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Immuno > Immuno 1: Hypersensitivity and allergy > Flashcards

Immuno 1: Hypersensitivity and allergy Flashcards

1
Q

During appropriate immune reactions, there should be no tissue damage

A

F. May be concomitant tissue damage as a side effect, but as long as pathogen is eliminated quickly will be minimal and repaired easily

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2
Q

Approrpaite immune tolerance occurs to what

A

Appropriate immune tolerance occurs to self, and to foreign harmless proteins:

Food, pollens, other plant proteins, animal proteins, commensal bacteria

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3
Q

What does development of appropriate immune tolerance involve

A

Involves antigen recognition and generation of regulatory T cells and regulatory (blocking) antibody (IgG4) production

Antigen recognition in context of “danger” signals leads to immune reactivity, absence of “danger” to tolerance

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4
Q

Hypersemsitivity reactions invole immune responses against what

A

Harmless foreign antigens (allergy, contact hypersensitivity)
Autoantigens (autoimmune diseases)
Alloantigens (serum sickness, transfusion reactions, graft rejection)

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5
Q

Outline the 4 types of hypersenstivity reactions

A

Type I : Immediate Hypersensitivity
Type II : Antibody-dependent Cytotoxicity
Type III : Immune Complex Mediated
Type IV : Delayed Cell Mediated

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6
Q

t/f diseases often fit into a distinct catgory of immune hypersensitivity

A

F… lots are a mixture

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7
Q

Examples of Type 1 immediate hypersestivity

A 
Anaphylaxis
Asthma
Rhinitis
-Seasonal
-Perennial
Food Allergy
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8
Q

What occurs in type 1 immediate hypersenstivity

A

1^o Antigen exposure:

  • Sensitisation not tolerance
  • IgE antibody production
  • IgE binds to Mast Cells & Basophils

2^o Antigen Exposure

  • More IgE Ab produced
  • Antigen cross-links IgE on Mast Cells/Basophils
  • Degranulation
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9
Q

Outline the 2 categoties of type II antibody-dependent hypersenstivity

A

Organ-specific autoimmune diseases

Autoimmune cytopenias (Ab mediated blood cell destruction)

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10
Q

Give examplesof the type II organi-soecific autoimmune diseases, adnd the antibody :

Myasthaenia gravis

Glomerulonephritis

Pemphigus vulgaris

Pernicious anaemia

A
  • Myasthenia gravis (Anti-acetylcholine R Ab)
  • Glomerulonephritis (Anti-glomerular basement membrane Ab)
  • Pemphigus vulgaris (Anti-epithelial cell cement protein Ab)
  • Pernicious anaemia (Intrinsic factor blocking Abs)
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11
Q

Outline types of type II, autuimmune cytopenias

A

Haemolytic anaemia
Thrombocytopenia
Neutropenia

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12
Q

T/f.. pernicious anaemia is an example of an autoimmune cytopenia

A

F…. it is an organ specific aurommune disease

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13
Q

Give 2 examples of tests for speicifc autoanibodies

A

Immunofluorescence

ELISA eg anti-CCP (Cyclic Citrullinated Peptide Abs for Rheumatoid Arthritis)

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14
Q

Outline type III reactions

A

Formation of Antigen-Antibody complexes in blood

Complex deposition in blood vessels/tissue

Complement & cell activation

Activation of other cascades eg clotting

Tissue damage (vasculitis)

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15
Q

Outline examples of tissue damage (vasculitis) as part of type III immune complex hypersenstivity

A

Systemic lupus erythematosus (SLE)

Vasculitides (Poly Arteritis Nodosum, many different types)

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16
Q

Outline why vasculitis occurs in type III hypersensitivty

A

Antibodies bound to antigen then deposit in vessel walls (or tissue) and activate complement (C3) and cellular activatin (monocyte/neutrophil)

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17
Q

What are the most common sites of vasculitis in type III hypersensitivity

A

Skin
Renal (glomerulonephritis)
Joints
Lung

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18
Q

Give examples of type IV delayed hypersensitivty responses

A 
Chronic graft rejection
GVHD
Coeliac disease
Contact hypersensitivity
Many autoimmune diseases….
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19
Q

