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Immunology year 2 > Hypersensitivity and allergy > Flashcards

Hypersensitivity and allergy Flashcards

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1
Q

How many of YOU have allergic sensitisation (atopy)?

A

50% of university students

However, only 30% will experience symptoms.

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2
Q

When do appropriate immune responses occur and what is the end result

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

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3
Q

What do appropriate immune responses depend on

A

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

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4
Q

What is the function of the immune system most of the time

A

Tolerance

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5
Q

Describe appropriate immune tolerance

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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6
Q

What does immune tolerance involve

A

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

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7
Q

How does the immune system know whether to tolerate or respond to an antigen

A

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

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8
Q

Ultimately, when do hypersensitivity reactions occur

A

Hypersensitivity Reactions occur when immune responses are mounted against
Harmless foreign antigens (allergy, contact hypersensitivity) i.e innocuous antigens- they would cause no damage themselves- but inappropriate immune activation leads to damage.
Autoantigens (autoimmune diseases)
Alloantigens (serum sickness, transfusion reactions, graft rejection)

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9
Q

State the Gel and Coombs classification for hypersensitivity reactions

A 
Classified by Gell & Coombs:-
Type I   : Immediate Hypersensitivity
Type II  : Antibody-dependent Cytotoxicity
Type III : Immune Complex Mediated
Type IV : Delayed Cell Mediated

Note: many diseases involve a mixture of types

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10
Q

Give an example of an all-antigen

A

Allo-antigens are antigens present in only SOME individuals (i.e. ABO blood groups).

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11
Q

Give some examples of type 1 hypersensitivity

A 
Anaphylaxis
Asthma
Rhinitis
Seasonal
Perennial
Food Allergy
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12
Q

Define atopy and allergy

A

The immunologic definition of atopy is an immediate hypersensitivity reaction to environmental antigens mediated by IgE. Such reactions tend to run in families; these families are said to have inherited the atopy trait. Although the term allergy was originally defined as any altered reactivity to exogenous antigens, it is now often used synonymously with atopy. In this and most texts, allergy is defined as immediate hypersensitivity mediated by IgE.

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13
Q

Describe the pathogenesis of type 1 immediate hypersensitivity

A

10 Antigen exposure
Sensitisation not tolerance
IgE antibody production
IgE binds to Mast Cells & Basophils

20 Antigen Exposure
More IgE Ab produced
Antigen cross-links IgE on Mast Cells/Basophils
Degranulation

Degranulation leads to release of prostalgnaldins, leukotrienes, histamines (airways) which leads to the inflammation, reduction in BP and airway obstruction seen in anaphylaxis.

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14
Q

Describe how the presentation of type 2 antibody-dependent hypersensitivity depends on the target tissue

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)
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15
Q

Describe the autoimmune cytopenias associated with type 2 hypersensitivity reactions

A

Autoimmune cytopenias (Ab mediated blood cell destruction)
Haemolytic anaemia
Thrombocytopenia
Neutropenia

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16
Q

Describe how we can test for specific autoantibodies in type 2 hypersensitivity reactions

A

Test for specific autoantibodies
Immunofluorescence
ELISA eg anti-CCP (Cyclic Citrullinated Peptide Abs for Rheumatoid Arthritis)

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17
Q

What are the key features of immune-mediated hypersensitivity (type 3)

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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18
Q

State some common examples of type 3 hypersensitivity reactions

A

Systemic lupus erythematosus (SLE)

Vasculitides (Poly Arteritis Nodosum, many different types)

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19
Q

Where is vasculitis common in type 3 hypersensitivity

A 
Vasculitis:
Renal (glomerulonephritis) 
Skin
Joints
Lung

Immune complex deposits in blood vessels in these regions- leading to complement activation, recruitment of monocytes and neutrophils — inflammation

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20
Q

What are the Th1 mediated type 4 delayed type hypersensitivity reactions

A 
Chronic graft rejection
GVHD
Coeliac disease
Contact hypersensitivity
Many autoimmune diseases….
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21
Q

What are the Th2 mediated type 4 hypersesensitivity reactions

A

Asthma
Rhinitis
Eczema

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22
Q

What are the different types of Type 4 hypersensitivity reactions

A

Th1
Cytotoxic
Th2

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23
Q

Summarise the mechanisms of type 4 hypersensitivity

A

Transient/Persistent Ag
T cell activation of macrophages, CTLs
Much of tissue damage dependent upon TNF & CTLs

APC presents antigen to Th1 cell
Th1 releases IL-2 to activate CTLs which release perforin to kill cells
Th1 also releases IFN-y to activate macrophages, which releases TNF to kill cells
In chronic reactions- Th1 will also release FGF to activate fibroblasts, which leads to angiogenesis and fibrosis.

