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Yr 2 MCD - Immuno > 1 - Hypersensitivity and Allergy > Flashcards

1 - Hypersensitivity and Allergy Flashcards

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1
Q

When do appropriate immune responses occur?

A

Appropriate immune responses occur to foreign harmful agents such as:

  • viruses
  • bacteria
  • fungi
  • parasites

Required to eliminate pathogens

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

Involves antigen recognition by cells of the immune system and antibody production

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2
Q

When do hypersensitivity reactions occur?

A

Hypersensitivity Reactions occur when immune responses are mounted against:

  • Harmless foreign antigens
    • allergy
    • contact hypersensitivity
  • Autoantigens (self antigens)
    • autoimmune diseases
  • Alloantigens (foreign antigens)
    • serum sickness
    • transfusion reactions
    • graft rejection
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3
Q

How are hypersensitivity reactions classified?

A

Classified by Gell & Coombs:-

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

Each involves distinct parts of the immune system reacting

NOTE: many diseases involve a mixture of types

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4
Q

What hypersensitivity conditions are classified as Type 1?

A

Anaphylaxis

Asthma

Rhinitis

  • Seasonal
  • Perennial (year-round)

Food Allergy

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5
Q

What events lead to a Type 1 hypersensitivity reaction?

A

STEP 1: PRIMARY Antigen Exposure

  • Sensitisation not tolerance
  • In allergy, you develop sensitisation
  • If no allergy, you develop tolerance
  • IgE antibody production
  • IgE binds to Mast Cells & Basophils

STEP 2: SECONDARY Antigen Exposure

  • More IgE Ab produced
  • Antigen cross-links IgE on Mast Cells/Basophils
  • Degranulation
  • Allergic reaction ensues
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6
Q

What does the clinical presentation of Type 2 hypersensitivity depend on?

A

Clinical presentation depends on target tissue

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7
Q

What conditions are classified as Type 2 hypersensitivity?

A

Organ-specific autoimmune diseases

  • 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)

Autoimmune cytopenias (Ab mediated blood cell destruction)

  • Haemolytic anaemia
  • Thrombocytopenia
  • Neutropenia
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8
Q

How do you test for Type 2 hypersensitivity?

A

Type 2 = Antibody-Dependent Hypersensitivity

Test for specific autoantibodies

  • Immunofluorescence
  • ELISA e.g. anti-CCP (Cyclic Citrullinated Peptide Abs for Rheumatoid Arthritis)
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9
Q

What is Type 3 Hypersensitivity?

A

TYPE 3 = Immune Complex Mediated Hypersensitivity

  • Formation of Antigen-Antibody complexes (immune complexes) in blood
  • Complex deposition in blood vessels/tissue
  • Complement & cell activation in site where complexes have been deposited
  • Activation of other cascades egclotting
  • Tissue damage (vasculitis)
    • Systemic lupus erythematosus (SLE)
    • Vasculitides (Poly Arthritis Nodosum, many different types)
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10
Q

In what conditions do you get Type 4 Hypersensitivity responses?

A

TYPE 4 = DELAYED HYPERSENSITIVITY RESPONSES

Th1 Mediated

  • Chronic graft rejection
  • GVHD
  • Coeliac disease
  • Contact hypersensitivity (on the skin)
  • Many autoimmune diseases….

Th2 Mediated

  • Asthma
  • Rhinitis
  • Eczema
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11
Q

What is the mechanism behind Type 4 Hypersensitvity responses?

A

THREE MAIN VARIETIES OF THESE RESPONSES

  • Th1
  • Cytotoxic
  • Th2

MECHANISMS

Th1 Mechanism

Antigen taking up by Antigen-Presenting Cell

Presented to Th1 cell

Produces lots of IFN-γ

This leads to:

  1. Macrophage activation and then TNF production
  2. Activates fibroblasts, leading to angiogenesis and fibrosis
  3. Leads to IL-2 production which activates CTLs which produce proteins perforin which kills cells

General Mechanism

Transient/Persistent Ag

T cell activation of macrophages, CTLs

Much of tissue damage dependent upon TNF and CTLs

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12
Q

What is Type 4 Hypersensitivity?

