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POM > Immuno - Hypersensitivity > Flashcards

Immuno - Hypersensitivity Flashcards

1
Q

What is the immune system role in hypersensitivity?

A
  • Over-reacting to harmless environmental particles: pollen, animal dander, drugs
  • Activation lead to inflammation cause pain & discomfort
  • Produce wide range of toxic molecules and protein result in tissue damage –> potentially fatal
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2
Q

What is an antigen?

A

A molecule/ar structure that can be recognised by antibody/adaptive immune system

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3
Q

What does it mean by requiring pre-sensitised immune system?

A

Having an existing adaptive immunological memory

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4
Q

How do we activate naive T-cells?

A

Encounter specific antigen for rapid proliferation (Clonal expansion)
Results in both effector and memory cells (differenciation)

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5
Q

How are different types of hypersensitivity triggered?

A

Depend on classes and subclasses of antibodies

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6
Q

How do we know what type of T-cells are generated?

A

Depends on what cytokines it’s exposed to

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7
Q

What are the 4 types of hypersensitivity?

A

Type I - Immediate/anaphylactic (allergen)
Type II - Antibody-mediated cytotoxic
Type III - Immune complex driven disease
Type IV - Delayed-type/ T-cell mediated

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8
Q

Which hypersensitivity reaction involve formation of antibody-antigen complex?

A

Type I-III

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9
Q

Which hypersensitivity reaction is initiated by T-cells?

A

Type IV

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10
Q

What does IgG do?

A

Activates complement & Fc receptor mediated phagocytosis?

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11
Q

What does IgA (dimer) do?

A

Cross mucosal epithelium

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12
Q

What does IgE do?

A

Mast cell degranulation

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13
Q

What classes of antibodies are there?

A

IgG, IgD, IgE, IgA (dimer connected by J chain) , IgM (pentamer connected with J chains & disulphide bonds)

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14
Q

What antibody mediates type I hypersensitivity?

A

IgE - usually only made in response to parasitic / potent venom
- Now produced against allergens (common multivalent environmental antigens)

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15
Q

What are examples of allergens?

A
  • Food (peanuts)
  • Plants (timothy grass/birch trees)
  • Animal dander (cats/dogs)
  • Drugs (penicillin/sulphonamides)
  • Insect products (bee venom/dust mites)
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16
Q

What test is used to test for Type I hypersensitivity?

A

Skin Prick test (expose skin to small amount of allergens)

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17
Q

What is a positive reaction for skin prick test?

A

Inflamed, raised tissue (aka Wheal & flare)

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18
Q

What is type I hypersensitivity? Examples?

A

Allergic reaction provoked by re-exposure to allergen

Asthma, allergic rhinitis, atopic dermatitis

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19
Q

What is the initial sensitization of type I?

A
  1. Generation of Type 2 CD4 T-cell (Th2) & B-cell follicular helper CD4 T-cell (Tfh)
  2. Tfh produces type II cytokines IL-4 & IL-13 (which promotes B cell to produce antigen specific IgE)
  3. IgE bound to surface of innate immune cells (mast cells & basophils - express high affinity IgE receptors)
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20
Q

What does Tfh do?

A

Produces type II cytokines IL-4 & IL-13 (which promotes B cell to produce IgE

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21
Q

What is the mechanism of sensitized Type I re-exposure to allergens?

A

Allergen encountering bound IgE causes rapid crosslinking & degranulation of mast cell/basophils

Release of histamine (a host of cytokine):

  • recruit other cell
  • promote further Th2 differentiation + highly active smooth muscle contracting molecules (leukotrienes & prostaglandins)
22
Q

What are IgE receptors?

A

Fc epsilon receptor I (FCER!)

23
Q

What are the phases of response in type I hypersensitivity?

A
  1. Early phase (within mins od exposure) - bioactive small molecules produced by mast cells
  2. Later response (few hours) - recruitment of early inflammatory cells (eg neutrophils)
  3. Late response (3-4days) - lots of eosinophils recruited + Th2 cells present
24
Q

What are the uses of histamine and heparin (primary) Leukotrienes (secondary) ?

A

Increase vascular permeability

Smooth muscle contraction

25
Q

What do prostaglandins mediate?

A

Vasodilation, contraction of pulmonary smooth muscle, platelet aggregation

26
Q

What are some examples of CD4 T-cells?

A

Th1 - produce molecules that promote control of intracellular pathogens
Th2 - alllergic & anti-helminth reponse
Tfh - B cell help in germinal centers
Th17 - Inflammation
Induced Treg - regulation, suppression of immune/inflammatory responses

27
Q

What is type II hypersensitivity?

