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Year 3 - Immunology > Lec 3 - hypersensitivity > Flashcards

Lec 3 - hypersensitivity Flashcards

1
Q

Contrast the mechanisms of Types I, II, III and IV hypersensitivity.

  1. Define the roles of allergen, IgE, mast cells, inflammatory cells, mediators and cytokines in Type I hypersensitivity.
  2. Explain the pathophysiology of early and late phase allergic reactions.
  3. Define atopy.
  4. Illustrate the clinical effects of Type I Hypersensitivity.
    1) Define the roles of antibody, complement, Fc receptor bearing cells and ADCC in Type II hypersensitivity.
    2) Illustrate the clinical effects of Type II hypersensitivity.
A
  1. Define the pathophysiology of immune complex formation in localised and systemic Type III hypersensitivity.
  2. Explain the factors involved in formation of abnormal immune complexes.
  3. Illustrate the clinical effects of Type III hypersensitivity.
  4. Define the roles of haptens, carrier proteins, Th1 cells, Th17 cells, antigen presenting cells and monocytes/macrophages in Type IV hypersensitivity - SEE SLIDE 8 AGAIN
  5. Illustrate the clinical effects of Type IV hypersensitivity
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2
Q

Describe type 1 hypersensitivity

  • AKA …
  • inappropriate response to an
  • the inappropriate response arises from the foreign antigen being presented to what kind of T cell which then induces B cells to inappropriately synthesise which Ig
  • Above Ig triggers what cells to produce allergic reaction
  • response time
A

AKA allergy

ALLERGEN

Presented to Th2 cell which induces cytokine (IL-4) release –> IgE by B cells

Mast cells and eosinophils to degranulate

Within minutes of exposure

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3
Q

Elements involved in type I hypersensitivity

A 
Allergen
IgE, 
Mast cell/ basophil, 
Th2 cells
Eosinophils
Genes
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4
Q

Types of allergens in type 1 hypersensitivity

A

AIRBORNE - pollens, house dust mite

INGESTED - nuts, seafood

OCCUPATIONAL - latex, drugs (hospital), industrial

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5
Q

Type 1 hypersensitivity is caused by a combo of what factors

A

Genetic factors
Environmental influences
Immune reactivity

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6
Q

What genetic factor is imposed in type 1 hypersensitivity + describe this

A

Atopy - genetic tendency to produce IgE to normally innocuous allergens (not everyone with atopy gets allergies)

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7
Q

Type 1 hypersensitivity presentations

A

Rhinitis
Asthma

Anaphylaxis

Dermatitis
Angioedema
Urticaria
Eczema

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8
Q

What cytokine is produced by Th2 cells in type 1 hypersensitive to induce IgE production by B cells

A

IL-4

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9
Q

Difference between EARLY and LATE phase allergic reaction

IgE production in type 1 hypersensitivity bind to mast cells and trigger them to release mediators which differentiate the early and late phase

What mediators are released in the
-early
-late
phase

A

Early (within minutes) - histamine, heparin
(preformed granules)

Late (within hours) - leukotrienes, prostaglandins
(new mediators)

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10
Q

The genetics of allergies has been associated with polymorphisms of a gene encoding what protein

A

Fillagrin (expressed by keratinocytes and involved in maintaining epithelial barriers and moisturising surfaces)

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11
Q

Physiological effects of mediators released by mast cells in anaphylaxis

A

Vasodilation
Increased vascular permeability
Fluid shift from vascular to extravascular spaces –> severe fall in BP

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12
Q

Physiological effects of mediators released by mast cells in allergic rhinitis

A

Vasodilation
Oedema
Increased mucus secretion
Smooth muscle contraction within lungs –> airflow reduction

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13
Q

Treatment options for type 1 hypersensitivity

A

AVOID ALLERGEN

Pharma:
B2 agonists, e.g. salbutamol
Antihistamines 
Sodium cromoglycate 
Steroids
Leukotriene antagonists, e.g. montelukast
Desensitisation immunotherapy
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14
Q

Tests for type 1 hypersensitivity

A 
Skin prick test
IgE levels (RAST test)
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15
Q

Describe type 2 hypersensitivity

  • mediated by which 2 immunoglobulins
  • what is the mechanism of each of the above 2 immunoglobulins once it has bound to the antigen
A

IgG or IgM reacting with antigens on surface of self or foreign cells

IgM activates complement and IgG binds its Fc portion to antigen which stimulates phagocytes