Outline the three main varieties of type IV delayed hypersensitivity reaction

A

Th1
Cytotoxic
Th2

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20
Q

Outlne the mechanisms of type IV hypersensitivtiy

A

Transient/Persistent Ag

T cell activation of macrophages, CTLs

Much of tissue damage dependent upon TNF & CTLs

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21
Q

Give an example of how a type IV hypersensity rreaction might occur

A

Antigen is presented on an APC

APC presented to Th1, which releases IFN-g, FGF and IL-2

IFN-g activates macrophages which release TNF

FGF activates fibroblast which casues angiogenesis and fibrosis

IL-2 causes cytotoxic T lymphocytes to release perforin

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22
Q

Nickel is a type II mediated hypersensitvitiy

improve

A

F. Type 4… as it contact hypersenstivity (contact dermatits)

inflammation only where the nickle is present e.g. if a nickel thimble was worn

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23
Q

Outline the immune reactant for each hypersensitivty reaction

A

I- IgE
II-IgG
III- IgG
IV- Th1/Th2/CTL

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24
Q

t/f inflammation is part of all immune reactions

A

T

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25
Q

What is inflammation and what is a common feature of it

A

This is the body’s response to tissue injury

  • It is a rapid attempt to bring the body’s defences to the site of injury
  • A common feature of inflammation is immune cell recruitment (sites of injury/infection) and activation
  • Once the immune cells reach the site, they release cytokines that leads to the features of inflammation
  • Inflammatory mediators include complement, cytokines, etc.
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26
Q

What are the signs of inflammation

A

Redness
Heat
Swelling
Pain

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27
Q

What are the features of inflammation

A

Vasodilatation, increased blood flow
Increased vascular permeability
Inflammatory mediators & cytokines
Inflammatory cells & tissue damage

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28
Q

Increased vascular permeability is caused by which mediators

A

C3a, C5a, histamine, leukotrienes

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29
Q

Which cytokines are involved in inflammation

A

IL-1, IL-6, IL-2, TNF, IFN-γ

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30
Q

Which chemokinesa re involved in inflammation

A

IL-8/CXCL8, IP-10/CXCL10

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31
Q

What can happen to cells during inflammation

A

Inflammatory cell infiltrate
Cell trafficking – chemotaxis
Neutrophils, macrophages, lymphocytes, mast cells
Cell activation

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32
Q

Overall, which 4 things occur in infkamation

A

Increased vascular permeability

Cytokines

Chemokines

Inflammatory cell infiltrate

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33
Q

What is atopy

A

a form of allergy in which there is a hereditary of constitutional tendency to develop hypersensitivity reactions (e.g. hay fever, allergic asthma, atopic eczema) in response to allergens (atopens). Individuals with this predisposition - and conditions provoked in them by contact with allergens - are described as atopic.

34
Q

What is the prevalence of atopy

A

Common - prevalence of atopy is 50% in young adults in UK

35
Q

How does the severity of allergy vary

A

mild occasional symptoms
severe chronic asthma
life threatening anaphylaxis

36
Q

T/f the genetic risk factors of atopy is usually monogenic

A

~80% of atopics have a family history

Polygenic

37
Q

Which genes are linked to raised IgE, asthma atopy

A

genes of IL-4 gene cluster (chromosome 5) linked to raised IgE, asthma, atopy

38
Q

Which genes are linked to atopa and asthma

A

genes on chromosome 11q (IgE receptor) linked to atopy and asthma

39
Q

Which genes are linked to eczema

A

genes linked to structural cells linked to eczema (filaggrin) and asthma (IL-33, ORMDL3, CDHR3)

40
Q

What are the environmental risk factors for atopy

A

Age - increases from infancy, peaks in teens, reduces in adulthood

Gender - asthma more common in males in childhood, females in adults

Family size - more common in small families

Infections- early life infections protect

Animals - early exposure protects

Diet - breast feeding, anti-oxidants, fatty acids protect

41
Q

Give examples of type 1 hypersensitivty mediated inflammation

A

Anaphylaxis, urticaria, angioedema

TYPE 1- IgE

42
Q

Give examples of type 2 mediated inflammation

A

Idiopathic/chronic urticaria

TYPE II- IgG

43
Q

Give examples of confitions involving mixe inflammaiton.

Which hypersensitivt yreactions are these mediated by

A

Asthma, rhinitis, eczema

Mesiated by

type I hypersensitivity (IgE mediated)
type IV hypersensitivity (chronic inflammation)

44
Q

What is rewquired for expression of allergic disease

A

Development of sensitisation to allergens instead of tolerance (primary response - usually in early life)

Further allergen exposure to produce disease (memory response - any time after sensitisation)

45
Q

Outline sensitisation of atopic airway disease

A

Dendritic cell samples the airway

Presents antigen to naive T cell

T cell decides whether to be tolerant to the antigen (in which case it becomes Treg) or auto-immune disease (Th1) or an allergic response (Th2)

If Th2 route was chosen, then Th2 cells will then proliferate and produce IL-4 and IL-13, which makes B cell produce IgE, not IgG antibodies

IgE which is specific to the antigen will bind to plasma cells and cause IgE production

IgE bind to mast cells

46
Q

Outline what happens in subsequent exposure, following sensitisation in atopic disease

A

Same process with dendritic cell

But the antigen will be presented to Th2 memory cells from the sensitisation stage

Which will then cause more IL4 and IL13 to make more IgE.

