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Principles > Immunology: principles and primary immune disease > Flashcards

Immunology: principles and primary immune disease Flashcards

0
Q

What is an antibody?

A

A protein produced in response to an antigen and has the property of binding specifically to that antigen

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1
Q

What are the components of the innate immune system?

A 
Complement 
Acute phase proteins
Phagocytes
Eosinophils
Basophils and mast cells
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2
Q

What is an antigen?

A

Any substance which can stimulate the adaptive immune system

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3
Q

What are antibodies produced by?

A

B lymphocytes

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4
Q

What do antibodies provide defence against?

A

Most bacteria

Viruses

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5
Q

What are cytokines?

A

A diverse collection of small proteins and peptides which are produced in response to antigens, inflammation and tissue damage

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6
Q

What do cytokines do?

A

They play a key role in coordinating the immune system - they modulate the behaviour of cells by binding to specific cytokine receptors on target cells

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7
Q

Where are compliment proteins produced?

A

Liver

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8
Q

What are acute phase proteins?

A

Produced in the liver in response to inflammatory signals

Basically - inflammatory markers

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9
Q

What are the functions of acute phase proteins?

A

Modulate immune responses to micro organisms

Tissue repair and healing

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10
Q

Where does the development of leukocytes occur?

A

Primary lymphoid tissue - bone marrow, thymus

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11
Q

Where are mast cells found?

A

Resident in tissues e.g. Mucosal tissues

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12
Q

Where are basophils found?

A

Blood

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13
Q

What is characteristic of mast cells and basophils?

A

Highly granular cells

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14
Q

What is released by mast cells and basophils when activated?

A

Pathogens/allergens
Histamine
Toxic substances
Cytokines

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15
Q

What immune response are mast cells and basophils important in?

A

Responses to parasites e.g. worms

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16
Q

Which immune cells play a role in allergic disease?

A

Eosinophils

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17
Q

What is the function of eosinophils?

A

Defence against large pathogens that cannot be dealt with by phagocytes

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18
Q

What are the phagocytes present in blood?

A

Neutrophils

Monocytes

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19
Q

What are the phagocytes present in tissues?

A

Macrophages

Dendritic cells

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20
Q

What are neutrophils?

A

Also known as polymorphonuclear cells
Most common circulating leukocyte
First immune cells recruited for damage, inflammation, infection

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21
Q

What are monocytes?

A

Precursors of tissue-resident macrophages

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22
Q

What is the purpose of monocytes and macrophages?

A

Detection, phagocytosis and destruction of pathogens and dead cells
Antigen presentation
Cytokine production

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23
Q

What are dendritic cells?

A

Antigen presenting cells - they capture and process antigens and present them to T cells to induce adaptive immune responses

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24
Q

Which lymphocytes are involved in the innate immune system?

A

Natural killers cells

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25
Q

Which lymphocytes are involved in the adaptive immune system?

A

T cells

B cells

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26
Q

What is the major function of natural killer cells

A

Detection and targeted killing of abnormal body cells e.g. cancerous cells, viral infections

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27
Q

What is the function of B cells?

A

Production of antigen-specific antibodies

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28
Q

What pathogens do T cells have a key role in defence against?

A

Viruses
Fungi
Mycobacteria

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29
Q

What are the two major T cell types?

A

CD4+ (T helper cells)

CD8+ (cytotoxic T cells)

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30
Q

What is inflammation?

A

Tissue response to injury of infection - promotes tissue healing and repair and disposes of cell debris and pathogens

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31
Q

What is lysozyme?

A

Anti-bacterial enzyme that digests bacterial cell walls

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32
Q

How is the classical complement activation pathway initiated?

A

Binding of the C1 complex to antibody-antigen immune complexes

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33
Q

What is the C3 convertase in complement activation pathways?

A

C4b2a

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34
Q

How is the lectin pathway of complement activation initiated?

A

Lectins bind to carbohydrates in the cell wall of microorganisms

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35
Q

How is the alternative pathway of complement activation initiated?

