Hypersensitivity and Allergy Flashcards
What does an exaggerated response cause
Tissue damage (hypersensitibity)
Allergy Hypersensitivity vs Autoimmunity Hypersensitivity
Allergy - foreign material recognised but self material damaged
Autoimmunity - Self material recognised and self material damaged
Type 1 hypersensitivity
Immediate hypersensitivity or atopic allergy
Caused by IgE being cross linked on the surface of mast cells
What are type 2,3 and 4 hypersensitivities referred to as
Type 2 Hypersensivity - Antibody dependent hypersensitivity
Type 3 Hypersensitivity - Immune complex hypersensitvity
Type 4 Hypersensitivity - Delayed time hypersensitvity
*note that type 4 is mediated by cells not antibodies
What 3 factors mediate type I hypersensitivity
Mast Cells
IgE
Allergens
Examples of Type I Allergies
Allergic rhinitis (hayfever) Allergic Asthma Eczema Food Allergies Anaphylaxis
(don’t memorise just be vaguely aware)
What does the mast cell cause during type I allergy
Release of mediators causing oedema and smooth muscle contraction
Sensitisation
Allergen crosses the mucosal surfaces and enters body
Phagocytosed into APC
Does the same for allergen as it would for antigen; presents on MHC complex II
Peptide of that protein is presented to a TH2 cell
TH2 cell causes class switching in B cells to produce IgE antibodies against that allergen that sit on the surface of the mast cell via their Fc receptors
Which interleukins are released by Th2 cells during type I hypersensitivity and what do they each do
IL10: inhibits Th1 activity and activates mast cells
IL4: Activates B cells and causes class switching
IL5: Activates Eosinophils
What happens on subsequent exposure to the same allergen (Elicitation)
Mast cell degranulates as the IgE antibodies are bound - releases inflammatory mediators which lead to the allergic reaction
Atopic subject
Person predisoposed to having high levels of IgE
thus predisposed to allergies
such as hay fever, perennial rhinitis, asthma and atopic eczema
What are some mediators released during reactions of type I hypersensitivity
Histamine Heparin Tryptase Arachidonic Acid Leukotrienes-D4 Prostaglandin-D2 TNFa IL-4
Would there be an anaphalactic response to a bee sting on the first time? Why/Why not?
No IgE antibodies against phospholipase A (protein causing reaction) have been made that are bound to mast cells
Why do dust-mites cause allergy
We do not have an allergic response to the mites themselves; instead we have a response to their faecal matter
Route of Entry and Bodily Response for Systemic Anaphylaxis
Route of Entry:
Intravenous either directly or through absorption of food into blood
Reponse: Full body mast cell degranulation Oedema Increased Vascular Permeability Tracheal Occlusion Circulatory Collapse Death
Route of Entry and Bodily Response for Acute Uticaria
Subcutaneously
Local increase in blood flow and vascular permeability
Route of Entry and Bodily Response for ALlergic Rhinitis
Inhalation
Oedema and Irritation of nasal mucosa
Route of Entry and Bodily Response for Asthma
Inhalation
Bronchial Constriction, Increased mucous production, Airway Inflammation
Route of Entry and Bodily Response for Food Allergy
Oral
Vomiting Diarrhea Pruritus Uticaria Anaphylaxis
Urticaria
Hives
Allergic Response in Asthma
Allergen enters the airways and causes IgE to crosslink on mast cell surface; causing the acute and chronic responses:
Acute Phase: Vasodilation, increased vascular permeability and cellular recruitment causing tissue damage
Chronic Phase: Eosinophils are recruited into airways; they release cytotoxic mediators to attack airways like they would do to a parasite
How to detect an allergy
Skin tests where a tiny amount of the allergen is pricked into the skin to prompt an immune response
Mechanism II of hypersensitivity
e.g. Allergic Haemolytic Anaemia
Mediated by antibodies;
- IgG
- IgA
- IgM
Caused by neutrophils releasing their mediators and antibody binding to a target leading to tissue damage
Rhesus Haemolytic disease of a newborn
Example of Type II Hypersensitivity
IgG goes through the placenta of the SECOND foetus of RhD+ blood type when mother is RhD- (first foetus familiarises the mother’s body with the allergen) and causes damage to the unborn foetus by attacking the RhD protein
Mechanism of Type III Hypersensitivity
e.g. Dermatitis
Immune complex formation; too many are formed so the immune system cannot effectovely clear them leading to their deposition in the skin which causes damage and necrosis
Extrinsic Allergic Alveolitis
Example of Type III Hypersensitivity
Immune complexes deposit into the alveoli and cause fibrosis and inflammation
Mechanism of Type IV Hypersensitivity
e.g. Contact Dermatitis
T cells activate macrophages that lead to tissue damage