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24
Q

Describe a common example of cell-mediated type 4 hypersensitivity

A

Nickel

Contact Hypersensitivity

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25
What is a common feature of the hypersensitivity reactions
Common Feature – inflammation Immune cell recruitment to sites of injury and/or infection activation Inflammatory mediators – complement, cytokines, etc
26
What are the key features of inflammation
Vasodilatation, increased blood flow Increased vascular permeability Inflammatory mediators & cytokines Inflammatory cells & tissue damage
27
What are the key signs of inflammation
Redness Heat Swelling Pain
28
What are the key mediators of inflammation
Increased vascular permeability Caused by:- C3a, C5a, histamine, leukotrienes Cytokines IL-1, IL-6, IL-2, TNF, IFN-γ Chemokines IL-8/CXCL8 (neutrophils), IP-10/CXCL10 (lymphocytes) Inflammatory cell infiltrate Cell trafficking – chemotaxis Neutrophils, macrophages, lymphocytes, mast cells Cell activation
29
Summarise allergy
``` Common - prevalence of atopy is 50% in young adults in UK Severity varies - mild occasional symptoms severe chronic asthma life threatening anaphylaxis Risk factors - genetic and environmental ```
30
Describe the genetic risk factors for allergy
~80% of atopics have a family history Polygenic 50-100 genes linked to asthma/atopy genes of IL-4, 5, 13 gene cluster (chromosome 5) linked to raised IgE, asthma, atopy genes on chromosome 11q (IgE receptor) linked to atopy and asthma genes linked to structural cells linked to eczema (filaggrin) and asthma (IL-33, ORMDL3, CDHR3)
31
Describe the environmental risk factors for allergy
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
32
What is happening to the prevalence in allergies in the UK
Increasing yearly | Indicates change in environment playing a major role- genetic won't have had time to influence change in suceptibility
33
Summarise the different types of inflammation in allergy
Anaphylaxis, urticaria, angioedema type I hypersensitivity (IgE mediated) Idiopathic/chronic urticaria type II hypersensitivity (IgG mediated) Asthma, rhinitis, eczema: mixed inflammation type I hypersensitivity (IgE mediated) type IV hypersensitivity (chronic inflammation)
34
What is key for the expression of allergic disease
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)
35
Describe sensitisation in allergic airway disease
Allergen comes into contact with the ciliated epithelium of the lungs Dendritic cell underling the epithelium process the allergen and presents it to CD4+ T cells Instead of differentiating into T-reg, which would induce tolerance, they differentiate into Th2 Th2 activate B cell proliferation and differentiation (via IL-4 and IL-13) into plasma cells which synthesise and release IgE (switch from IgG)
36
Describe what happens upon second exposure to the antigen in allergic airway disease
In second exposure, the allergens are presented by APCs to memory Th2 cells, which then release IL-5, which causes eosinophil degranulation Th2 cells also release IL-4 and IL-13, which stimulate production of IgE by plasma cells The antigens crosslink the IgE on the surface of mast cells causing degranulation Eosinophils and mast cells release the mediators of inflammation
37
Summarise the key features of 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 Treatments that prevent the activation of eosinophils effective at treating allergic diseases
38
Summarise the key features of mast cells
Tissue resident cells IgE receptors on cell surface ``` Crosslinking of IgEs leads to Mediator release Pre-formed histamine cytokines toxic proteins Newly synthesized leukotrienes prostaglandins ```
39
Summarise neutrophils
Important in virus induced asthma severe asthma atopic eczema 55-70% of blood leukocytes Polymorphonuclear cells (PMNs) nucleus contains several lobes Granules contain digestive enzymes Also synthesize oxidant radicals cytokines leukotrienes
40
Summarise the acute phase of the immunopathogenesis of asthma
Acute inflammation of the airways mast cell activation & degranulation Pre stored mediators histamine Newly synthesised mediators prostaglandins, leukotrienes acute airway narrowing due to : smooth muscle contraction - leukotrienes mucus secretion -leukotrienes vascular leakage and thus airway wall oedema all these obstruct the lumen of the airways -- bronchoconstriction
41
Describe the two phase response to the single allergen challenge
