1. hypersensitivity and allergy

Question 1

what causes hypersensitvity?

Answer 1

exaggerated immune response

Question 2

type 1 hypersensitivity

what is it known as

which cells are involved

Answer 2

atopic allergy

mast cells, IgE, Th2

Question 3

mechanism for atopic allergy

Answer 3

1. foreign allergen enters body- engulfed and presented
2. Th2 cells recognise- IL4 stimulate B cells to produce IgE antibodies -> bind to mast cells
3. mast cells with IgE, cross linked by specific allergens, once allergen binds become activated and release histamine etc. degranulation and synthesis of newly formed mediators (leukotrienes,PG)

induces inflammation on SM

4. later response- Th2 release IL5 that stimulate eosinophils- can result in chronic tissue damage

Question 4

Those suffering from atopic allergies- what are they predisposed to produce?

Answer 4

higher levels of IgE

Question 5

IgE structure compared to IgA, IgE

Answer 5

extra heavy domain replacing hinge region

Question 6

half life of IgE

Answer 6

IgG is protected from degradation and is released back to circulation

if pH changes then IgE becomes degraded

Question 7

how do different types of atopic disorders arise?

Answer 7

different types of allergen and route of exposure

Question 8

what may drvie Th2 production

Answer 8

hygiene hypothesis

Question 9

how can you assess sensitivity to specific allergens?

Answer 9

skin prick test

intra-dermal exposure induces a wheal and flare reaction.

Question 10

asthma- what is the acute and chronic responses caused by?

Answer 10

acute; inflammatory mediators cause increased mucus secretion and SM contraction leading to airway obstruction

recruit cells from circulation

chronic: caused by cytokines and eosinophils- release inflammatory mediators

Question 11

type II tissue damage mechanism

Answer 11

• IgG, IgA or IgM antibodies that bind to cell surface membranes or connective tissue components.
• activate complement and/or trigger neutrophils to release digestive products and reactive oxygen species.
• haemolytic rhesus anaemia induced by antigens that bind to erythrocytes: if antibodies are generated against these antigens, then erythrocyte lysis can result.
• IgG only antibody that can cross placenta

Question 12

tissue damage type III mechanism

Answer 12

• Involves several soluble antigens and antibodies cross-linking to form a lattice structure known as an immune complex (IC) that may precipitate out of solution and/or become lodged in tissues. Immune complexes can activate complement and neutrophils leading to tissue damage.
• An example is allergic alveolitis caused by production of antibodies to inhaled fungal spores. Immune complex formation in the walls of the alveoli leads to inflammation and fibrosis. This results in breathlessness due to poor gas exchange across the alveolar walls (as distinct from the wheezing in asthma that is due to constriction of the bronchi).
• farmers lung, pigeon fanciers lung

Question 13

what normally happens to immune complexes?

Answer 13

bound to complement and made into small complexes by solubilsation

deposited into erthryocyte bound complexes

phagocytosed

Question 14

type IV tissue damage mechanism

Answer 14

• Involves activation of helper T cells (principally T_H1 cells) by the interaction with antigen presenting cells. The activated T_H1 cells secrete cytokines, eg. IL-2 that can activate T_C cells and IFN-gamma that can activate macrophages (and possibly lead to granuloma formation).
• Reactions of this type are seen in the chronic phases of the mycobacterial infections that cause tuberculosis and leprosy.
• Contact allergens that induce a type IV hypersensitivity reaction seen clinically as contact dermatitis include metals (eg. nickel, chromium) and plant products (eg. poison ivy).