A

Delayed Hypersensitivity Responses

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13
Q

Give an example of a Type 4 Delayed-Type Cell-Mediated Hypersensitivity response

A

Nickel

  • Contact Hypersensitivity
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14
Q

Summarise the different forms of hypersensitivity reactions

A
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15
Q

What are the features of inflammation?

A

IMMUNE CELL

  • recruitment to sites of injury/infection
  • activation

INFLAMMATORY MEDIATORS

  • complement
  • cytokines
  • etc.

Features of Inflammation

Vasodilatation (increased blood flow)

Increased vascular permeability

Inflammatory mediators and cytokines

Inflammatory cells and tissue damage

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16
Q

What are the signs of inflammation?

A

Redness

Heat

Swelling

Pain

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17
Q

What occurs in inflammation?

A

Immune cell recruitment to sites of injury and/or infection

Immune cell activation

Inflammatory mediators also have a role e.g. complement, cytokines etc.

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18
Q

What cytokines are pro-inflammatory?

A
  • IL-1
  • IL-6
  • IL-2
  • TNF
  • IFN-γ
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19
Q

What chemokines are involved in attracting inflammatory cells?

A
  • IL-8/CXCL8
  • IP-10/CXCL10
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20
Q

What caused increased vascular permeability in inflammation?

A

Caused by:

  • C3a
  • C5a
  • Histamine
  • Leukotrienes
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21
Q

By what mechanisms do inflammatory cells infilitrate tissues?

A

Cell Trafficking (Chemotaxis)

  • Neutrophils
  • Macrophages
  • Lymphocytes
  • Mast Cells

Cell Activation

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22
Q

List some common allergens

A

Animal fur

Pollen

House dust mites

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23
Q

What is atopic?

A

Denoting a form of allergy in which a hypersensitivity reaction such as eczema or asthma may occur in a part of the body not in contact with the allergen.

