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IMM005 > Allergy and hypersensitivity > Flashcards

Allergy and hypersensitivity Flashcards

1
Q

What are the three ways the immune system can go wrong?

A

React to innocuous agent

Being deficient and not working

Reacting to self during autoimmunity

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2
Q

Define hypersensitivity

A

Damage to the host arising from an immune response

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3
Q

Causes of hypersensitivity

A

Autoimmunity

Side effect of response to pathogen

Transplantation

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4
Q

How many types of hypersensitivity are there?

A

6

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5
Q

Features of type I hypersensitivity

A

Mast cells

IgE

Generally allergies

Immediate

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6
Q

Which cells are involved in type I hypersensitivity?

A

Mast cells

B cells

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7
Q

Why is type I hypersensitivity immediate?

A

Since all the components involved are preformed

All you need is for the allergen to bind to its receptors

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8
Q

What is the half-life of IgE?

A

2.5 days in serum

12 weeks if bound to mast cells

IgE lasts longer when bound to its receptor

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9
Q

When does IgE become elevated?

A

Certain parasitic diseases

Hyper IgE syndrome

Allergy

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10
Q

What agents promote class switching to IgE in B cell immunoglobulins?

A

IL-4

IL-13

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11
Q

What agent inhibits IgE?

A

Interferon-y

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12
Q

What is the main mechanism underlying Type I hypersensitivity?

A

IgE-mediated mast cell degranulation

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13
Q

Describe the organ affected and the symptoms caused due to type I sensitivity

A

Upper respiratory tract - hay fever

Lower respiratory tract - atopic asthma

Skin - allergic eczema

Systemic - peanuts

Infection - worm

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14
Q

Which inflammatory granules are released by mast cells?

A

Histamine

Serotonin

TNFa

Prostaglandins

Leukotrienes

First two = stored, released immediately
Last three = newly synthesised, chronic effects

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15
Q

What is necessary for Type I hypersensitivity to take place?

A

IgE antibody acting on mast cells and eosinophils

Th2 cells releasing IL4, IL5 and IL13 to cause IgE class switching

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16
Q

What are the two main components describing the predisposition to allergies?

A

Genes

Environment

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17
Q

Which genes are related to allergy sensitivity?

A

FcRe

HLA-DQ

IL-2R

IL-4R

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18
Q

What are the three ways to treat allergies?

A

Allergen avoidance

Pharmacotherapy

Immunotherapy

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19
Q

Describe some drugs used to treat allergies

A

Corticosteroids - suppress transcription of proinflammatory genes

Sodium cromoglycate - blocks mediator release from mast cells, reducing IgE []

Anti-histamines

Motelukast - leukotriene receptor antagonist

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20
Q

Describe immunotherapes used to treat allergies

A

Omalizumab - anti-IgE and anti-FcER

Repeated low dose antigen over a period of years

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21
Q

What is type II hypersensitivity?

A

Antibody mediated killing

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22
Q

What are the two ways type II hypersensitivity manifests?

A

Antibody-mediated killing

Formation of antibodies that block physiological function

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23
Q

Describe how type II hypersensitivity causes antibody-mediated killing

A
  1. Antibody binds to target due to loss of tolerance or increased antigenicity of the cell (foreign antigen embeds into the cell)
  2. Fc from antibody (IgG) activates anything with an Fc receptor
  3. Complement cascade leads to killing and damage
24
Q

When does type II hypersensitivity occur?

A

Transplantation - hyperacute transplant rejection

Haemolytic disease of the newborn

Autoimmune diseases

25
Q

When does haemolytic disease of the newborn take place?

A

When the mother is Rhesus factor negative, but the baby is Rhesus factor positive

26
Q

Describe the process behind Haemolytic disease of the newborn

A
  1. First pregancy, nothing happens to the baby
  2. During birth, the mother may come in contact with the RhD+ child
  3. The mother mounts an immune response against this protein, and forms anti-D antibodies
  4. In the second baby. the antibodies are ready
  5. The antibodies cross the placenta and coat the blood cells of the RhD+ baby
27
Q

What is a possible treatment of Haemolytic disease of the newborn?

A

Overloading the system to mask out anti-D to prevent mother from being sensitised

28
Q

What does a newborn who suffered haemolytic disease look like?

A

Blue

Blood cells are killed by mothers immune cells

29
Q

Example of an autoimmune disease with type II hypersensitivity

A

Goodpasture’s

Antibody attacks type IV collagen

Especially damages kidneys

30
Q

What is another example of type II hypersensitivity?

