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1Principles of Biomedicine - MD1 > 68 - Immunopathology > Flashcards

68 - Immunopathology Flashcards

1
Q

Types of hypersensitivity

A

Type 1 - Immediate type (IgE, mast cells, lipid mediators)
Type 2 - Antibody mediated (IgM, IgG bound to antigen)
Type 3 - Immune complex (IgM, IgG complex deposition)
Type 4 - Delayed type hypersensitivity (CD4+ mediated)

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2
Q

Aspects of atopy
1)
2)
3)

A

1) High levels of IgE
2) Large numbers of eosinophils
3) Large numbers of Il-4-secreting Th2 cells

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3
Q

Allergy

A

Immune-mediated inflammatory response to common environmental antigens that are otherwise harmless

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4
Q

Relationship between [IgE] and atopy

A

Positive correlation. Those at risk of anaphylactic shock have more IgE than those predisposed to hayfever.

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5
Q 
Common features of allergens
1)
2)
3)
4)
5)
6)
A

1) Individuals are repeatedly exposed to allergens via mucosal route
2) Allergens are highly soluble proteins, carried by small particles (if inhaled)
3) If ingested, slowly-degraded molecules
4) Very stable
5) High solubility in body fluids
6) Introduced in very low doses

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6
Q

Adaptive immune response induced by allergens

A

Th2

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7
Q 
Examples of type 1 reactions 
1)
2)
3)
4)
A

1) Systemic anaphylaxis (EG: antibiotics, venoms, peanuts)
2) Allergic rhinitis (pollen, dust mites)
3) Asthma (blockage of the airways)
4) Food allergens

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8
Q

Phases of type 1 allergic response
1)
2)

A

1) Sensitisation

2) Response (have an immediate and a delayed phase)

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9
Q

Sensitisation
1)
2)
3)

A

1) Low dose antigen through mucosal route promotes Th2 activation (IL-4 stimulates Th2 differentiation)
2) Th2 release IL-4, IL-5 and IL-13
3) IL-5 stimulates IgE isotype switching

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10
Q

What releases IL-4?

A

Th2 cells, basophils

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11
Q

What do DCs release to stimulate Th2 bias?

A

IL-33, which recruits basophils, which then release IL-4

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12
Q

How do DCs bias to Th2?

A

Indirectly, through recruiting basophils with IL-33.

Basophils then release IL-4, which biases Th2 differentiation

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13
Q

Locations of mast cells

A

Mucosal, epithelial tissues, near blood vessels

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14
Q

Effects of mast cell IgE crosslinking
1)
2)

A

1) Degranulation

2) Synthesis of inflammatory lipid mediators, cytokines and chemokines

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15
Q

Preformed mediators in mast cells

A

Histamine

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16
Q

Lipid mediators synthesised by mast cells

A

Leukotrienes, prostaglandins

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17
Q

Cytokines synthesised and secreted by mast cells

A

IL-3, IL-4, IL-5, IL-13 (Th2-type cytokines)

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18
Q

Immediate phase of allergy
1)
2)
3)

A

1) Redness - vasodilation
2) Soft swelling - oedema
3) Dependent upon IgE
Soluble mediator phase

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19
Q

Late phase of allergy
1)
2)

A

1) Hard swelling - accumulation of leukocytes
2) Neutrophil, Th2, eosinophil infiltration
Cellular phase

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20
Q

Wheal

A

Localised swelling around allergic challenge

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21
Q

How long after challenge does late phase occur?

A

8-12 hours

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22
Q

Effect of allergy on GIT

A

1) Increased fluid secretion
2) Increased peristalsis
3) Leads to diarrhoea, vomiting

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23
Q

Effect of allergy on skin
1)
2)
3)

A

1) Increased fluid secretion
2) Increased vasodilation
3) Leads to swelling, itching, urticaria

24
Q

Effect of allergy on airways
1)
2)
3)

A

1) Decrease bronchial diameter
2) Increase mucus
3) Leads to nasal blockage, coughing, phlegm, asthma

25
Q

Effect of allergy on blood vessels
1)
2)

A

Increased blood flow

Increased permeability

26
Q

Where ar eeosinophils present?

A

Mucosal linings

27
Q

Which stage of allergic response are eosinophils found?

A

Late stage

28
Q

What do eosinophils release?