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16
Q

Once antibody has bound to the relevant antigen in type 2 hypersensitivity, damage can arise in what 4 ways

A

Complement activation
Fc binding and stimulation of phagocytes
Antibody dependent cellular cytotoxicity (ADCC)
Effects on target cell function - inhibit/stimulate function

17
Q

How does antibody dependent cellular cytotoxicity (ADCC) work in type 2 hypersensitivity

A

Effector cell of the immune system (probably NK cell) lyses the target cell, whose membrane surface antigens have been bound by specific antibodies

18
Q

Clinical effects of type II hypersensitivity

A

Haemolytic reactions, e.g. after blood transfusion, autoimmune haemolysis, drug induced haemolysis

Haemolytic disease of the newborn

Hyperacute graft rejection

Some organ specific autoimmune diseases, e.g. Grave’s disease, pemphigus, goodpasture’s syndrome

19
Q

Describe type 3 hypersensitivity

  • AKA
  • characterised by
  • can also involve what Igs
  • signs & symptoms generally manifest how long after antigen exposure
A

AKA immune complex disease

EXCESSIVE/ABNORMAL immune complexes of antigen and antibody that cause damage at the site of production or circulate and damage elsewhere

IgM or IgG

4-10 hours

20
Q

Immune complex formation is a normal physiological process but it is pathological in type 3 hypersensitivity and causes symptoms due to predisposing factors in either the antigen involved or in the immune response to that antigen

The end result of abnormal immune complex formation is that the complexes precipitate out into tissues and cause inflammation

This inflammation tends to take one of two main forms:

A

Systemic illness where immune complexes are deposited throughout many tissues (SERUM SICKNESS)

Localised disorder where complexes form locally in tissues, rather than depositing in blood (ARTHUS REACTION)

21
Q

Difference between serum sickness and arthus reaction in type 3 hypersensitivity

A

Serum sickness - systemic deposition of immune complexes

Arthus reaction - localised immune complexes

22
Q

Small immune complexes form in type 3 hypersensitivity when antibody levels are … and antigen levels are …

A

Antibody low

Antigen high

23
Q

Large immune complexes form type 3 hypersensitivity when antibody levels are … and antigen levels are …

A

Antibody high/normal

Antigen low/normal

24
Q

How are immune complexes usually broken down

What happens to this process in type 3 hypersensitivity?

A

Transported (usually attached to red cells) to the liver and spleen where phagocytes such as Kupffer cells take up and destroy the complexes

This process fails and immune complexes are not cleared

25
Q

Clinical effects of Type III hypersensitivity

  • kidney
  • systemic
  • resp
A

Immune complex deposition in kidney

  • GN, e.g. post-streptococcal
  • Nephrotic syndrome
  • Renal failure

Systemic
-SLE

Resp

  • farmer’s lung
  • bird fancier’s lung
26
Q

Describe type 4 hypersensitivity

  • AKA
  • mediated by
  • inappropriate response to
  • how long for clinical response to occur
A

Delayed hypersensitivity

Th1 and/or Th17 cells and their CYTOKINES

Inert (unreactive) environmental substances, e.g. nickel, drugs, cosmetics) or as a reaction to infection with certain micro-organisms

48-72 hours

27
Q 
Define the roles of 
-haptens, carrier proteins
-antigen presenting cells
-Th1 cells
-TNF
in Type IV hypersensitivity
A

Haptens - in type 4 reactions, the antigen is usually of TOO LOW MOLECULAR WEIGHT TO EVOKE IMMUNE RESPONSE so…

Carrier proteins - …haptens. need to bind to a host protein called a CARRIER to produce sufficient antigenic bulk to stimulate immune response

APCs - macrophages and dendritic cells present antigen to T cells

Th1 cells - recognise foreign antigen upon presentation and stimulate cytokine production –> inflammation

TNF - secreted by macrophages and T cells and stimulates MOST OF THE DAMAGE IN TYPE 4

28
Q

What substance produced by macrophages and T cells and stimulates much of the damage in delayed hypersensitivity

A

Tumour necrosis factor

29
Q

What conditions can type 4 delayed hypersensitivity lead to

A

RA
MS
IBD

(all are affected by Th1/Th17 cells and macrophages causing inflammation)

30
Q

Treatment options of type 4 hypersensitivity

A

Prevention/ avoidance of contact with antigen

Anti-inflammatory drugs

  • corticosteroids
  • NSAIDs
  • drugs that block TNF, IL-6
  • monoclonal antibodies against B cells

Year 3 - Immunology (6 decks)

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