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Flashcards in Immunology Deck (116):
1

What is vaccination?

Deliberate administration of antigens to produce immunological memory

2

When are long lived T and B cells generated?

Adaptive immune response

3

Where do long lived plasma cells reside?

Bone marrow

4

In immunological memory, how does IgG clear infection before symptoms occur?

Direct neutralisation of bacteria
Rapid mobilisation of phagocytes and complement
IgA blocks bacterial binding to mucous membranes

5

What are naïve B and T cells?

Mature but not yet activated (induce a strong response in 14-21 days)

6

What can naïve B and T cells become?

Effector or memory cells

7

What have memory B cells already undergone?

Ig class switching and hypermutation

8

What is immunisation?

The process through which an individual develops immunological memory to a disease

9

What is active immunisation?

Protection by the persons own immune system- usually permanent

10

What is passive immunisation?

Protection transferred by another person or animal- temporary

11

What are the two types of active vaccination?

Live attenuated vaccines or inactive vaccines e.g. killed, subunit or toxoid

12

What are some features of inactivated vaccines?

Do not multiply, not as effective, antibody based (not T cell), will diminish with time, multiple doses

13

What can under-inactivation cause?

Pathogens or toxins within the body

14

What can over-activation cause?

Ruins conformation of the antigen so there can be no antibody binding

15

What are some features of a live attenuated vaccine?

Similar to natural infection, organism must replicate, needs 1 dose

16

What is the advantage of inactivated vaccines over live attenuated ones?

Generally safer and easier to store

17

What is the most common example of natural passive immunisation?

Through transfer of maternal antibodies in placenta and maternal antibodies through breast milk

18

What antibody is transferred across the placenta?

IgG

19

What are examples of therapeutic passive immunisation?

Human immunoglobulin or monoclonal antibodies

20

What makes some organisms difficult to create vaccinations for?

Chronic/latent disease or rapidly evolving infections

21

What are some new approach vaccinations?

Mucosal vaccines, intranasal vaccine and preventative vaccines against cancer causing viruses

22

What is primary immunodeficiency?

Inherited abnormalities associated with a failure of development of components of the immune system

23

What are the hallmarks of immunodeficiency?

Serious, persistent, unusual, recurrent infections

24

What is classed as recurrent infection?

2 major or 1 major and recurrent minor infections in one year

25

What are typical features of immunodeficiency in general?

Weight loss, failure to thrive, severe skin rash, chronic diarrhoea, mouth ulcers, autoimmune disease, family history

26

What is more common, primary or secondary immunodeficiency?

Secondary

27

What are causes of secondary immunodeficiency?

Physiological, infections, treatment, malignancy, nutritional disorders

28

What do defects of phagocyte production usually cause?

Failure to produce neutrophils or a failure of their maturation

29

What is Kostmann Syndrome?

Rare autosomal recessive disorder of severe chronic neutropenia

30

What are signs of Kostmann Syndrome?

Infections after birth, fever, irritability, ulcers, failure to thrive

31

What is the supportive treatment for Kostmann Syndrome?

Prophylactic antibiotics and antifungals

32

What is the definitive treatment for Kostmann Syndrome?

Stem cell transplant, granulocyte colony stimulating factor

33

What is leukocyte adhesion deficiency?

Genetic defect in leukocyte integrins to cause a failure of neutrophil adhesion and migration

34

What does leukocyte adhesion deficiency show?

Leukocytosis (high WCC) and localised bacterial infections

35

What are opsonins?

Binding enhancers for phagocytosis

36

What do opsonin defects cause?

Defective phagocytosis but not significant disease

37

In general, how are phagocyte deficiencies treated?

Oral/IV antibiotics, surgical drainage of abscess, bone marrow transplant

38

What is chronic granulomatous disease?

Failure of oxidative killing mechanisms. It is x-linked deficiency of NADPH oxidase

39

What does CGD result in?

