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Immunology > 1. Hypersensitivity and allergy > Flashcards

1. Hypersensitivity and allergy Flashcards

1
Q

What are alloantigens?

A
  • Antigen present only in some individuals
  • Capable of inducing the production of an alloantibody in people that lack it
  • e.g. blood group antigens
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2
Q

What are the 4 types of hypersensitivity?

A
  • Type I - immediate hypersensitivity
  • Type II - antibody-dependent cytotoxicity
  • Type III - immune complex mediated
  • Type IV - delayed cell mediated
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3
Q

Give examples of type I hypersensitivity

A
  • Anaphylaxis
  • Asthma
  • Rhinitis
  • Food allergy
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4
Q

Outline the mechanism of type I hypersensitivity

A
  • 1st antigen exposure - sensitisation
  • IgE production
  • IgE binds to mast cells + basophils
  • 2nd antigen exposure
  • More IgE produced
  • Antigen cross-links IgE on mast cells + basophils
  • Degranulation and release of inflammatory mediators
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5
Q

What happens in type II hypersensitivity?

A
  • The antibodies produced by an immune response binds to antigens on the patient’s own cell surfaces
  • B cell proliferation
  • IgG and IgM bind - classical complement
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6
Q

Give examples of organ-specific autoimmune diseases (type II hypersensitivity) and the antibodies they involve

A
  • Myasthenia gravis - anti-acetylcholine receptor antibodies (muscles become weak)
  • Glomerulonephritis - anti-glomerular BM antibodies (cause of kidney disease)
  • Pemphigus vulgaris - anti-epithelial cell cement protein antibodies (blistering skin condition)
  • Pernicious anaemia - intrinsic factor blocking antibodies (prevents vit. b12 absorption)
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7
Q

Give examples of autoimmune cytopenias (antibody-mediated blood cell destruction) (type II hypersensitivity)

A
  • Haemolytic anaemia - red cells
  • Thrombocytopenia - platelets
  • Neutropenia - neutrophils
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8
Q

What is bullous pemphigoid?

A
  • Blistering skin disorder
  • Antibodies against BM proteins
  • More robust blisters than pemphigus due to deeper inflammation in the skin
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9
Q

How can you test for specific antibodies?

A
  • Immunofluorescence

* ELISA

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10
Q

Outline the progression of a type III hypersensitivity response

A
  • Excess antigen
  • Formation of antigen-antibody complex in the blood
  • Can’t get through small blood vessels easily - complexes deposit in the vessels and tissues
  • Leads to complement activation and cell recruitment
  • Activation of other cascades e.g. clotting
  • Tissue damage - inflammation of blood vessels (vasculitis)
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11
Q

Give an example of a type III hypersensitivity autoimmune disease

A

Systemic lupus erythematosus (SLE)

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12
Q

Given an example of a vasculitis disorder

A

Polyarteritis nodosa - systemic necrotising vasculitis

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13
Q

What are the most common sites of vasculitis?

A
  • Renal (glomerulonephritis)
  • Skin
  • Joints
  • Lungs
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14
Q

Give examples of type IV hypersensitivity reactions/disorders

A

Th1
• Chronic graft rejections
• Coeliac disease
• Contact hypersensitivity

Th2 (all others are Th1)
• Asthma
• Rhinitis
• Eczema

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15
Q

What does a Th1 type IV hypersensitivity reaction mainly involve?

A

Production of lots of gamma-interferon by Th1

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16
Q

Which cytokines does Th2 release in type IV hypersensitivity?

A
  • IL-4
  • IL-5
  • IL-13
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17
Q

What cells can T helper cells activate in type IV?

A
  • Macrophages

* Cytotoxic T lymphocytes

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18
Q

Do type IV hypersensitivity reactions depend on a transient antigen presence or a persistant antigen?

A

Both

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19
Q

What is a lot of tissue damage in type IV dependent on?

A

TNF-alpha

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20
Q

What is asthma caused by (in terms of Ig and immune cells)?

A
  • IgE binding to mast cells

* Induction of T cells producing Th2 type cytokines

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21
Q

What are the features of inflammation?

A
  • Vasodilation
  • Increased vascular permeability
  • Inflammatory mediators + cytokines
  • Inflammatory cells + tissue damage
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22
Q

What are the signs of inflammation?

A
  • Redness
  • Swelling
  • Heat
  • Pain
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23
Q

What causes increased vascular permeability in inflammation?

A
  • C3a
  • C5a
  • Histamine
  • Leukotrienes
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24
Q

Which cytokines are released during inflammation?

