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Immunology > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

What is a hypersensitivity reaction?

A

An inappropriate immune response to non-infectious antigens that results in tissue damage and disease

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2
Q

What are the different types of hypersensitivity reactions?

A

Type 1: immediate hypersensitivity

Type 2: cytotoxic hypersensitivity

Type 3: serum sickness and Arthus reaction

Type 4: delayed-type hypersensitivity, contact dermatitis

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3
Q

What causes immediate hypersensitivity?

A

Immediate hypersensitivity results from exposure to allergens in the environment

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4
Q

Describe the immune response to immediate hypersensitivity

A

Host immune response is characterised by IgE antibodies bound to mast cells

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5
Q

What are the effects of IgE in response to immediate hypersensitivity?

A

IgE is specific to the allergen and cross-links to activate (mast) inflammatory cells to release mediators

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6
Q

Summarise the immune response to immediate hypersensitivity

A

Immune reactant: IgE

Antigen: soluble e.g. allergen

Effector Mechanism: Mast cell activation + degranulation

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7
Q

Give examples of immediate hypersensitivity

A

Allergic Rhinitis
Anaphylaxis
Eczema (skin)
Asthma (airways)

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8
Q

How can we induce a immediate hypersensitivity reaction?

A

A Type I hypersensitivity reaction can be induced via injection or scratching an allergen on skin

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9
Q

What are the effects of the immune response to an immediate hypersensitivity reaction?

A

Mast cells release inflammatory mediators causing leakage of plasma fluid into surrounding tissue = wheal (local oedema - bump on skin)

Vasodilatation = erythema = flare response

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10
Q

What is systemic anaphylaxis?

A

An exaggerated allergic response

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11
Q

How does systemic anaphylaxis occur?

A

Exposure to allergen causes rapid allergic reaction indicated by vasodilatation and fluid release = oedema

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12
Q

Why is systemic anaphylaxis dangerous?

A

Angioedema (face) can restrict the airways and lead to death

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13
Q

How is systemic anaphylaxis treated?

A

Require adrenaline on hand to treat reaction

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14
Q

What is cytotoxic hypersensitivity?

A

Hpersensitivity reactions in response to altered components of human cells

E.g. penicillin attaches to surface of RBCs which immune system flags as foreign

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15
Q

Outline a cytotoxic hypersensitivity reaction to penicillin

A
  1. Platelet / RBC covered in a drug (e.g. penicillin)
  2. Immune systems generates IgG response to drug
  3. IgG activates macrophages and complements = inflammation
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16
Q

What allergens cause cytotoxic hypersensitivity?

A

Some drug allergies

Penicillin

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17
Q

Describe the autoimmune cytotoxic hypersensitivity response

A

IgG antibodies disrupt normal functions of the receptor by either:

  • uncontrollable activation
  • blocking receptor function
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18
Q

Describe the normal release of Thyroxine and TSH

A

Pituitary releases TSH which acts on thyroid to release thyroxine

Thyroxine in blood causes -ve feedback = reduces TSH production

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19
Q

Outline how cytotoxic immune response can lead to Grave’s disease

A

In Thyrotoxicosis / Grave’s an immune response is generated against TSH receptors causing long term stimulation of TSHR

Release of thyroxine leads to excess levels with no -ve feedback

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20
Q

What are the consequences of autoimmune cytotoxic hypersensitivity reactions?

A

Grave’s disease
Myasthenia Gravis
Haemolytic disease (newborn)

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21
Q

Outline the ways Type II HS reactions cause myasthenia Gravis

A

Antibodies block / destroy nAchR on postsynaptic junctions

Antibodies block / destroy nAchR at junction between nerve and muscle

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22
Q

How does haemolytic disease of newborns occur?

A

Blood group antigen (Rhesus) causes immune response when:

  • RhD -ve mother
  • RhD +ve foetus

Occurs at time of delivery

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23
Q

How does baby normal dissociate from maternal circulation?

A

Normally embryonic chorion isolates foetus from maternal circulation

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24
Q

How does HDN affect maternal circulation?

A

During incompatibility, embryonic chorion disruption causes release of red cells in maternal circulation

Mother produces antibodies against RhD+ foetus - 1st child is safe

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25
Q

What are the consequences of HDN on foetus during 2nd pregnancy

A

During 2nd pregnancy, antibodies previously stimulated can cross placenta and attack fetal RBCs with RhD resulting in death

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26
Q

What causes serum sickness (Type 3 HS)?

A

Presence of soluble antigen e.g. tetanus / diphtheria toxoids can cause serum sickness /arthus reaction

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27
Q

How do toxoids cause serum sickness / arthus reaction?

A

Large IgG response generated at site of injection causes immune complexes

These activate cells around capillaries to produce inflammatory response with activated complement

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28
Q

How does arthus reaction arise?