Asthmatic Baseline- PEF already slightly low due to tonic bronchoconstriction Inhale allergen (e.g dust) - early response- acute and dramatic decrease in PEF- due to mast cell degranulation Then get a late response a couple of hours later- due to cellular response- Type 4- eosinophils, lymphocytes, neutrophils etc -- constantly inhaling allergen- so risk always present to some degree
42
Summarise the immunopathogensis of the late phase of asthma
``` Chronic inflammation of the airways Cellular infiltrate Th2 lymphocytes, eosinophils Smooth muscle hypertrophy Mucus plugging Epithelial shedding Sub epithelial fibrosis ``` Mediators released by eosinophils include peroxidase, eosinophil major basic protein, and cationic protein, which all cause direct damage to bronchial tissue. As a result of the chronic allergic inflammation, the bronchial smooth muscle is hypertrophic, and mucus secretion is increased; airflow becomes persistently, rather than intermittently, reduced.
43
Summarise the key 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 Reduced & variable peak flow (PEF) Reversible and episodic nature important in diagnosis
44
When may an asthmatic take their reliever inhaler
Upon symptoms- don't prevent attacks- just treats them as they occur
45
What are the two different types of allergic rhinitis
Seasonal - hay fever - grass, tree pollens Perennial - perennial allergic rhinitis HDM, pets
46
What are the symptoms of allergic rhinitis
``` Symptoms sneezing rhinorrhoea itchy nose, eyes nasal blockage, sinusitis, loss of smell/taste ``` In severe cases- may have nasal polyps
47
Describe the key features of allergic eczema
``` 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 ```
48
Summarise the difference in food allergies between adults and infants
Infancy-3yrs egg, cows milk Children/adults peanut, nuts, shell fish, fruits, cereals, soya
49
Describe the different reaction types to food allergies
Mild Itchy lips, mouth, angioedema, urticaria Severe Nausea, abdominal pain, diarrhoea, collapse, wheeze Anaphylaxis Collapse- due to vasodilation- loss of blood pressure
50
Essentially, what is meant by anaphylaxis
Anaphylaxis: severe generalised allergic reaction Uncommon, potentially fatal Generalised degranulation of IgE sensitised mast cells
51
Describe the symptoms of anaphylaxis
``` Symptoms: 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 ```
52
Describe the different systems involved in anaphylaxis
Systems: Cardiovascular - vasodilatation, cardiovascular collapse Respiratory - bronchospasm, laryngeal oedema Skin - vasodilatation, erythema, urticaria, angioedema GI - vomiting, diarrhoea- due to vascular leakage and oedema of G.I tract
53
Describe the different investigations used in the diagnosis of anaphylaxis
``` Careful history essential Skin prick testing RAST (blood specific IgE): Total IgE Lung function (asthma) ``` RAST= • RAST (radioallergosorbent test) – tests the amount of specific IgE antibodies in the blood Place allergen on membrane- place sample of patient's blood on membrane- radioisotope will bind to IgE bound to the allergen.
54
Describe the emergency treatment of anaphylaxis
Emergency Treatment EpiPen & Anaphylaxis kit antihistamine, steroid, adrenaline Seek immediate medical aid
55
Describe the prevention of anaphylaxis
``` Prevention Avoidance of known allergen Always carry a kit & EpiPen Inform immediate family & caregivers Wear a MedicAlert® bracelet ```
56
Summarise the treatment for allergic rhinitis
anti-histamines (sneezing, itching, rhinorrhoea) nasal steroid spray (nasal blockage)- better for perennial- anti-histamines ineffective at preventing nasal blockage cromoglycate (children, eyes)- mast cell inhibitor
57
Summarise the treatment for eczema
emollients- to thicken the skin barrier | topical steroid cream
58
generally, what can be used to treat severe hypersensitivity reactions
If severe anti-IgE, anti-IL-4/-13, anti-IL-5 mAb anti IL-5- will prevent activation and recruitment of eosinophils
59
Describe the stepwise asthma treatment
Step 1. Use short acting b2 agonist drugs as required by inhalation Salbutamol - if mild and intermittent - don't prevent Step 2. Inhaled steroid low-moderate dose Beclomethasone/budesonide (50-800mg per day) Fluticasone (50-400mg per day) used to prevent Step 3. Add further therapy Add long acting bronchodilators, leukotriene antagonist High dose inhaled steroids - up to 2mg per day via a spacer Step 4. Add courses of oral steroids, SLIT, azithromycin Prednisolone 30mg daily for 7-14 days Anti-IgE, anti-IL-5, anti-IL-4/-13 monoclonal Abs more severe as you go down
60
When is immunotherapy effective
