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Immunity and Pathology 1 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent

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2
Q

What type is allergy?

A

hypersensitivity reaction (type 1)

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3
Q

What is an allergen?

A

antigen that causes an allergic reaction

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4
Q

What is type 1 hypersensitivity and what are examples?

A

IgE mediated via mast cells and basophils

atopy, anaphylaxis

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5
Q

What is type 2 hypersensitivity and what are examples?

A

cytotoxic responses via NK cells, complement and CD8+ T cell

haemolytic anaemia

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6
Q

What is type 3 hypersensitivity and what are examples?

A

immune responses complex via complement and neutrophils

serum sickness

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7
Q

What is type 4 hypersensitivity and what are examples?

A

cell mediated responses via T cells and macrophages

sarcoidosis
tuberculous (TB)
crohns

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8
Q

If there is a genetic predisposition for allergy what is this called?

A

atopy

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9
Q

What can the allergic reaction lead to?

A

anaphylaxis

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10
Q

What can allergens be?

A

proteins and haptens

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11
Q

What are haptens?

A

any small molecule that can be recognised by a specific antibody but cannot elicit an immune response

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12
Q

To elicit an immune response, what must a hapten do?

A

must be chemically linked to a protein molecule (carrier) to elicit antibody or/and T cell responses

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13
Q

When are IgE producing B cells activated?

A

during first exposure (sensitisation)

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14
Q

Where does IgE bind?

A

to Fc receptor on mast cells or CD63 on basophils

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15
Q

What does second exposure in IgE cause?

A

binds rapidly and causes immediate degranulation

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16
Q

What T cell causes proliferation of IgE?

A

TH2

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17
Q

What are the main roles of histamine?

A
  • Immune cell recruitment
  • Neurotransmitter
  • Vasodilator
  • Endothelial constriction
  • Bronchoconstrictor
  • Increase vessel permeability
18
Q

What are examples of cutaneous atopy (localised) type 1 hypersensitivity?

A

– allergic rhinitis (hay fever)
– atopic dermatitis (allergic eczema)
– asthma (lower respiratory tract)

19
Q

What is systemic anaphylaxis (systemic)?

A

– Anaphylactic shock throughout body
– Arises from mast cell degranulation
– Anaphylatoxins also produced by complement cascade (can be type II/III)

20
Q

What are tests that can be done to identify an allergy?

A

skin prick/patch test (for skin allergies)
blood test for IgE levels
food challenges

21
Q

What are drugs used for allergy and how do they work?

A

– Anti-histamines – compete with histamine for receptors
– Hydrocortisone – block histamine synthesis
– Cromoglycate – stabilises mast cells stops histamine release
– Epinephrine – best immediate treatment for anaphylactic shock reverses effects of granules (vasoconstriction, relaxes muscles)

22
Q

What are immunological treatments?

A

– Hypo- or de- sensitisation
– repeat injections of allergen – IgE to IgG production

23
Q

How do anti histamines work?

A

– compete with histamine for receptors (found on multiple cell types)
* Histamine receptors have basal activity
* Can be inverse agonists or antagonists

24
Q

How does epinephrine work?

A
  • increases peripheral vascular resistance
  • improves blood pressure
  • reverses peripheral vasodilation
  • causes bronchodilation
  • reduces inflammatory mediator release
25
Q

How is complement activated in type 2 hypersensitivity?

A

by IgG or IgM binding to an antigenic cell (cell surface auto-antigens or haptens/allergens

26
Q

What are cells lysed by in type 2 hypersensitivity?

A

– Membrane attack complex formation (complement)
– Antibody dependent cell mediated cytotoxicity (natural killer cells or CD8+ T cells)

27
Q

What are examples of type 2 hypersensitivity?

A
  • Transfusion of mismatched blood type
  • Autoimmune hemolytic anaemia
28
Q

What does type 3 hypersensitivity involve?

A

reactions against soluble antigens circulating in serum.

29
Q

What do antibody-antigen immune complexes deposited in organs in type 3 hypersensitivity reactions lead to?

A

– Complement activation
– Neutrophil recruitment
– Inflammation-mediated damage

30
Q

What are examples of type 3 hypersensitivity?

A

– Arthus reaction
– Serum sickness
– Oral erythema multiforme (EM)

31
Q

What is Arthus reaction?

A

hypersensitivity reaction where antibody-antigen complexes are localised (e.g blood vessel walls)

32
Q

What can Arthus’s reaction arise from?

A

injected particles (booster vaccines)
inhaled or ingested allergens

33
Q

What is serum sickness?

A

systemic form of Arthus reaction
complexes lodge in many different tissues

34
Q

What is oral erythema multiforme characterised by?

A

crusty blistering of oral mucosa

35
Q

What is oral erythema multiforme caused by?

A

deposition of immune complexes (IgM immune complexes) in the microvasculature of the oral mucous membrane

36
Q

What can oral erythema multiforme arise from?

A

acute inflammatory response to HSV

hypersensitivity to drugs e.g Trimethoprimsulfamethoxazole

37
Q

What is trimethoprimsulfamethoxazole administered for?

A

to treat urinary or lower respiratory tract infections.

38
Q

What’s type 4 hypersensitivity?

A

T cell-mediated hypersensitivity (no antibodies)

39
Q

What is type 4 hypersensitivity sometimes called?

A

Sometimes called delayed hypersensitivity as takes time to recruit T cells (adaptive immune response)

40
Q

What cells does type 4 hypersensitivity involve?

A

CD4+ T cells (inflammation induced damage via macrophages)

CD8+ T cells (direct damage of cells – cytotoxicity)

41
Q

What are examples of type 4 hypersensitivity?

A
  • Contact dermatitis
  • Tissue graft rejection
  • Response to intracellular pathogens (e.g., TB) – characterised by the formation of granulomas in lung tissue.
  • Oral diseases – Orofacial granulomatous (OFG)
42
Q

What happens in contact dermatitis?

A

Localized T cell reaction at site of antigen exposure

Immunity and Pathology 1 (13 decks)

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