IL5 released by Th2 to recruit eosinophils and activate them.

Eosinophils then release inflammatory mediators

IgE bound to mast cells undergoes crosslinking with the antigen

Causes degranulation of mast cells and release of inflammatory mediators

47
Q

Eosinophils make up what proportion of blood leukocytes

A

0-5% of blood leukocytes

48
Q

T/F most eosinophils present in tissues

A

T…. Present in blood, most reside in tissues

49
Q

What is the nucleus of an eosinophil like

A

Nucleus - two lobes

50
Q

What is contained in the granules of eosinophils

A

Toxic proteins…. the grnules arfe LARGE

51
Q

What is an effect of eosinophil activation

A

TISSUE DAMAGE

52
Q

T/F mast cells are tissue resident cells

A

T

53
Q

How are mast cells avtivated

A

IgE receptors on cell surface

54
Q

What happens upon IgE cross linking to mast cells (what mediators are contained there)

A

MEDIATOR RELEASE

  1. Pre-formed:
    - Histamines
    - Cytokines
    - Toxic proteins
  2. Newly synthesised
    - leukotrienes
    - prostaglandings
55
Q

Which disease are neutorhils important in

A

virus induced asthma
severe asthma
atopic eczema

56
Q

What proportion of blood leukocytes are neutrophils

A

55-70% of blood leukocytes

57
Q

Neutrophils are aka

A

Polymorphonuclear cells (PMNs)

58
Q

What is the nucleus of a neutrophil like

A

Nuecleus several lobes

59
Q

What is contained within the granules of neutrophils

what else do neutrophils synthesise

A

digestive enzymes

Also synthesize
oxidant radicals
cytokines
**leukotrienes

60
Q

Outline the pathology of asthma

A

Acute airway inflammation

Mast cell activation and degranulation

  • -> release of prestored mediators (e.g. histamine, leading to airway wall oedema)
  • -> release of newly synthesised mediators (prostaglandins and leuktrienes)

LEADS TO:

Acute airway narrowing (airway smooth muscle contraction)

61
Q

What are the three things in asthma that cause airway narrowing

A

Airway wall oedema (due to vascular leakage)

mucus secretion and

airway smooth muscle contraction

(NOTE: these are all due to the mediators released from the mast cell activation and degranulation)

62
Q

What happens upon exposure to asthama causing antigen to peak flow

A

PEF starts at less than 100% (as asthmatic so reduced anyway)

EARLY RESPONSE:
Initially, there is a rapid and significant reduction in PEF in response to antigen exposure. This is due to the immediate hypersensitiviy (IgE mediated, mast cell activation, acute airway narrowing due to the oedema, mucus and contraction)

This recovers quickly (within an hour)

However, over 2-8hrs there is then another reduction in PEF , the

LATE RESPONSE:
There is cell-mediated delayed type hypersensitivity in which lymphocyte and eosinophil mediated infmallation occurs (Th2 cells activate eosinohils, leading to IL4 and IL5 release)

Important to remember that asthma is a mixture of type I and type IV.

This graph is on somebody who has already been sensitised to antigen and had subsequent exposures already.

So what happens when you give them allergen

You get type I reaction straight away (due to IgE cross-linking)

Then later you get cell mediated type IV reaction which is when Th2 activates eosinophils. This is not accounted for by type I, which only involves mast cell/basophil degranulation

63
Q

Outline the chronic airway inflammation in asthma

A

So we had early and late response which are referring to acute onset inflammation

Not there is also CHRONIC INFLAMMATIONlON

  1. Cellular infiltrates (Th2 lymphocytes and eosinophils, from delayed type hypersensitivity)
  2. Smooth muscle hypertrophy
  3. Mucus plugging
  4. Epithelial shedding
  5. Sub-epithelial fibrosis
64
Q

What are the important clinical features of asthma

A

REVERSIBLE generalised airway obstruction (–> chronic episodic wheeze)

Bronchial hyperresponsiveness (–>bronchial irritability)

