Hypersensitivity and Allergy

Question 1

What does an exaggerated response cause

Answer 1

Tissue damage (hypersensitivity)

Question 2

Allergy Hypersensitivity vs Autoimmunity Hypersensitivity

Answer 2

Allergy - foreign material recognised but self material damaged

Autoimmunity - Self material recognised and self material damaged

Question 3

Type 1 hypersensitivity

Answer 3

Immediate hypersensitivity or atopic allergy

Caused by IgE being cross linked on the surface of mast cells

Question 4

What are type 2, 3 and 4 hypersensitivities referred to as

Answer 4

Type 2 Hypersensitivity - Antibody dependent hypersensitivity

Type 3 Hypersensitivity - Immune complex hypersensitivity

Type 4 Hypersensitivity - Delayed time hypersensitivity
*note that type 4 is mediated by cells not antibodies

Question 5

What 3 factors mediate type I hypersensitivity

Answer 5

Mast Cells
IgE
Allergens

Question 6

Examples of Type I Allergies

Answer 6

Allergic rhinitis (hayfever)
Allergic Asthma
Eczema
Food Allergies
Anaphylaxis

(don’t memorise just be vaguely aware)

Question 7

What does the mast cell cause during type I allergy

Answer 7

Release of mediators causing oedema and smooth muscle contraction

Question 8

Sensitisation

Answer 8

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

Question 9

Which interleukins are released by Th2 cells during type I hypersensitivity and what do they each do

Answer 9

IL10: inhibits Th1 activity and activates mast cells

IL4: Activates B cells and causes class switching

IL5: Activates Eosinophils

**4+5+(Th1)=10 if that helps

Question 10

What happens on subsequent exposure to the same allergen (Elicitation)

Answer 10

Mast cell degranulates as the IgE antibodies are bound - releases inflammatory mediators which lead to the allergic reaction

Question 11

Atopic subject

Answer 11

Person predisoposed to having high levels of IgE

thus predisposed to allergies
such as hay fever, perennial rhinitis, asthma and atopic eczema

Question 12

What are some mediators released during reactions of type I hypersensitivity

Answer 12

Histamine
Heparin
Tryptase
Arachidonic Acid
Leukotrienes-D4
Prostaglandin-D2
TNFa
IL-4

Question 13

Would there be an anaphalactic response to a bee sting on the first time? Why/Why not?

Answer 13

No IgE antibodies against phospholipase A (protein causing reaction) have been made that are bound to mast cells

Question 14

Why do dust-mites cause allergy

Answer 14

We do not have an allergic response to the mites themselves; instead we have a response to their faecal matter

Question 15

Route of Entry and Bodily Response for Systemic Anaphylaxis

Answer 15

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

Question 16

Route of Entry and Bodily Response for Acute Urticaria

Answer 16

Subcutaneously

Local increase in blood flow and vascular permeability

Question 17

Route of Entry and Bodily Response for ALlergic Rhinitis

Answer 17

Inhalation

Oedema and Irritation of nasal mucosa

Question 18

Route of Entry and Bodily Response for Asthma

Answer 18

Inhalation

Bronchial Constriction, Increased mucous production, Airway Inflammation

Question 19

Route of Entry and Bodily Response for Food Allergy

Answer 19

Oral

Vomiting
Diarrhea
Pruritus
Uticaria
Anaphylaxis

Question 20

Urticaria

Answer 20

Hives

Question 21

Allergic Response in Asthma

Answer 21

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

Question 22

How to detect an allergy

Answer 22

Skin tests where a tiny amount of the allergen is pricked into the skin to prompt an immune response

Question 23

Mechanism II of hypersensitivity

Answer 23

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

Question 24

Rhesus Haemolytic disease of a newborn

Answer 24

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

Question 25

Mechanism of Type III Hypersensitivity

Answer 25

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

Question 26

Extrinsic Allergic Alveolitis

Answer 26

Example of Type III Hypersensitivity

Immune complexes deposit into the alveoli and cause fibrosis and inflammation

Question 27

Mechanism of Type IV Hypersensitivity

Answer 27

e.g. Contact Dermatitis

T cells activate macrophages that lead to tissue damage