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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
When does haemolytic disease of the newborn take place?
When the mother is Rhesus factor negative, but the baby is Rhesus factor positive
26
Describe the process behind Haemolytic disease of the newborn
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
What is a possible treatment of Haemolytic disease of the newborn?
Overloading the system to mask out anti-D to prevent mother from being sensitised
28
What does a newborn who suffered haemolytic disease look like?
Blue Blood cells are killed by mothers immune cells
29
Example of an autoimmune disease with type II hypersensitivity
Goodpasture's Antibody attacks type IV collagen Especially damages kidneys
30
What is another example of type II hypersensitivity?
Formation of antibodies that block cell receptors No killing is involved, but prevents the organ from functioning correctly
31
Example of type II hypersensitivity not caused by cell death
Myasthenia gravis Blocking of the receptors to ACh
32
What is type III hypersensitivity mediated by?
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
Describe the process of type III hypersensitivity
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 4. Macrophages try to eat them, but the complexes are unable to 5. Macrophages carry out frustrated phagocytosis
34
What is frustrated phagocytosis?
Macrophages are activated and releasing their inflammatory factors without degrading the antibody-antigen complex
35
Where is type III hypersensitivity seen?
Allergies: Farmer's lung (hay exposure) Infections: post-streptococcal glomerulonephritis Autoimmune diseases: SLE
36
What is post-streptococcal glomerulonephritis?
Following infection with streptococci, cross-reactivity can lead to kidney damage
37
What mediates Type IV hypersensitivity?
T cells Both CD4+ and CD8+ subclasses Cause symptoms through separate mechanisms
38
Which cytokines are increased during type IV hypersensitivity?
TNFa IFN-y
39
When does type IV hypersensitivity take place?
Allergy - contact dermatitis Tuberculin skin reaction to mycobacterial antigens Infections - TB granuloma
40
How does type IV hypersensitivity cause skin rashes?
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
What test screens for latent TB infection?
Mantoux test Involves injection of tuberculinin in the skin
42
How does type IV hypersensitivity cause granulomas in TB?
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
What did type V hypersensitivity used to be a subclass of?
Type II hypersensitivity
44
What molecule is involved in type V hypersensitivity?
Antibodies
45
What is the mechanism behind type V hypersensitivity?
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
Example of a condition caused by type V hypersensitivity
Grave's disease Agonist to TSHR on thyroid gland Increases thyroid hormone release
47
What is innate hypersensitisation?
Hyperactivation of the innate immune system
48
Examples of innate hypersensitisation
Sepsis Toxic shock syndrome
49
Describe the mechanism behind toxic shock syndrome
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
What conditions is chronic inflammation linked to?
Atherosclerosis Alzheimer's Type II diabetes Inflammageing
51
What test is done to look for allergies?
Skin prick allergy test
52
Describe the process behind a skin prick allergy test
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
What causes dust allergy?
Fecal pellets of D. Farinae Each pellet contains 0.2 ng of the allergen
54
What is the main difference between type II and type III hypersensitivity?
Unlike type II hypersensitivities, antigen-antibody complexes in type III are not membrane-bound
55
Describe how CD4+ cells become activated in type IV hypersensitivity
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
What autoimmune conditions are caused by type IV hypersensitivity?
Type I diabetes Multiple sclerosis Hashimoto's thyroiditis
57
Features of innate hypersenstivities
Chronic inflammation Innapropriate responses Overactivation of macrophages

IMM005 (17 decks)

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