Cough

Mucus

Breathlessness

Chest tightness

Responds to treatment (COPD doesn’t)
Spontaneous variation
Reduced and variable PEF

65
Q

What are the important clinical features of allergic rhinitis

A

Note the mechanism is very similar to asthma in terms of type 1 and then type 4

Seasonal (hay fever, grass, tree pollens)

Perennial (house dust mites or pets)

Symptoms: sneezing, rhinorrhoea, itchy nose and eyes, nasal blockage, sinusitis, loss of smell/taste

66
Q

Outline the clinical features of allergic eczema

A

Atopic dermatitis is allergy due to genetics, contact dermaitis is at the site of the chemical exposure=type IV)

Chronic itchy skin rash

Flexures of arms and legs

HDM sensitisation and dry cracked skin

Complicated by bacterial and (rarely) viral infections (early childhood, herpes simplex)

50% clears by 7 years
90% by adulthood

67
Q

Outline the important clinical features of food allergy

A

Mild: itchy lips, mouth, angioedema, urticaria

Severe: nausea, abdominal pain, diarrhoea, collapse, wheeze, ANAPHYLAXIS

68
Q

What are the most common food allergens in infants and adults

A

Infancy-3yrs
egg, cows milk

Children/adults
peanut, nuts, shell fish, fruits, cereals, soya

69
Q

What is anaphylaxis

A

severe generalised allergic reaction

Generalised degranulation of IgE sensitised mast cells

70
Q

Symptoms of anaphylaxis

A

itchiness around mouth, pharynx, lips

swelling of the lips, throat and other parts of the body

wheeze,

chest tightness,

dyspnoea

faintness,

collapse

diarrhoea & vomiting

death if severe & untreated

71
Q

Which systems are involved in anaphylaxis

A

Systems:
Cardiovascular - vasodilatation, cardiovascular collapse

Respiratory - bronchospasm, laryngeal oedema

Skin - vasodilatation, erythema, urticaria, angioedema

GI - vomiting, diarrhoea

72
Q

How can food allergens be tested

A

Careful history essential

Skin prick testing

RAST (blood specific IgE):

Total IgE

Lung function (asthma)

73
Q

What is the emergency treatment of anaphylaxis

A

EpiPen & Anaphylaxis kit

  • ->antihistamine, steroid, adrenaline
  • -> Seek immediate medical aid
74
Q

How is anaphylaxis prevented

A

Avoidance of known allergen
Always carry a kit & EpiPen
Inform immediate family & caregivers
Wear a MedicAlert® bracelet

75
Q

How is allergic rhinitis treated

A

anti-histamines (sneezing, itching, rhinorrhoea)

nasal steroid spray (nasal blockage), if the inflammation is cell mediated (anti-histamine only helps if it’s just due to type 1)

cromoglycate (children, eyes)= a mast cell stabiliser

76
Q

How is eczema treated

A

emollients
topical steroid cream
(as mostly cell mediated)

77
Q

What drugs are now used for sever rhinitis and eczema

A

anti-IgE, anti-IL-4/-13, anti-IL-5 mAb

78
Q

What is the treatment for asthma

A
  1. Short acting b2 agonist drugs as required by inhalation (SALBUTAMOL,)
  2. Inhaled steroid low-moderate dose (Beclomethasone/budesonide or flutocasone, 40-800micrograms )
  3. Add further therapy
    - long acting bronchodilators, leukotriene antagonist
    - high dose inhaled steroids via spacer (2milligrams, much higher)
  4. Add oral steroids, SLIT (sub lingual immune therapy), azithromycin
    - prednisolone (30mg)
    - Anti-IgE, anti-IL-5, anti-IL-4/-13 monoclonal Abs
79
Q

When is immunotherapy used

A

Effective for single antigen hypersensitivities

  • Venom allergy - bee or wasp stings
  • Pollens
  • HDM
  • Antigen used is purified
80
Q

Why is azithromycin given for asthma treatment eventually

A

Asthma may be due to bacteria colonisaton of the lungs

81
Q

How can immunotheray be given

A

Subcutaneous immunotherapy (SCIT)
3 years needed
Weekly/monthly 2hr clinic visits

Sublingual immunotherapy (SLIT)
3yrs needed
Taken at home

Can be used for anaphylaxis or severe allergic rhinitis for example

82
Q

Differentiate pemphigus and pemphigoid

A

Pemphigus is Abs directed at intercellular cement

Pemphigpoid is Abs directed at the basement membrane

Immuno (5 decks)

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