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Hypersensitivity Flashcards

1
Q

What is inflammation?

A

an immune response aimed at eliminating the inciting cause

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2
Q

What are the possible inciting causes?

A

invading microorganisms, particulate materials (allergens, prostheses), altered self cells (growth disorders, cell injury), transformed malignant cells (neoplasia)

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3
Q

Hypersensitivity definition

A

a state of altered reactivity in which the body reacts with an immune response to a foreign agent (e.g. allergen)

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4
Q

Allergen definition

A

an antigen (protein) that causes an allergic reaction

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5
Q

What hypersensitivity classification are allergic reactions?

A

type I hypersensitivity

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6
Q

Where are allergens found?

A

airborne (e.g. pollen or dust), food, medication

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7
Q

What is the difference between a food allergy and an intolerance?

A

a food allergy is a hypersensitivity reaction involving the immune system whereas a food intolerance disrupts the digestive system

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8
Q

Examples of allergies that must be considered for dental treatments

A

latex, anaesthetics, antibiotics, metals

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9
Q

What is the name of the system used to classify hypersensitivity reactions?

A

Gell and Coombs’s classification

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10
Q

What molecules can cause type I hypersensitivity (allergies)?

A

allergens or haptens

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11
Q

Haptens definition

A

small (non-protein) molecules that can be recognised by a specific antibody but cannot elicit an immune response

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12
Q

How would haptens be able to cause an immune response?

A

If haptens are chemically linked to a protein molecule (carrier)

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13
Q

Example of a hapten

A

Antibiotic (can bind to proteins in body to cause immune response - results in inflammation against hapten and carrier)

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14
Q

Which is the most common type of hypersensitivity?

A

type I hypersensitivity

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15
Q

Which antibody mediates type I hypersensitivity?

A

IgE antibody

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16
Q

Which cell produces antibodies?

A

plasma cells (B cells)

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17
Q

What is the action of IgE in type I hypersensitivity reactions?

A

IgE (constant region) binds to receptors on mast cells and basophils. When the antigen binds to IgE this induces degranulation.

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18
Q

Which receptor on mast cells do IgE antibodies bind to?

A

Fc receptors

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19
Q

Which receptor on basophils do IgE antibodies bind to?

A

CD63

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20
Q

Which immune cells are involved in type I hypersensitivity reactions?

A

mast cells, basophils, eosinophils

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21
Q

How is IgE produced in type I hypersensitivity reactions?

A

Allergens (or haptens) are recognised by PRRs on innate immune cells. Antigen presentation activates the adaptive immune system via MHCII-TCR interactions which results in differentiation into TH2 cells. TH2 cells activate B cells to differentiate into plasma cells which produce IgM before class switching to IgE in the first exposure to the allergen.

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22
Q

Examples of Pattern Recognition Receptors on innate immune cells that recognise allergens (or haptens bound to proteins)

A

TLRs, Protease-activated receptors (PARs)

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23
Q

What happens in the second exposure to the allergen?

A

IgE recognises the allergen and binds rapidly causing immediate degranulation of immune cells to release histamine.

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24
Q

What is the effect of histamine?

A

vasodilation, increased vascular permeability, smooth muscle constriction / bronchoconstriction, neurotransmission