A

Toxic granule-derived basic proteins and free radicals

Chemical mediators which activate epithelial cells, recruit and activate inflammatory cells

29
Q

Regulation of eosinophils

A

Very tight, as can release very toxic products.

IL-5 stimulates eosinophil release from the bone marrow

30
Q

Why are too many eosinophils recruited in allergy?

A

Mast cells, Th2 release IL-5

31
Q

How are eosinophils attracted to site of allergy?

A

Epithelial cells release eotaxins (chemokines)

32
Q

Effect of activation on eosinophils

A

Increased number of FceRI on surface, increased IgE binding, which lowers threshold of activation

33
Q 
Examples of drugs used to to treat hypersensitivity
1)
2)
3)
4)
A

1) Epinephrine
2) Inhaled beta-adR agonists
3) Antihistamines
4) Corticosteroids

34
Q 
Epinephrine effects
1)
2)
3)
4)
A

1) To treat anaphylaxis, asthma
2) Reforms tight junctions between epithelial cells (reduce oedema)
3) Bronchodilator
4) Accelerates heart rate (if too much oedema, drop in bp)

35
Q

Chemical in Ventolin

A

Albuterol (beta-adR agonist)

36
Q 
Side effects of corticosteroids 
1)
2)
3)
4)
A

1) Bone demineralisation
2) Skin thinning
3) Weight gain
4) Immunosuppression

37
Q

Effectiveness of corticosteroids over time

A

Effectiveness wanes over time

38
Q

Treatment for allergy that addresses cause

A

Desensitisation.
Administration of increasing doses of allergen.
Induces T cell tolerance

39
Q 
How does tolerance induce T cell tolerance?
1)
2)
3)
4)
A

1) Decreased allergen-induced proliferation (anergy)
2) Deviation of secreted cytokines
3) Stimulation of apoptosis
4) Production of Treg
Exact mechanism not well-known

40
Q

T cells involved in type IV hypersensitivity

A

CD4+, sometimes CTL

41
Q

How is a type IV hypersensitivity elicited?
1)
2)
3)

A

1) Microbial infection (Chronic infection, EG: TB)
2) Intradermal injection of protein antigens
3) Contact with chemicals which are absorbed through skin

42
Q

Cytokine most implicated in type IV hypersensitivity

A

IFNg

43
Q

Examples of type IV hypersensitivity
1)
2)
3)

A

1) Contact sensitivity (EG: Poison ivy, adhesives, Mantoux test)
2) TB infection
3) Coeliac disease

44
Q

How long does it take for a type IV hypersensitivity response to come about?

A

A few days

45
Q

DTH

A

Delayed-type hypersensitivity (type IV)

46
Q

Allergen in poison ivy

A

Pentadecacatechol

47
Q 
Mechanism of contact hypersensitivity
1)
2)
3)
4)
5)
A

1) Pentadecacatechol haptenates
2) Taken up by an APC, taken to a lymph node (DC is licensed)
3) Memory T cells are formed (sensitisation)
4) On re-exposure, activation of effector memory T cells, central memory T cells.
5) IFNg release. Leads to recruitment of macrophages to site, which leads to redness, soreness, blister

48
Q

How does TB lead to type IV?

A

1) Infects alveolar macrophage
2) Macrophage releases IFNg, is activated
3) Activated macrophages release IL-8, TNFa

49
Q

Proportion of those infected with TB who clear disease

A

90%

50
Q

Haplotype that predisposes to coeliac

A

Over 90% of patients are DQ2 positive

51
Q

Diagnostic test for coeliac

A

Test for autoantibodies to gliadins and tissue transglutaminase

52
Q

Foods that contain gliadins

A

Wheat, rye, barley

53
Q

Amino acids that gliadins are rich in

A

Glutamine (30%) and proline (15%)

54
Q

Peptides that HLA DQ2 preferentially binds to

A

Those with negatively charged anchoring chains are positions 4, 7

55
Q

Ability of unmodified gluten to bind HLA DQ2

A

Poor. Positively-charged anchoring chains at positions 4,7

56
Q

How is gluten made to bind to HLA DQ2?

A

Modified by tissue transglutaminiase.

Deamidated gliadin peptides have negatively-charged side chains at positions 4, 7

57
Q

Sensitisation phase of coeliac

A

1) Gliadin from food changed by tissue transglutaminase.
2) This is detected by HLA DQ2 on an APC
3) This goes to MALT, stimulates Th1 cells.

1Principles of Biomedicine - MD1 (157 decks)

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