Hypersensitivity Flashcards
Hypersensitivity
exaggerated, inappropriate adaptive immune response to harmless environmental antigens
Sometimes inflammatory reactions and tissue damage result
Can be provoked by range of antigens
not manifest on first contact with Ag
usually appears on subsequent contact
Hypersensitivity is classified into X types.
4 types.
Type I, II, II, and IV
Types I, II, III - Antibody mediated
Type IV - mediated by T cells and macrophages
In practice these types do not always occur in isolation
Common causes of hypersensitivity:
Pollen, Peanuts, Drugs, Poison Ivy, etc.
Type I (Immediate) Hypersensitivity:
- IgE response (sensitization) to innocuous environmental antigens
- IgE is located mainly in tissues, binds to FcƐRI on mast cells, basophils and activated eosinophils
- Second encounter with allergen triggers release of inflammatory mediators
- Produces acute inflammatory reaction within minutes
- Symptoms of varying severity, from running nose (rhinitis) to breathing difficulties and even death by asphyxiation
IgE - FcƐRI is very high affinity binding, which is what makes type I so fast (and so termed “immediate”)
Mast Cells:
- Resident in mucosal and epithelial tissues lining body surfaces
- Present in all vascularized tissues except CNS and retina
- Maintain tissue integrity
- Alert immune system to local trauma and infection
- Facilitate repair of damage caused by infection or wounds
- 50-200 granules fill the cytoplasm
FcƐRI on mast cells:
- Allergic individuals make IgE responses to innocuous antigens (allergens)
- FcƐRI is cross-linked
- Rapid degranulation causing release of inflammatory mediators like histamine
Eosinophils:
- Release toxic mediators in IgE response
- Mostly resident in connective tissue underlying mucosal epithelia
- In inflammatory response, cytokines and chemokines at site induce eosinophils to express FcεRI
Basophils:
- Granules contain similar, but not identical, set of mediators to those of mast cells
- Recruited to tissue under appropiate stimulation
- Similar effector function to eosinophils
Allergic reactions have an immediate reaction followed by a late-phase reaction
TRUE OR FALSE
TRUE
Systemic anaphylaxis:
- Caused when allergens reach the bloodstream and activate mast cells throughout the body
- Should be treated immediately with epinephrine (adrenaline)
Treatments for Type I hypersensitivity:
Avoidance
Anti-histamines
Epinephrine/Adrenaline
Desensitisation
Type II Hypersensitivity:
Antibody-dependent cytotoxic hypersensitivity
Occurs in 12-18 hours of exposure to antigen
Occurs when IgG or IgM binds to either a
self-antigen or a foreign antigen on human cells leading to phagocytosis, killer cell activity or complement-
mediated lysis
Damage is restricted to particular cells/tissues
bearing the antigen
Examples of Type II Hypersensitivity reaction:
- Blood transfusion reactions when ABO incompatible blood is transferred
- Haemolytic disease of the newborn
Type III hypersensitivity:
Mediated by persistence and deposition of small IgG-antigen immune complexes
Tend to circulate in blood and become deposited in blood vessel walls
When they accumulate, they fix complement and trigger inflammatory reactions by interacting with Fc receptors and complement receptors on leukocytes and mast cells
C3a stimulates mast cells to release histamine causing urticaria
C5a recruits inflammatory cells to site
Platelets accumulate, clots form, blood vessels burst causing skin haemorrhage
Type IV hypersensitivity:
Delayed-type hypersensitivity (occurs 1-3 days after exposure to antigen)
Mediated by antigen-specific effector T cells
Amount of antigen required is 100-1000 times greater than that required to produce Ab-mediated hypersensitivity reactions