A

Spontaneous hydrolysis of C3

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36
Q

What is the alternative C3 convertase involved in the alternative pathway?

A

C3bBb

37
Q

Which bacteria is the alternative pathway of complement activation vital against?

A

Meningococcus

38
Q

In complement activation, what happens after the hydrolysis of C3?

A

Splitting of C5

Aggregation of other compliment proteins to form the membrane attack complex

39
Q

What are the functions of complement?

A 
Membrane attack complex
Opsonisation
Chemotaxis
Clearance of immune complexes
Inflammation
40
Q

What is complement mediated opsonisation?

A

Coating of micro organisms by immune proteins e.g. C3b, antibodies, CRP

41
Q

Where do phagocytes express their receptors for opsonins?

A

On their cell surface - this facilitates the uptake of microorganisms

42
Q

What dissolves the immune complexes that trigger the classical complement activation pathway?

A

C3b binding

43
Q

Which complement protein binds to the surface of pathogens to initiate the membrane attack complex?

A

C5b

44
Q

How does the membrane attack complex work?

A

Inserts into target cell walls, putting a hole in the membrane causing osmotic cell lysis of the pathogen

45
Q

What complement proteins are anaphylatoxins?

A

C3a and C5a

46
Q

How do anaphylatoxins work?

A

Bind to receptors on mast cells & basophils, causing degranulation
Vasoactive substances and chemotactic factors cause the recruitment of phagocytes to the site of infection

47
Q

What ensures that the complement system is kept under tight control at all times?

A

Only cleaved components are active
Have very short half life
Complement inhibitors - C1 inhibitor, factor I, factor H, C4 binding protein

48
Q

What infection might deficiency of the complement pathway be associated with?

A

Recurrent meningococcal infection

49
Q

Which structures on the pathogen are recognised by innate leukocytes?

A

PAMPS

50
Q

What are toll-like receptors?

A

Receptors which specifically bind different pathogen components e.g. dsRNA, DNA, extra cellular proteins and sugars

51
Q

At sites of inflammation, endothelial cells become activated. What do they express to recruit leukocytes?

A

Adhesion molecules - selectins and ICAMs

Chemokines

52
Q

What do selectins allow the leukocyte to do?

A

Weakly bind to endothelial cells and roll along the cell surface

53
Q

How do leukocytes bind firmly to endothelial cells?

A

Chemokines activate leukocytes

Leukocytes bind strongly to endothelial cells via integrins (receptors on leukocyte) binding to ICAMs (endothelium)

54
Q

What is the name given to the process of the leukocyte squeezing through the endothelial layer?

A

Diapedesis

Transmigration

55
Q

Once leukocytes are in tissues, how do they get to the site of inflammation?

A

Follow a chemokine gradient

56
Q

What is oxidative killing?

A

Neutrophils and macrophages can phagocytose and destroy pathogens by generating lethal toxic oxygen and nitrogen free radicals

57
Q

In which leukocyte - neutrophils or macrophages - is oxidative killing particularly important?

A

Neutrophils

58
Q

What is the crucial enzyme in oxidative killing?

A

NADPH oxidase complex

59
Q

What is a granuloma?

A

A collection of immune cells that walls off the mycobacteria, but does not eradicate them

60
Q

What activates B cells?

A

Antigen engagement

Requires a strong signal

61
Q

Why do B cells need T cells?

A

To help respond to protein antigens

To help B cells switch the antibody type

62
Q

Where are T cells produced and where do they mature?

A

Bone marrow

Mature in thymus

63
Q

What is the structure of the T cell antigen receptor (TCR)?

A

A membrane bound heterodimer with alpha and beta chains

64
Q

Which immune cells are involved in cell-mediated immunity?

A

T cells

65
Q

What are T dependant antigens?

A

Large proteins that are able to activate both T and B cells
They produce several types on antibody - IgM, IgG, IgE, IgA
They stimulate immunological memory

66
Q

What are T independent antigens?