A

Destruction of cells by IgM & IgG binding to cells

28
Q

What are the consequences of Type II hypersensitivity?

A

Tissue injury

  • Local & systematic inflammation
  • Cell depletion (loss of function/ balance in organ)
29
Q

What are some causes of Type II?

A
  • Mismatched blood transfusion
  • Haemolytic disease of the newborn
  • Graves disease - secretion of thyroid hormone
  • Immune thrombocytopenia - abs against platelet surface protein
30
Q

How is Type II sensitized?

A
  • Exposure to foreign antigen

- Aberrant response to self-antigen (IgM/G recognise)

31
Q

What are the disease mechanism for type II?

A
  1. Anti-receptor activity
  2. Antibody dependent cell-mediated cytotoxicity (ADCC)
  3. Classical activation of complement cascade
32
Q

What is and how does ADCC work?

A

Antibody dependent cell-mediated cytotoxicity

  • Abs-ag complex bound by Fc receptors (expressed by granulocytes & NK cells)
  • cause direct lysis of target cell & release of inflammatory mediators, chemokines & cytokines
33
Q

What does the complement cascade cause?

A

Inflammation
Opsonisation
Recruitment & activation of immune cells
Lysis of cell

34
Q

How does the complement cascade work?

A

Antibody recognised by complement components leading to the formation of MAC (membrane attack complex form pores) on cell surface leading to cell death (due to loss of osmotic integrity)

35
Q

What is type III hypersensitivity?

A

Non-cell bound abs-(self)ag complex not cleared as deposited in vessel wall/tissue - promotes inflammation & tissue damage

36
Q

What are the symptoms of Type III hypersensitivity?

A 
Fever
Rashes
Joint pain
Protein in urine
Arthritis (joint)
Glomerulonephritis (kidney)
Vasculitis (blood vessel)
37
Q

What are some autoimmune diseases involving Type III?

A

Rheumatoid Arthritis
Multiple Sclerosis
SLE - Systematic lupus erythematous

38
Q

Give example of antibody-mediated diseases. Type III

A 
Persistent infections (Hepatitis)
Serum sickness - when given anti-serum to snake venom, Abs recognises it so 2nd exposure will cause inflammation
39
Q

What is SLE?

A

Systematic Lupus Erythematous

- autoimmune disease that increases apoptosis + clearance of that material

40
Q

What is the childhood form of SLE?

A

Juvenile-onset SLE (rare)

activates all components of innate & adaptive immune system

41
Q

What is the mechanism for SLE?

A
  1. Develop IgG against DNA/protein present in nucleus - forming persistent immune complex deposits & variety of pathologies
  2. Antibody-nuclear antigen immune complex deposit in tissue cause local inflammation
42
Q

What are the characteristics of SLE?

A
  • Increase in apoptosis + clearance of it
  • Saturation of physiological process to remove lupus cluster in surface bleb of apoptotic cells AMPLIFIES immune exposure
43
Q

What is type IV hypersensitivity?

A

Memory T-cell response promote inflammation

44
Q

How is Type IV sensitized?

A

Naive T-cells presented to APC/DCs to generate memory T-cells

45
Q

What is the most common type IV example?

A

Contact dermatitis (exposure to poison ivy)

46
Q

What happens when exposed to poison ivy?

A

Urushiol molecule act as hapten (binds to skin protein) & presented to DCs –> T-cell clonal selection –> drives Th1 response

  • response is small, rarely result in antibody production
47
Q

What happens when re-exposed to poison ivy?

A

Memory cells produce cytokines (Eg IFN-gamma) which promote pro-inflammatory activation of macrophages

  • Cause swelling + oedema + form blister-like lesions (cytotoxic T cell/Memory T-helper/macrophages/cytokines)
48
Q

What other contact antigens also drive Th1 base inflammation?

A

Nickel salts / hairdyes / intracellular pathogens (Measles virus/ TB)

49
Q

What other type IV reactions are there?

A
  • Positive tuberculin skin test - measure previous exposure to TB (inject M.tb into skin)
  • Any memory T-cell capable of immune overreaction
    eg Asthma (Th2 –> produce soluble mediators promotes Bronchoconstriction)
    Inflammation & rejection of tissue graft - CD8 T-cells kill transplanted cells
50
Q

How many types of hypersensitivity can contribute to pathology at the same time?

A

More than 1

eg Asthma  
Type I (Generation after exposure - allergy)
Type IV (Th2 --> produce soluble mediators promotes Bronchoconstriction)

POM (22 decks)

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