Excessive inflammation and granuloma formation, recurrent deep bacterial and fungal infections, failure to thrive, lymphadenopathy, hepatosplenomegaly

40

What is the prophylactic treatment for CGD?

Prophylactic antibiotics and antifungals

41

What is the definitive treatment for CGD?

Stem cell transplant, gene therapy

42

What are organisms which can hide from the immune system in cells?

Salmonella, chlamydia, rickettsia

43

Where is it common for organisms to hide in the body?

Macrophages

44

What is reticular dysgenesis?

Failure to produce neutrophils, lymphocytes, monocytes/macrophages, platelets

45

How is reticular dysgenesis treated?

Only by stem cell transplant

46

What is SCID?

Failure to produce lymphocytes in the thymus

47

When are signs of SCID?

Unwell by 3 months, persistent diarrhoea, failure to thrive, infections of all types, family history

48

What is the commonest form of SCID?

X-linked mutation in the IL2 receptor which results in the inability to produce cytokines

49

What is the clinical presentation of SCID?

Low/absent T cells, normal/increased B cells, poorly developed lymphoid tissues

50

How is SCID treated?

Prophylactic antibiotics, stem cell transplant, gene therapy

51

What is DiGeorge syndrome?

Defect of the 3rd/4th pharyngeal pouch so there is failure of thymus development which results in T cell immunodeficiency

52

What are physical signs of DiGeorge syndrome?

Low set ears, high forehead, cleft palate, small mouth

53

What are clinical signs of DiGeorge syndrome?

Hypocalcaemia, T cell lymphopenia, congenital heart disease, recurrent bacterial and viral infections, frequent fungal infection

54

What is the treatment for DiGeorge syndrome?

Prophylactic antibodies and treatment of infection and immunoglobulin replacement

55

What is the good thing about DiGeorge syndrome?

T cell function improves with age

56

What do antibody deficiencies present as?

Recurrent bacterial infections

57

What is Bruton's X-linked Hypergammaglobulinaemia?

Failure to produce mature B cells

58

What is selective IgA deficiency?

A genetic component which only affects about 1/3rd of sufferers

59

What is CVID?

Lots of different diseases, low IgG/IgA/IgE

60

How does CVID present?

Recurrent bacterial infections associated with autoimmune disorder

61

What type of hypersensitivity reactions are allergic responses?

Type 1

62

What is an allergic response?

IgE mediated antibody response to an external antigen

63

What antibodies do non-atopic episodes involve?

IgG and IgA

64

Allergen specific T cells are activated by allergen derived peptides in allergic reactions. What does this cause?

Differentiation of CD4+ T cells into effector Th2 cells which produce cytokines

65

Which interleukins does Th2 produce to synthesise IgE by B cells?

IL4, 13 and 5

66

What does the production of IgE during allergic responses result in?

Eosinophil and mast cell recruitment to the site of allergen

67

Abnormal response to allergens is the normal response to what?

Helminth infection

68

Mast cells release preformed substances. What are these?

Histamine, heparin and tryptase

69

Mast cells synthesise molecules on demand. What are these?

Leukotrienes, prostaglandins and cytokines

70

What do mast cells express receptors for?

The Fc region of the IgE antibody

71

When do clinical features of allergic responses occur?

Within minutes

72

What are clinical features of allergic responses?

Urticaria, angioedema, asthma, allergic rhinitis, conjunctivitis and anaphylaxis

73

In extrinsic asthma, what does the release of histamine and other inflammatory mediators result in?

Muscle spasm (bronchodilation and wheeze), mucosal inflammation and inflammatory cell infiltrate (secretions)

74

What do non-allergic responses occur as a result of?

Spontaneous mast cell degranulation

75

What can non-allergic responses occur as a result of?

Drugs, thyroid disease, idiopathic, physical urticaria

76

What is the management of type 1 hypersensitivity reactions?

Allergen avoidance, block/prevent mast cell activation, anti-inflammatory agents, management of anaphylaxis, immunotherapy

77

What drugs block mast cell activation?

Sodium cromoglicate

78

What drugs prevent mast cell activation?