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24
Q

Outline the prevalence of atopy in UK

A

Prevalence of atopy is 50% in young adults in UK

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25
Explain how the severity of atopy can differ
**SEVERITY CAN VARY** Mild * e.g. occasional symptoms Severe * e.g. chronic asthma Life-Threatening * e.g. life threatening anaphylaxis
26
What are the overall risk factors for allergy?
Genetic Environmental
27
Outline genetic risk factors that can cause allergies
80% of atopics have a family history Polygenic * 50-100 genes liked to ashtma/atopy * genes of IL-4 gene cluster (chromosome 5) linked to raised IgE, asthma, atopy * genes on chromosome 11q (IgE receptor) linked to atopy and asthma * genes liked to structural cells linked to eczema (flaggrin) and asthma (IL-33, ORMDL3, CDHR3)
28
Outline environmental risk factors that can cause allergies
**AGE** * increases from infancy * rare in infancy * peaks in teens * reduces in adulthood **GENDER** * asthma more common in males in childhood and females in adults **FAMILY SIZE** * more common in small families * only child has higher risk of allergy/asthma **INFECTIONS** * early life infections are protective **ANIMALS** * early exposure is protective * children that grow up on farms have very low incidence of allergies **DIET** * breast-feeding = protective * anti-oxidants = protective * fatty acids = protective
29
What is happening to the prevalence of allergies in the UK?
Allergies are increasing in the UK * asthma, hayfever and eczema have all increased * believed to be due to environmental changes * especially, decreased infectious disease incidence
30
What are the types of inflammation in allergy?
Anaphylaxis/Urticaria/Angioedema * type 1 hypersensitivity (IgE mediated) Idiopathic/Chronic Urticaria * type 2 hypersensitivity (IgG mediated) Asthma/Rhinitis/Eczema * mixed inflammation * type 1 hypersensitivity (IgE mediated) * type 4 hypersensitivity (chronic inflammation)
31
What does expression of atopy require?
* 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) _DIAGRAM:_ Lumen of the airway depicted Smooth muscle cells lining airway Dendritic cells just under surface of epithelium * Sample allergens using their processes * Process allergen * Present peptides from allergen Presented to naive T cells Tolerance: Becomes Treg cell Autoimmunity: Th1 response Allergy (Sensitisation): Th2 response _Th2 response (Allergy)_ Th2 cells proliferate Cytokines IL-4 and IL-13 These cytokines tell B cells to produce IgE instead of IgG IgE is specific to the peptide allergen IgE binds to plasma cells More IgE producion _Subsequent Exposure_ IgE already being produced and present on mast cells Intake of allergen Allergen peptide presented by dendritic cells T cells become Th2 More IL-4 and IL-13 More IgE IL-5 also produced which leads to eosinophil recruitment and activation Eosinophils produce mediators of inflammation This combines with mast cell response which is degranulation and inflammatory mediator recruitment Expression of allergic disease SENSITISATION NOT TOLERANCE
32
What are eosinophils?
0-5% of blood leukocytes Present in blood, most reside in tissues Recruited during allergic inflammation Generated from bone marrow Nucleus * two lobes Contain large granules * toxic proteins Lead to tissue damage
33
What are mast cells?
Tissue resident cells IgE receptors on cell surface Crosslinking of IgEs leads to: Multiple granules in cytoplasm * Mediator release * Pre-formed: * histamine * cytokines * toxic proteins * Newly synthesized: * leukotrienes * prostaglandins
34
What are neutrophils?
Important especially in: * virus induced asthma * severe asthma * atopic eczema 55-70% of blood leukocytes Polymorphonuclearcells (PMNs) * nucleus contains several lobes Granules contain * digestive enzymes Also synthesize * oxidant radicals * cytokines * leukotrienes
35
What is the immunopathogenesis of asthma?
**Acute inflammation of the airways** 1. Mast Cell Activation and Degranulation * Pre-stored mediators * histamine * Newly synthesised mediators * prostaglandins * leukotrienes * Acute airway narrowing * Airway wall oedema
36
Outline the two-phase response to single allergen challenge
Initially, PEF is still lower than average due to pre-exisiting condition (e.g. asthma) Pathogen inhalation Acute rapid response due to: * Mast cell activation * Degranulation * Mediators: * Prostaglandins * Histamine * Leukotrienes * These cause airway narrowing due to: * Mucus * Smooth muscle * Oedema This recovers fairly rapidly within an hour Then there's another late response without inhalation of the allergen as a cell-mediated response * Lymphocyte driven inflammation * Eosinophil driven inflammation Occurs 2-8 hours after a single large-dose inhalation
37
What are the important clinical features of asthma?
Reversible generalised airway obstruction * chronic episodic wheeze Bronchial hyperresponsiveness * bronchial irritability Cough Mucus production Breathlessness Chest tightness Response to treatment Spontaneous variation * due to variation in allergen exposure Reduced and variable peak flow (PEF)
