Hypersensitivity Type 1 Flashcards
Hypersensitivity type 1 has to do with which antibody?
Immunoglobulin E (IgE) antibody
What’s the time frame on reactions resulting from type 1 hypersensitivity?
Almost immediate (within minutes)
What type of hypersensitivity are most allergies? Is there a genetic component?
Type 1
There is a genetic predisposition to over-reaction to certain allergens (antigens)
Give examples of things that can activate a type 1 hypersensitivity
Breathe in
Take in
Contact with skin
What are the two steps of an allergic reaction?
- First exposure - sensitisation
- Subsequent exposure - gets serious
How does a genetic predisposition to allergies work?
Genes code for T helper cells that are more hypersensitive to certain antigens
Allergies can run in families
What happens in the sensitisation phase of an allergic reaction?
The body comes into contact with the allergen (ie pollen)
Allergen gets picked up by APC immune cells (ie dendritic cells or macrohages) in the airway membranes
Migrates molecules to the lymph nodes (happens even if person is not allergic)
APC presents antigen to naive T helper cells -> primed Th cell
Th2 releases IL-4 -> Tells B cell to undergo antibody class-switching from IgM to IgE (specific for that antigen)
Th releases IL-5 -> stimulates production/activates eosinophils (granulocyte)
Antigen specific IgE molecules (cytotropic) have high affinity for Fc-epsilon receptors on mast cells (granulocyte)
IgEs bind to Fc-epsilons on mast cell surface
How does a naive T helper cell turn into a mature specialised T helper cell?
APC presents antigen to naive T helper cells
If the person is allergic, the APC will also express co-stimulatory molecules
Naive Th cell binds to the antigen and costimulatory molecule -> becomes primed Th cell
Interleukin molecules (cytokines) aid here (ie IL-4, IL-5, IL-10 help form Th2)
What are eosinophils?
Granulocytes
Can degranulate to release toxic substances that can damage invading and nearby host cells
What are cytotropic antibodies?
Antibodies that bind to other cell surfaces
What happens in the second exposure phase of an allergic reaction?
The mast cell with antibodies attached binds the allergen
Needs two adjacent antibodies to attach to an allergen so they can ‘cross-link’
Cross-linking signals to the mast cell to degranulate
Degranulation releases pro-inflammatory molecules called mediators
Mediators cause allergic symptoms
What are mediators?
Pro-inflammatory molecules/cells
Released by mast cells
Examples
- Histamine
Binds to H1 receptors
Causes smooth muscle around bronchi to contract > makes it more difficult to breathe
Cause blood vessel dilation and increased wall permeability > fluid enters interstitial space > oedema (swelling) + urticaria (hives)
- Proteases
The effect of these molecules causes the early phase reactions (within minutes)
What are late phase reactions?
Occur 8-12 hours after the second exposure
More immune cells (Th2 cells, eosinophils, basophils (granulocyte)) recruited to location of allergen due to pro-inflammatory molecules and cytokines produced in early phase
Cytokines and leukotrienes recruited/released (smaller molecules made of fatty acids - facilitate communication between a local group of cells)
Leukotrienes (LTB4 and LTC4) cause smooth muscle contraction and vasodilation, and can attract immune cells (neutrophils, mast cells, eosinophils) to their location even after the allergen is gone
What is anaphylactic shock?
A large load of allergen (or very sensitive person)
Severe symptoms (inreased vascular permeability, airway constriction)
Can’t supply vital organs with enough oxygen rich blood
What are treatments for type 1 hypersensitvity?
- Antihistamines
Reduce vascular permeability and bronchoconstriction - Corticosteroids
Reduce the inflammatory response - Epinephrine
Constricts blood vessels and helps prevent anaphalactic shock