Antihistamines, leukotriene receptor antagonists

79

What are anti-inflammatory agents?

Corticosteroids

80

What is given to manage anaphylaxis?

Adrenaline

81

What do type II hypersensitivity reactions involve?

Direct cell killing

82

What are type II hypersensitivity reactions triggered by?

Antibody binding to an antigen on the cell surface or extracellular matrix

83

What is the result of type II hypersensitivity reactions?

Cell lysis or inflammatory reactions at the site of antibody deposition

84

When the antibody binds to a cell surface antigen, what does this result in?

Activation of complement for cell lysis and opsonisation

85

What antibodies are involved in type II hypersensitivity reactions and why?

IgG and IgM as they activate complement

86

Complement activation results in the activation of C3. What does this cause?

Chemotaxis, solubilisation of immune complexes, direct killing of bacteria and opsonisation

87

What type of bacteria does complement generally kill and how?

Directly encapsulated bacteria through the membrane attack complex

88

What complement proteins are involved in type II hypersensitivity reactions?

C3a and C5a

89

How does direct cell killing take place in type II hypersensitivity reactions?

Through B cells producing antibodies directed against the cell membrane protein

90

What other immune system components are involved in type II hypersensitivity reactions?

Eosinophils and natural killer cells

91

What are clinical examples of type II hypersensitivity reactions?

Blood cells (transfusion reactions), Goodpasture's syndrome, myasthenia gravis, binding of antibodies to TSH receptor

92

How are type II hypersensitivity reactions managed?

Removal of the pathogenic antibody (blood removed by cell separator) or immunosuppression

93

What are type III hypersensitivity reactions?

Immune complex mediated

94

What is the key feature of type III hypersensitivity reactions?

Antibodies binding to soluble antigens

95

What triggers type III reactions and what happens to these?

Excess antigens- antibody binds to them to form small immune complexes

96

Where are the immune complexes of type III reactions found?

Trapped in blood vessels, joints and glomeruli

97

What is activated in type III reactions?

Complement

98

What is the result of type III reactions?

Antibody mediated phagocytosis and infiltration and activation of neutrophils and macrophages to result in tissue damage

99

A clinical example of type III reactions is farmer's lung. What happens here?

Inhaled fungal particles are deposited which stimulates antibody binding

100

What does immune complexes in the walls of the alveoli and bronchioles result in?

Leukocyte accumulation and activation

101

What are symptoms of leukocyte accumulation in the lungs?

Wheezing and malaise 4-8 hours after antigen exposure. Can also be dyspnoea, pyrexia and a dry cough

102

What are other examples of type III hypersensitivity reactions?

Acute hypersensitivity pneumonitis, systemic lupus erythematosus

103

What is the difference between types II and III reactions?

Type II is localised and type III is systemic

104

How do you test for type III reactions?

Test for specific IgG antibodies

105

How do you manage type III reactions?

Allergen avoidance, steroids, immunosuppression

106

What are type IV reactions?

Delayed hypersensitivity

107

What are autoimmune examples of type IV reactions?

Type 1 diabetes, psoriasis, rheumatoid arthritis

108

What are non-autoimmune examples of type IV reactions?

Nickel hypersensitivity, TB, leprosy, sarcoidosis, cellular rejection of organ transplant

109

What differentiates type IV reactions?

T cell mediated

110

In type IV hypersensitivity reactions, what is generated on initial sensation to an antigen?

Effector Th1 cells

111

What happens on subsequent exposure to antigens in type IV reactions?

Activation of Th1 cells, recruitment of macrophages, lymphocytes and neutrophils to cause persistent inflammation

112

What do Th1 cells activate in type IV reactions?

Interferon gamma cytokines

113

What is poison ivy an example of?

Type IV reaction

114

What is sarcoidosis?

Multi-system granulomatous disease

115

What type of immune response is involved in sarcoidosis?

Non specific response involving T cells and macrophages

116

What does sarcoidosis result in?

Persistent production of activated cytokines