A

Previous vaccination = elevated antibodies

If vaccinated again = more immune complexes form
High levels of antigens can cause localised inflammation

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29
Q

Outline the process of arthus reaction formation

A
  1. Activate mast cells to release inflammatory mediators.
  2. inflammatory cells invade site
  3. Blood vessel permeability + blood flow increased.
  4. Platelets accumulate = occlusion of small blood vessels, hemorrhage, and appearance of purpura
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30
Q

What causes serum sickness?

A
  • large intravenous doses of soluble antigens (e.g. drugs)

IgG antibodies produced form small immune complexes with antigen in excess

immune complexes deposited in tissues e.g. blood vessel walls

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31
Q

What causes tissue damage during serum sickness?

A

Tissue damage is caused by complement activation and the subsequent inflammatory responses

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32
Q

How does antivenom cause serum sickness?

A
  • large amounts of horse Ig
  • Vasculitis rash on skin
  • nephritis; immune complexes deposited in kidney ⇒ fatal
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33
Q

What causes farmers lung?

A
  • hay mold inhaled into lungs

- localised inflammation; immune complexes

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34
Q

What are the consequences of farmer’s lung?

A

Antigen inhaled (mold etc.) that forms immune complexes with alveoli

Complexes stimulate an inflammatory response within lung resulting in fibrosis, granulation + inflammation

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35
Q

What causes hypersensitivity pneumonitis?

A
  • Dusts, bacteria, fungi
  • Farmer’s lung - thermophilic actinomycosis
  • Pigeon breeder’s lung - protein derived from birds
36
Q

Describe the histology of hypersensitivity pneumonitis

A
  • Interstitial pneumonia
  • Non-caseating granulomas in 2/3rd patients
  • Interstitial fibrosis, honeycombing & obliterative bronchiolitis
  • Intra-alveolar infiltrate
37
Q

What determines Type III HS reaction pathology?

A

Antigen dose and route of delivery determine the pathology observed in type III hypersensitivity reactions

38
Q

What are the effects of Type III HS due to a High IV dose?

A
  • Vasculitis: Blood vessel walls
  • Nephritis: renal glomeruli
  • Arthritis: joint spaces
39
Q

What are the consequences of Type III HS in subcutaneous tissue?

A

Causes arthus reaction due to immune complexes forming in perivascular areas

40
Q

What is the effect of an inhaled Type III HS allergen?

A

Farmer’s lung leads to immune complexes forming in alveolar / capillary interfaces

41
Q

What are the 2 types of delayed-type hypersensitivity?

A
  • Th1 (intracellular bacteria)

- Th2 (worm infection / allergens)

42
Q

Outline the Th1 mediated delayed-type reaction

A
  1. Antigen activates Th1 cells
  2. Cytokines (IFN-y + !L-12) released
  3. Macrophages tstimulated o release cytokines / chemokines to recruit specific cells (granuloma) to inflammation site

~2-3 days for reaction

43
Q

Name an antigen that induces a Th1 mediated delayed-type hypersensitivity response

A

Tuberculin

44
Q

Describe the Th2 mediated delayed-type HS reaction

A

Cells produce IL-4 + IL-5 cytokines that recruit IgE and eosinophils to site of inflammation

45
Q

Why does a delayed response occur in Type IV HS reactions?

A

T cell mediated Macrophages recruit cytokines / chemokines that recruit further immune cells to inflammation site
- takes 24 -72 hrs

46
Q

Give examples of Type IV HS disorders

A

Contact dermatitis
Tuberculoid Leprosy
Poison Ivy

47
Q

Describe how a mantoux test is carried out

A

Subcutaneously inject tuberculin extract (bacilli)
Wait ~2-3 days for reaction
Ulceration shows sensitisation

48
Q

What is tuberculoid leprosy?

A

Tuberculoid leprosy is a strong Th1 response in response to tuberculin bacilli presence resulting in typical granuloma

49
Q

How does poison ivy cause a delayed-type hypersensitivity reaction?

A

People previously sensitised to pentadecacatechol (in poison ivy) can develop a strong contact dermatitis type reaction upon re-exposure

50
Q

What is allergy?

A

Defined as “disease following a response by the immune system to an otherwise innocuous antigen”

51
Q

What is the significance of IgE?

A

First line of defence against worms and allergies

52
Q

How do IgE molecules create an immune response?

A

Binds FcεR1 receptor on mast cells

Coats mast cells to react when in the presence of antigen

53
Q

Outline the simple allergy IgE reaction

A
  1. First exposure to pollen
  2. IL-4 drives B cells to produce IgE in response to pollen antigens
  3. Pollen-specific IgE binds to mast cells
54
Q

What causes allergic sensitisation?

A

Exposure to Allergen is critical, this includes:

  • Nature of the allergen
  • Dosage of Allergen (high vs. low)
  • Timing
  • Location of Priming

Role of pro-allergic dendritic cells and cytokines

Genetic predisposition to Allergy

55
Q

How does the environment affect allergy cases?

A

Microbiome altered due to increased cleanliness - lack of diversity (aseptic environment) may cause sensitivity to more allergens

56
Q

What are some common allergens?