``` Effective for single antigen hypersensitivities Venom allergy - bee or wasp stings Pollens HDM Antigen used is purified ```
61
Describe subcutaneous immunotherapy
Subcutaneous immunotherapy (SCIT) 3 years needed Weekly/monthly 2hr clinic visits designed to induce tolerance - not sensitisation done in clinic- in case of sever anaphylactic reaction
62
Describe sublingual immunotherapy
Sublingual immunotherapy (SLIT) Can be taken at home 3yrs needed
63
When does allergy occur
Allergy occurs when a damaging immune response develops to an otherwise innocuous foreign substance, the antigen involved is referred to as the allergen. Most allergic disease is produced by mixed type I and type IV hypersensitivity reactions. Type I is immediate hypersensitivity/IgE- mediated Type IV is cell mediated chronic inflammation
64
What is the difference between allergy and atopy
Atopy is the tendency to produce abnormally high IgE responses to otherwise harmless foreign environmental substances. Allergic disease is the expression of a disease caused by atopy
65
Summarise the immunopathogenesis of allergic disease
Specific IgE produced on first exposure IgE binds to Fc receptors on mast cells Re-exposure to allergen cross-links IgE with mast cell activation (synthesis of prostaglandins/leukotrienes) and degranulation (histamine and other mediators) produce vasodilation, and permeability of blood vessels with fluid entering mucosal tissues with swelling (oedema), increased mucus secretion (rhinorrhoea, sputum production), neural stimulation (cough, sneezing, itch). Chronic inflammation with lymphocyte and eosinophil activation and infiltration
66
Describe the clinical manifestation of different organs in response to allergens
nose allergic rhinitis inhaled bronchi allergic asthma inhaled blood circulation anaphylactic shock oral/mucosal contact/inhaled skin allergic eczema skin contact
67
What is allergic rhinitis often associated with
often associated with: sinusitis, otitis media, allergic conjunctivitis, asthma
68
What is the prevalence of asthma in the U.K
Asthma is common (4-20% UK population)
69
What factors can precipitate an acute asthma attack
Factors that may precipitate acute attack of asthma: Viral infectionAllergen exposureCold air / Exercise Irritants Emotional stress
70
State the common causes of anaphylaxis
Bee and wasp stings ie venom allergy Food e.g. peanut allergy, shellfish, fruits and vegetables Drug allergy e.g. penicillin Where allergen is introduced directly into the blood e.g. bee sting, the reaction can be almost instantaneous with cardiovascular collapse the predominant feature. Where the allergen is absorbed through skin or mucosa e.g. peanut allergy, the reaction may develop more slowly, but is still very rapid. Milder forms of urticaria/angioedema much more common that full anaphylaxis.
71
Describe anaphylactoid reactions
Anaphylactoid/anaphylaxis-like reactions are clinically identical to anaphylaxis but the mast cell activation is not due to IgE-mediated allergy. No prior exposure is required. A number of other mast cell triggers may operate instead e.g. complement activation by radiocontrast media, direct stimulation of mast cells by opiates, alcoholic drink constituents or food colours e.g. tartrazine. The treatment of the acute episode is the same
72
Summarise the investigations and diagnosis of allergy
Careful history is essential Immediate hypersensitivity (type I) skin prick tests very useful to confirm presence of atopy and identify possible causative allergens Specific IgE measurement (RAST) only necessary if: On antihistamines Extensive skin disease Presence of dermatographism Very young baby Previous anaphylaxis Skin test solution not available Challenge with allergen e.g. for food allergy, occupational allergy Other tests e.g. total IgE, lung function tests for asthma
73
What is the immune reactant in type 2 hypersensitivity
IgG Responds to either: cell or matrix antigen -- complement , macrophages, NK cells - -some drug allergies (penicillin) cells surface receptor -- antibody alters signalling- chronic urticaria
74
What is the immune reactant in type 3 hypersensitivity
IgG Responds to soluble antigen -- complement and phagocyte activation serum sickness, Arthur reaction
75
Describe the different types of type 4 hypersensitivity
Th1 - soluble antigen - macrophage activation - contact dermatitis, TB Th2- soluble antigen - eosinophil activation - chronic asthma and allergic rhinitis CTL - cell-associated antigen - cytotoxicity - contact dermatitis

Immunology year 2 (5 decks)

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