A
  • IL-1
  • IL-6
  • IL-2
  • TNF
  • IFN-γ
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25
Which chemokines are released during inflammation and what do they do?
* IL-8/CXCL8 - attracts neutrophils | * IP-10/CXCL10 - attracts lymphocytes
26
What is atopy?
* Form of allergy * Hereditary or constitutional tendency to develop hypersensitivity reactions in response to allergens (atopens) * e.g. allergic asthma, hay fever, atopic eczema
27
How common is atopy?
Very - 50% of young adults in the UK
28
Give examples of the varieties of atopy
* Mild occasional symptoms * Severe chronic asthma * Life threatening asthma
29
Give examples of some genetic risk factors to atopy
(genetic component is polygenic) • IL-4 gene cluster (Chr5) linked to raised IgE, asthma and atopy • Chromosome 11q genes (IgE receptor) linked to asthma and atopy • Structural cell genes linked to eczema (filagrin) and asthma (IL-33)
30
How does the risk of atopy change with age?
* Increases from infancy * Peaks in teens * Reduces in adulthood
31
How does gender influence asthma (atopy)?
* More common in males in childhood | * More common in females in adults
32
How is the risk of atopy different depending on family size?
More common in small families
33
How does early life exposure to infections and animals affect atopy?
Protects from reactions
34
What type of hypersensitivity is anaphylaxis, urticaria and angioedema?
Type I
35
What type of hypersensitivity idiopathic/chronic urticaria?
Type II
36
What type of hypersensitivity asthma, rhinitis and eczema?
* Type I | * Type IV
37
When an APC activates the CD4+ T cells, they become specific and can become...
* Th1 (producing IFN-gamma) * Th2 (leads to B cell activation) * Treg (if harmless antigen)
38
What happens when the allergens are presented by APCs to the memory Th2 cells?
* Th2 releases IL-5 * This causes the degranulation of eosinophils * Th2 also releases IL-4 and IL-13 * This stimulates the production of IgE by plasma cells * IgE then becomes mobilised onto the surface of mast cells * Antigens then cross-link with IgE and cause degranulation of mast cells * Massive release of inflammatory mediators - allergic reaction
39
How many nucleus lobes do eosinophils have?
2
40
What are in the large granules in eosinophils?
Toxic proteins
41
What are the pre-formed and newly synthesised mediators in mast cells?
Pre-formed • histamine • cytokines • toxic proteins Newly synthesised • leukotrienes • prostaglandins
42
What allergies/hypersensitivies are neutrophils important in?
* Virus induced asthma * Severe asthma * Atopic eczema
43
What do neutrophil granules contain?
Digestive enzymes
44
What 3 processes cause airway narrowing in asthma?
* Vascular leakage leading to airway wall oedema * Mucus secretion * Smooth muscle contraction around the bronchi
45
There is cellular infiltration of which cells in chronic asthma?
Th2 and eosinophils
46
What happens to the epithelium in chronic asthma?
* Epithelial shedding | * Sub-epithelial fibrosis
47
What are some of the clinical features of asthma?
* Reversible generalised airway obstruction - chronic episodic wheeze * Bronchial hyper-responsiveness * Cough, mucus, breathlessness, chest tightness * Spontaneous variation * Response to treatment * Reduced and variable peak expiratory flow (PEF)
48
What are the 2 types of allergic rhinitis and give an example of each?
* Seasonal e.g. hay fever | * Perennial (long lasting) e.g. animal allergens
49
What are the symptoms of allergic rhinitis?
* Sneezing * Rhinorrhoea * Itchy nose and eyes * Nasal blockage, sinusitis, loss of smell/taste
50
What is allergic eczema?
* Chronic itchy skin rash | * Most common in the flexures of the arms and legs
51
What is the relation between allergic eczema and house dust mites?
House dust mite proteins can get through the dry, cracked skin => sensitisation
52
What can cause allergic eczema complications?
Bacterial and (rarely) viral infections e.g. HSV
53
When does allergic eczema usually clear?
* 50% by 7 years | * 90% by adulthood
54
What are the mild and severe allergic reactions to food?
Mild • itchy lips and mouth • angioedema • urticaria ``` Severe • Nausea • Abdominal pain • Diarrhoea • Anaphylaxis ```
55
What is anaphylaxis and what are the symptoms?
Severe generalised allergic reaction - degranulation of IgE sensitised mast cells • itchiness around mouth, pharynx and lips • swelling of lips, throat, etc. • wheeze, chest tightness and dyspnoea • faintness • diarrhoea and vomiting • death if severe/untreated
56
What are the systemic effects in anaphylaxis
* CV - vasodilation, collapse * Resp - bronchospam, laryngeal oedema * Skin - vasodilation, erythema, urticaria, angioedema * GI - vomiting and diarrhoea
57
How can allergies be investigated and diagnosed?
* Careful history * Skin prick testing * RAST (radio-allergosorbent test) - IgE blood test * Measure total IgE * Lung function (for asthma)
58
What is the emergency treatment for anaphylaxis?
* EpiPen and anaphylaxis kit * Antihistamine (if mild) * Adrenaline (if severe)
59
How can anaphylaxis be prevented (+ safety precautions)?
* Avoidance of known allergen * Always carry an EpiPen and anaphylaxis kit * Inform immediate family and caregivers * Wear medicalert bracelet
60
What is the treatment for allergic rhinitis?
* Anti-histamines * Nasal steroid therapy * Cromoglycate (eye drops)
61
What is the treatment for eczema?
* Emollients | * Topical steroid cream
62
What is the treatment for allergic rhinitis/eczema if severe?
* Anti-IgE mAb * Anti-IL4/13 mAb * Anti-IL5 mAb
63
What is the treatment for asthma (4 steps)?
1) Short-acting beta-2 agonist by inhalation e.g. salbutamol 2) Inhaled steroid low-moderate dose e.g. beclomethasone, fluticasone 3) Add long-acting beta-2 agonist or leukotriene antagonist, or high dose inhaled steroids 4) Add courses of oral steroids and/or monoclonal antibodies
64
What is immunotherapy and when is it effective?
* Make people develop tolerance by exposing them to small amounts of the allergen * Effective for single antigen hypersensitivities * e.g. bee stings, pollens etc.
65
What are 2 types of immunotherapy?
* Subcutaneous immunotherapy (SCIT) - weekly/monthly 2hr clinic visits, 3 years * Sublingual immunotherapy (SLIT) - can be taken at home, 2-3 years

Immunology (5 decks)

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