A

Formation of antibodies that block cell receptors

No killing is involved, but prevents the organ from functioning correctly

31
Q

Example of type II hypersensitivity not caused by cell death

A

Myasthenia gravis

Blocking of the receptors to ACh

32
Q

What is type III hypersensitivity mediated by?

A

Immune complex mediated

What makes it different from type II is that the antigens are NOT embedded to the cell wall, but rather are soluble

33
Q

Describe the process of type III hypersensitivity

A
  1. Soluble antibody binds to soluble antigen, causing an immune complex
  2. Antigen-antibody complexes deposit in skin, kidney or lungs where the blood flows slower
  3. Macrophages try to eat them, but the complexes are unable to
  4. Macrophages carry out frustrated phagocytosis
34
Q

What is frustrated phagocytosis?

A

Macrophages are activated and releasing their inflammatory factors without degrading the antibody-antigen complex

35
Q

Where is type III hypersensitivity seen?

A

Allergies: Farmer’s lung (hay exposure)

Infections: post-streptococcal glomerulonephritis

Autoimmune diseases: SLE

36
Q

What is post-streptococcal glomerulonephritis?

A

Following infection with streptococci, cross-reactivity can lead to kidney damage

37
Q

What mediates Type IV hypersensitivity?

A

T cells

Both CD4+ and CD8+ subclasses

Cause symptoms through separate mechanisms

38
Q

Which cytokines are increased during type IV hypersensitivity?

A

TNFa

IFN-y

39
Q

When does type IV hypersensitivity take place?

A

Allergy - contact dermatitis

Tuberculin skin reaction to mycobacterial antigens

Infections - TB granuloma

40
Q

How does type IV hypersensitivity cause skin rashes?

A

Immune cells migrate to the surface

Travel to the lymph nodes

T cells become activated and migrate to the site on the skin where they replicate

41
Q

What test screens for latent TB infection?

A

Mantoux test

Involves injection of tuberculinin in the skin

42
Q

How does type IV hypersensitivity cause granulomas in TB?

A

Continuous activation of T cells in chronic local TB

Leads to the accumulation of large numbers of macrophages

Macrophages cannot clear it and join up to make giant cells

Giant cells form granuloma to corner the infection

43
Q

What did type V hypersensitivity used to be a subclass of?

A

Type II hypersensitivity

44
Q

What molecule is involved in type V hypersensitivity?

A

Antibodies

45
Q

What is the mechanism behind type V hypersensitivity?

A

Formation of antibody which acts as an agonist on the cell surface receptors

Causing the stimulation of that cell to carry out their function

46
Q

Example of a condition caused by type V hypersensitivity

A

Grave’s disease

Agonist to TSHR on thyroid gland

Increases thyroid hormone release

47
Q

What is innate hypersensitisation?

A

Hyperactivation of the innate immune system

48
Q

Examples of innate hypersensitisation

A

Sepsis

Toxic shock syndrome

49
Q

Describe the mechanism behind toxic shock syndrome

A

It is caused by a superantigen

This does not bind to a specific TCR on T cells, but rather lots of cells through the outside of the receptor at once

50
Q

What conditions is chronic inflammation linked to?

A

Atherosclerosis

Alzheimer’s

Type II diabetes

Inflammageing

51
Q

What test is done to look for allergies?

A

Skin prick allergy test

52
Q

Describe the process behind a skin prick allergy test

A

Scratch with needle dipped into different allergens

Wait for 20 minutes for the test response

Some responses are more delayed, requiring more time = T cell mediated

53
Q

What causes dust allergy?

A

Fecal pellets of D. Farinae

Each pellet contains 0.2 ng of the allergen

54
Q

What is the main difference between type II and type III hypersensitivity?

A

Unlike type II hypersensitivities, antigen-antibody complexes in type III are not membrane-bound

55
Q

Describe how CD4+ cells become activated in type IV hypersensitivity

A

APC displays antigen on MHC II receptor

IL-12 expression by APCs induces Th1 maturation

Th1 secrete IL-2 and IFN-y

Macrophage and T cell proliferation

Th17 activated and secrete IL-17, leading to neutrophil recruitment

Macrophages promote inflammation and leaky endothelium

56
Q

What autoimmune conditions are caused by type IV hypersensitivity?

A

Type I diabetes

Multiple sclerosis

Hashimoto’s thyroiditis

57
Q

Features of innate hypersenstivities

A

Chronic inflammation

Innapropriate responses

Overactivation of macrophages

IMM005 (17 decks)

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