A

House dust mite, pollens, cockroach etc

57
Q

How are allergens named?

A

Allergens are named systematically:

  • After source organism and order discovered
    e. g. Der p1 comes from Dermatophagoides pteronyssinus

Not all proteins are allergenic

58
Q

Describe the genetics of allergy

A

Most allergies are polygenic - however interaction between genes and environment can determine development of allergies

59
Q

What is the role of filaggrin?

A

Filaggrin links skin integrity and allergy

60
Q

What is the consequence of defective filaggrin?

A

When defective atopic dermatitis is greater due to increased access for allergens

61
Q

What factor determines the production of an allergic response?

A

Type of cell presenting the antigen initially can affect whether an allergic response is generated or not

62
Q

What cells are switched to ‘pro-allergic’ due to antigen presentation?

A

APCs within skin called langerhan cells (epidermis) and dendritic cells (dermis)

63
Q

What causes the switch of cells to pro-allergic?

A

Not Known but one Candidate Protein is TSLP
This may switch DC to a ‘pro-allergic’ state
(TSLP= Thymic stromal lymphopoietin)

64
Q

What are the effector mechanisms of the allergic immune response?

A
  1. First exposure to pollen
  2. IL-4 drives B cells to produce IgE in response to pollen antigens
  3. Pollen-specific IgE binds to mast cells
  4. Second exposure to pollen
  5. Acute release of mast-cell content causes allergic rhinitis (hay fever)
65
Q

Describe the structure of resting mast cells

A

Resting mast cells contain dense granules full of inflammatory mediators (histamine, leukotrienes etc.)

66
Q

How do activated mast cell structures change?

A

Activated mast cell releases all mediators revealing a different structure

67
Q

What are the 2 phases of an allergic response?

A

Allergic responses have an early and late phase

  • Early mediated by mast cells
  • Late mediated by T cells
68
Q

Describe the early allergic response

A

Early response = typical wheal & flare response (Type 1)

69
Q

What is a late allergic response charcterised by?

A

High allergen dose - recruitment of other immune cells to site of inflammation causes later reaction - more diffuse oedema and inflammation

70
Q

Describe the allergic reaction phases of the airways

A

Reduced FEV1 in airway inflammation ~30 mins after allergen inhalation

Recruitment of inflammatory cells causes late response lasting longer ~24hrs

71
Q

Outline primary sensitisation to allergens

A

> Mediated by B cells

DC activation: present antigen to T cells (Th2)
Activated Th2 produce IL-4, IL-13 which signal B cell IgE production

IgE lines mast cells ready for secondary allergen exposure
⇒ acute allergic reaction

72
Q

Describe the secondary allergen exposure

A

> Mediated by Th2

Recruitment of other immune cells e.g. eosinophils and mast cells mediate over a prolonged period of time

⇒ Chronic allergic reaction

73
Q

What effector mediators are produced by mast cells during early phase?

A
  • histamine
  • leukotrienes
  • prostaglandins
74
Q

What effect does histamine have during early phase?

A
  • increase vascular permeability

- smooth muscle contraction

75
Q

Describe the effects of leukotriene release during early phase allergic reactions

A
  • increase vascular permeability
  • smooth muscle contraction
  • mucus secretion
76
Q

What are roles of prostaglandin release in response to early phase allergic reactions?

A

Acts as chemoattractants for T cells, eosinophils and basophils

77
Q

What cytokines are released during late phase?

A
  • IL-4 + IL-13

- TNF-a

78
Q

What are the effects of IL-4 and IL-13?

A

promote Th2 activity

Activate IgE

79
Q

What is the effect of TNF-a during late phase allergic reaction?

A

promotes tissue inflammation

80
Q

How does mast cell activation effect GI tract?

A
  • inc. fluid secretion
  • inc. peristalsis

Expulsion of contents (diarrhoea + vomiting)

81
Q

What are the effects of mast cell activation on the airways?

A
  • dec. diameter
  • inc. mucus secretion

Congestion / blockage; wheezing, coughing, phlegm

Swelling + mucus secretion in nasal passages

82
Q

Describe the effects of mast cell activation on blood vessels

A
  • inc. blood flow
  • inc. permeability

Inc. fluid in tissues = more lymph to lymph nodes = more cells + proteins in tissues
- increased effector response in tissues

83
Q

Where are eosinophils found?

A

Located in the tissues and recruited to allergic reaction site

Express FcεRI upon activation

84
Q

What are the 2 effector functions of eosinophils?

A
  1. Release toxic granule proteins + free radicals to kill microorganisms / parasites and cause tissue damage
  2. Synthesise + release prostaglandins, leukotrienes and cytokines to amplify inflammatory response - activate epithelial cells + recruit leukocytes
85
Q

What does ate phase allergic response depend upon?

A

Late-phase reaction is dependent on allergen dose

Continued synthesis and release of inflammatory mediators

Immunology (14 decks)

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