Hypersensitivity Flashcards
What are the 4 types of Gel and Coomb classification?
1 - Immediate hypersenitivity
2 - Direct cell effects
3 - Immune complex mediated
4 - Delayed type hypersensitivity
Main antibody in hypersensitivity:
IgE antibody
Hygeine hypothesis:
In modern countries, decreased exposure to parasites has left immune system ‘untrained’
Children producing more Th2 more likely to develop allergens than children who switch to producing Th1
Vasoactive mediators (2):
Histamine
Tryptase
What is an allergen?
When T cells bind to an antigen that catalyses a reaction
Sensitisation process (5):
- Allergen picked up by immune cells in airways
- Antigen presenting cells migrate to lymph nodes
- If person is allergic, antigen presenting cells will express costimulatory molecules
- This results in the production of IgE by B cells
- Residual IgE antibodies then bind to circulating mast cells via Fc receptors
Antigen presenting cells (2):
dendritic cell
macrophages
How are TH2 cells made?
Naive T helper cell binds to antigen
Cytokines help T helper cells become TH2
Which cytokines help T helper cells become TH2?
Interleukin-4, 5 & 10
Which IL’s does TH2 release?
IL4 & IL5
What does IL5 stimulate:
Production of eosinophils
Mild symptoms of type 1 hypersensitivity (4):
- Hives
- eczema
- allergic rhinitis (hayfever)
- asthma
Severe symptoms of type 1 hypersensitivity
Large load of allergen can cause:
→ Inc vascular permeability
→ Airway constriction
→ Can’t supply vital organs
→ ANAPHYLACTIC SHOCK
Type 1 second exposure:
Allergen binds to IgE -coated mast cells and basophils causing degranulation
Histamine (mediator) released
Early phase reaction (minutes):
Bronchi: smooth muscle contraction; difficulty breathing
Blood vessels: dilation, increase permeability
Release of proteases + eosinophils
Late phase reaction (8-12 hours):
TH2 cells, Basophils, Eosinophils recruited to site of allergen
Release of IL-4, IL-5, IL-10
Type 2 is mediated by:
Tissue specific antibody to destroy specifc organ or tissue
IgM/IgG
Type 2 sensitisation phase:
generation of relevant IgM/IgG antibodies in a classical humoral immune response
Type 2 pathological phase:
Mediated by normal antibody effector functions
Type 2 lla reaction:
destruction of antigen-positive cells
Type 2 llb reaction:
stimulation of cell surfaces antigens
What happens when too many antibodies bind to receptors? (Type 2)
An increase in thyroid hormone production
Type 3:
Mediated by soluble immune complexes
- Large amounts of antigen-antibody complex not removed by macrophages
- Complexes lodge in capillaries
- Classical complement pathway activated leading to vasodilation and cell death
- Neutrophils are attracted to the area
- Neutrophils discharge killing antigens causing huge inflammation
Type 4 is mediated by:
T cells
How is type 4 driven by CD4+ T cells?
Activation of CD4+ T cells leads to proliferation and inc. in macrophage recruitment and activation
Hallmarks of type 4:
large number of macrophages at reaction site
takes 24-48 hours for symptoms to manifest
garnulomas often form due to infectious pathogens which cannot be cleared