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25
What is the cause of the itching sensation in allergies?
the release of the soluble mediator, histamine, by degranulation of mast cells and basophils can cause neurotransmission
26
Examples of type I hypersensitivity reactions
asthma, hay fever, anaphylaxis, atopic dermatitis (eczema)
27
What is the scientific name for eczema?
atopic dermatitis
28
Which allergens cause asthma?
dust mites, mold (environmental fungi)
29
Which allergen causes hay fever?
pollen
30
Examples of food allergens
peanuts, shellfish, wheat, dairy
31
Which allergens cause eczema?
anything - airborne particles
32
What is the name of the most severe allergic reactions?
anaphylaxis
33
Anaphylaxis definition
systemic allergic reaction that affects multiple tissues/organs
34
Why is inflammation amplified during anaphylaxis?
due to excessive degranulation
35
Which plasma factor system plays a prominent role in anaphylaxis?
complement cascade
36
Which pathways of complement do allergens activate?
classical pathway (indirectly) or alternative pathway
37
What is the action of the complement cascade in anaphylaxis?
production of complement proteins e.g. anaphylatoxins which drive excessive inflammation
38
What is the effect of anaphylaxis on the respiratory system?
bronchoconstriction, excess mucous production
39
What are the 2 types of inflammatory responses?
TH1 (targets microorganisms) and TH2 (targets allergens and parasites)
40
What does the TH1 inflammatory response target?
targets microorganisms e.g. bacteria, fungi, virus
41
What does the TH2 inflammatory response target?
targets allergens and parasites
42
Which type of inflammatory response takes over in allergy patients?
TH2
43
What are the different aetiologies of allergies?
genetic susceptibility and environmental factors
44
Example of a genetic susceptibility that increases risk of allergy development
mutation in filaggrin (structural protein) impairs skin barrier (eczema)
45
What environmental factors can cause allergies?
hygiene hypothesis and pollution/climate change
46
How can the hygiene hypothesis influence risk of allergy development?
by exposing a child to allergen at an early age, the immune system won't see the allergen as a threat and skews towards a TH1 response
47
How can pollution influence risk of allergy development?
rural areas have fewer pollutants therefore reduced risk of allergy development (doesn't align with hygiene hypothesis)
48
What are the 2 options of sequalae for allergies?
drugs or immunological treatment
49
What are the 3 types of drugs that can be used to reverse the action of histamine?
anti-histamines, hydrocortisone, epinephrine
50
How do anti-histamines treat allergies?
they are histamine receptor antagonists (blocks receptor on target cells)
51
How does hydrocortisone treat allergies?
by blocking histamine synthesis
52
How does epinephrine treat allergies?
by reversing the effects of granules leading to vasoconstriction and muscle relaxation (e.g. bronchodilation)
53
What immunological treatments may be undertaken to target a particular allergen?
hypo/de - sensitisation (injections of allergen) or potential class switching from IgE to IgG production
54
How many class switching from IgE to IgG reduce type I hypersensivity reactions?
IgE targets allergens while IgG targets microorganisms
55
Which soluble mediators drive type I hypersensitivity reactions (allergies)?
histamine and anaphylatoxins (complement proteins)
56
Outline of type II hypersensitivity
Involves the tagging of cells with IgG/IgM antibodies for removal (cytotoxicity)
57
Which antibodies are involved in type II hypersensitivity reactions?
IgG and IgM
58
Which plasma factor system is involved in type II hypersensitivity reactions?
complement system (causes lysis by membrane attack complex)
59
Which immune cells are involved in type II hyper sensitivity reactions?
complement and cytotoxic cells (NK cells and CD8+ T cells)
60
What do the IgG and IgM antibodies bind to in type II hypersensitivity reactions?
antigen usually bound to a host cell (self-antigen or allergen)
61
How is the target cell lysed in type II hypersensitivity reactions?
membrane attack complex formation via complement or antibody dependent cellular cytotoxicity via NK cells or CD8+ T cells
62
Two examples of type II hypersensitivity reactions
transfusion of mismatched blood types and autoimmune haemolytic anaemia
63
What happens when a type B patient is mistakenly given type A blood?
Type B patient expresses anti-A antibodies which bind to the type A RBCs, tagging them for cellular cytotoxicity via complement, NK cells and CD8+ T cells
64
What happens in autoimmune haemolytic anaemia?
IgG and IgM antibodies tag own erythrocytes for removal by cellular cytotoxicity
65
Which antibodies mediate type III hypersensitivity reactions?
IgG and IgM (same as type II hypersensitivity)
66
What do IgM / IgG antibodies bind to in type III hypersensitivity reactions?
soluble antigens (or allergens) circulating in blood (not attached to host cells unlike type II)
67
68
What happens in type III hypersensitivity reactions?
IgG/IgM antibodies bind to antigens forming antibody-antigen immune complexes which are deposited in blood vessel walls and tissues driving inflammation
69
How do type III hypersensitivity reactions cause damage?
the immune complexes embedded in the endothelium activates complement and attracts neutrophils which release enzymes that damage endothelial cells
70
Examples of type III hypersensitivity reactions?
systemic lupus erythematosus, rheumatoid arthritis, Sjogren's syndrome, oral erythema multiforme (all autoimmune diseases)
71
What is the name of the autoimmune disease in which the antibody-antigen immune complexes are deposited in the skin?
Lupus
72
What is the name of the autoimmune disease in which the antibody-antigen immune complexes are deposited in the joints?
rheumatoid arthritis
73
What is the name of the autoimmune disease in which the antibody-antigen immune complexes are deposited in the lips?
oral erythema multiforme
74
Which type of hypersensitivity reaction does not involve antibodies?
Type IV hypersensitivity reactions
75
What type of hypersensitivity reaction is IgE mediated?
type I
76
What type of hypersensitivity reaction involves cytotoxic responses?
type II
77
What type of hypersensitivity reaction involves an immune complex response?
type III
78
What type of hypersensitivity reaction is cell mediated?
Type IV (no Ig)
79
Why do type IV hypersensitivity reactions have a delayed response?
due to recruitment of T cells
80
81
What happens during type IV hypersensitivity reactions?
there is a localised T cell reaction at the site of antigen exposure
82
Which immune cells are involved in type IV hypersensitivity reactions?
CD4+ and CD8+ T cells and macrophages
83
How do CD4+ T cells cause damage in type IV hypersensitivity reactions?
CD4+ T cells differentiate into T helper cells that release cytokines to activate macrophages
84
How do CD8+ T cells cause damage in type IV hypersensitivity reactions?
direct damage via cytotoxicity
85
Examples of type IV hypersensitivity reactions
contact dermatitis and orofacial granulomatosis
86
What is contact dermatitis?
A skin rash that arises from encountering an allergen
87
What causes contact dermatitis?
usually environmental factors such as allergens or irritants
88
What is the difference between contact dermatitis and atopic dermatitis?
Contact dermatitis is type IV / delayed whereas atopic dermatitis is type I and occurs rapidly (allergens)
89
What happens in contact dermatitis?
APCs take up allergens in the skin and either migrate to lymph nodes for antigen presentation via MHCII to trigger CD4+ T cell differentiation into TH1 cells which activate macrophages OR APCs remain at skin barrier and undergo MHCI (all nucleated cells) presentation to CD8+ T cells resulting in cytotoxicity. Both pathways lead to inflammation
90
What is orofacial granulomatosis also known as?
oral Crohn's (similar morphology to Crohn's disease)
91
What is the clinical presentation of orofacial granulomatosis?
formation of granulomas in the soft tissue of the oral mucosa
92
Which cells are present in the granulomas of orofacial granulomatosis?
epithelioid macrophages, giant cells, M1 macrophages (pro-inflammatory), CD4+ and CD8+ T cells
93
How are giant cells formed?
by the fusion of epithelioid macrophages
94
What is the aetiology of orofacial granulomatosis?
unknown - particular allergen

BDS1 (105 decks)

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