38
Outline the daily PEF of a person with poorly controllled asthma
Use inhaler in order to increase PEF Exercise decreases PEF PEF decreases during sleep normally due to house dust-mites
39
What can cause allergic rhinitis?
**SEASONAL** * ​​hay-fever (grass, tree pollens) **PERENNIAL (year-round)** * perennial allergic rhinitis (HDM, pets)
40
What are the symptoms of allergic rhinitis?
Sneezing Rhinorrhoea Itchy nose Itchy eyes Nasal blockage Sinusitis Loss of smell/taste
41
What is allergic eczema?
Chronic itchy skin rash * Common in flexures of arms and legs House dust-mite sensitisation * HDMs can enter dry cracked skin so this makes it worse * 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
42
What percentage of allergic eczema cases are cleared by the age of 7 and what percentage by adulthood?
50% cleared by 7 years old 90% cleared by adulthood
43
What forms of food allergy most commonly affect infants and children/adults?
**INFANTS (3 YEARS)** * eggs * cows milk **CHILDREN/ADULTS** * peanuts * nuts * shell-fish * fruits * cereals * soya
44
What are the symptoms of mild food allergies?
Itchy lips Mouth Angiodema Urticaria (generalised all over body)
45
What are the symptoms of severe food allergies?
Nausea Abdominal Pain Diarrhoea Collapse Wheeze Anaphylaxis
46
What is anaphylaxis?
Severe generalised allergic reaction Uncommon Potentially fatal
47
What causes anaphylaxis biologically?
Generalised degranulation of IgE sensitised mast cells
48
What are the symptoms of anaphylaxis?
Itchiness around: * mouth * pharynx * lips Swelling of: * lips * throat * other parts of body Wheeze Chest tightness Dyspnoea Faintness Collapse Diarrhoea Vomiting Death (if severe and untreated)
49
What is the effect of anaphylaxis on different body systems?
**CARDIOVASCULAR** * vasodilatation * cardiovascular collapse **RESPIRATORY** * bronchospasm * laryngeal oedema **SKIN** * vasodilatation * erythema * urticaria * angioedema **GI** * vomiting * diarrhoea
50
How are allergies investigated and diagnosed?
Careful history is essential Skin-prick testing * Wheel of 3mm is diagnostic of allergy * Flare surrounds the wheel RAST (blood specific IgE): * Total IgE - not very specific * Lung function (asthma)
51
How do you treat anaphylaxis?
**EMERGENCY TREATMENT** ​EpiPen and Anaphylaxis Kit * antihistamine * steroid * adrenaline (epinephrine) Then seek immediated medical aid
52
How do you prevent anaphylaxis?
Avoidance of known allergen Always carry a kit and EpiPen Inform immediate family and caregivers Wear a MedicAlert bracelet
53
How do you treat rhinitis and eczema?
**ALLERGIC RHINITIS** * anti-histamines (sneezing, itching, rhinorrhea) * nasal steroid spray (nasal blockage) * cromoglycate (children, eyes) **ECZEMA** * emollients (keep skin barrier healthy without cracking so HDMs can't enter) * topical steroid cream **IF SEVERE:** * anti-IgE * anti-IL-4 * anti-IL-13 * anti-IL-5 mAb These are very effective, however they are also very expensive. Therefore, they are restricted to severe disease.
54
Outline asthma treatment
**STEP 1** Use short-acting β2 agonist drugs as required by inhalation * Salbutamol **STEP 2** Inhaled steroid low-moderate dose * Beclomethasone/Budesonide (50-800μg per day) * Flucticasone (50-400μg per day) **STEP 3** Add further therapy * Long-acting bronchodilators, leukotriene antagonist * High dose inhaled steroids - up to 2mg per day via a spacer **STEP 4** Add course of oral steroids, SLIT, azithromycin * Prednisolone - 30mg daily for 7-14 days * Anti-IgE, Anti-IL-5, Anti-IL-4/-13 monoclonal Abs
55
What is immunotherapy effective for?
Effective for single antigen hypersensitivities * Venom allergy - bee or wasp stings * Pollens * HDM This is done via subcutenous injection Build it up from low dose to high dose Helps to build tolerance Need to do the subcutaneous version it for 3 years to build good tolerance Antigen used is purified
56
What is SCIT?
Subcutaneous Immunotherapy (SCIT) * 3 years needed * weekly/monthly 2 hour clinic visits * still relatively expensive
57
What is SLIT?
Sublingual Immunotherapy (SLIT) * Can be taken at home * 3 years needed
58
When does appropriate immune tolerance occur?
Appropriate immune tolerance occurs to self, and to foreign harmless proteins: * food * pollens * other plant proteins * animal proteins * commensal bacteria 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
59
What kinds of responses would someone with asthma undergo daily?
Mixture of early Type 1 response and ongoing late, cell-mediated response at the same time
60
What are the features of asthma?
**Chronic inflammation of the airways** Cellular infiltrate * Th2 lymphocytes, eosinophils Smooth muscle hypertrophy Mucus plugging Epithelial shedding Sub-epithelial fibrosis This is all in addition to ongoing acute inflammation features
61
What is rhinorrhea?
Runny nose Nasal cavities filled with mucus

Yr 2 MCD - Immuno (5 decks)

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