A

Carbohydrates, lipids and nucleic acids that are only able to activate B cells and only produce IgM

67
Q

B cell antigen receptors can bind directly to large, intact molecules. What must happen to protein antigens in order to be recognised by T cells?

A

Antigens must be processed and presented to their T cell antigen receptor in complex with major histocompatibility complex (MCH) molecules

69
Q

What are major histocompatibility complex molecules?

A

The immune systems way of displaying peptide antigens to T cells

70
Q

What are “SPUR” infections?

A

Serious infections
Persistent infections
Unusual infections
Recurrent infections

71
Q

What are some of the clinical features of phagocyte deficiencies?

A

Recurrent infections - may affect common and unusual sites

Normal bacteria, unusual bacteria, mycobacteria and fungi

72
Q

What does the term “phagocyte deficiency” encompass?

A

Defects of phagocyte production, mobilisation and recruitment

73
Q

What is Kostmann syndrome?

A

Rare autosomal recessive disorder where neutrophils are not effectively produced, resulting in low circulating neutrophil count

74
Q

What is the clinical presentation of Kostmann syndrome?

A 
Infections, usually within 2 weeks after birth:
Recurrent bacterial infection
Systemic or localised infection
Non specific features:
Fever
Irritability
Oral ulceration
Failure to thrive
75
Q

Where is the defect in Kostmann syndrome?

A

In the neutrophil precursor

76
Q

How is Kostmann syndrome managed?

A

Prophylactic antibiotics
Prophylactic antifungals
Granulocyte colony stimulating factor (G-CSF)
Stem cell transplant

77
Q

What is leukocyte adhesion deficiency?

A

A rare primary immunodeficiency caused by genetic defect in leucocyte integrins (CD18)
Results in failure of neutrophil adhesion and migration

78
Q

What is the clinical picture of leukocyte adhesion deficiency?

A

Marked leukocytosis and localized bacterial infections that are difficult to detect
High circulating neutrophil count

79
Q

What receptors do phagocytes express that allow binding of antibody that is also bound to antigen?

A

Fc receptors

80
Q

What defects might result in ineffective opsonisation and phagocytosis?

A

Complement receptor defects

Antibody and complement production defects

81
Q

What causes chronic granulomatous disease?

A

Failure of oxidative killing mechanisms
Inability to clear organisms and excessive inflammation
results in failure to degrade chemoattractants and antigens, persistent accumulation of neutrophils, activated macrophages and lymphocytes:
This results in granuloma formation

82
Q

What is the clinical picture of chronic granulomatous disease?

A 
Recurrent deep bacterial infections, especially Staphylococcus, Aspergillus, pseudomonas cepacia
Mycobacteria, atypical mycobacteria
Recurrent fungal infections
Failure to thrive
Lymphadenopathy and hepatosplenomegaly
Granuloma formation
83
Q

How do you test for chronic granulomatous disease/assess whether neutrophils are capable of oxidative killing?

A

NBT (“nitroblue tetrazolium”) test

84
Q

How is an NBT test carried out?

A

Feed patient neutrophils source of E coli
Add dye that is sensitive to H202
If hydrogen peroxide is produced by neutrophils, dye changes colour

85
Q

How do CD8+ cytotoxic cells kill cells directly?

A

Production of pore-forming molecules: perforin
Triggering apoptosis of the target
Secrete cytokines e.g. IFNγ

86
Q

What is reticular dysgenesis?

A 
A rare genetic disorder of the bone marrow resulting in complete absence of granulocytes and decreased number of abnormal lymphocytes
Failure of production of:
Neutrophils
Lymphocytes
Monocyte/macrophages 
Platelets
87
Q

What is severe combined immunodeficiency?

A

Failure of production of lymphocytes

88
Q

What is the classical presentation of severe combined immunodeficiency?

A

Unwell by 3 months of age
Persistent diarrhoea
Failure to thrive
Infections of all types

89
Q

Why do diseases like SCID present roughly three months into life?

A

Maternal IgG protects neonate until then

90
Q

What is the most common form of SCID?

A

X-linked SCID

Genetic mutation in IL2 receptor

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