑ smooth muscle contraction, ↑ vascular permeability, & mucus production.
Cytokines promote: inflammation, IgE production, & amplify TH2 response.
Allergies treatment
Avoid exposure.
Use antihistamines, corticosteroids, or adrenaline.
Desensitisation or promoting IgA/IgG over IgE.
Type II hypersensitivity
IgG or IgM bind to antigens on cell surfaces → complement activation, phagocytosis, & cell lysis.
Ex.
haemolytic transfusion reactions → due to mismatched blood group antigens.
haemolytic disease of newborn → maternal IgG targets fetal RBCs.
Penicillin allergy.
How can penicillin trigger Type II hypersensitivity?
Binds to RBCs, forming neoantigens that elicit an IgG response → complement deposition & RBC destruction.
Type III hypersensitivity
IgG forms immune complexes with soluble antigens which deposit in tissues.
Triggers complement activation & attracts neutrophils → inflammation & tissue damage.
Affects areas like kidneys, joints, & blood vessels.
Ex. systemic lupus erythematosus (SLE) → immune complexes deposit in kidneys → vasculitis, neutropenia, & widespread tissue injury.
Type IV hypersensitivity
Mediated by CD4+/CD8+ T cells & occurs 1–3 days after antigen exposure.
Ex. tuberculin skin test: TH1 cells recognize antigen from M. tuberculosis → local inflammation 24–72 hours later.
Phases of Allergic Reaction
Immediate phase occurs within minutes due to histamine.
Late phase occurs 6–8 hours later & involves leukotrienes & cytokines, leading to chronic inflammation.
Asthma is a late-phase reaction that causes airway inflammation & bronchoconstriction.
Systemic Anaphylaxis
Allergens enter blood, activating mast cells systemically.
Symptoms develop rapidly & include vascular collapse & smooth muscle contraction.
Treated with adrenaline, which ↓ vascular permeability, relaxes smooth muscle, & stimulates heart.
Clinical Manifestations of Type I
Allergic rhinitis:
IgE-mediated response to airborne allergens (pollen, dust mites).
Mast cells in nasal mucosa release histamine & other mediators upon allergen exposure.
Symptoms: sneezing, nasal congestion, & itchy eyes, throat, & nose.
