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Foundations > Immunology > Flashcards

Immunology Flashcards

1
Q

Innate Immunity

A

Natural immunity that is present from birth and is generally non-specific and fast

Includes physical barriers, inflammatory mediators, complement proteins, acute phase proteins, immune cells

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2
Q

What does the immune system do

A

identifies and eliminates microorganisms by distinguishing self molecules from non self molecules and identifying danger signals

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3
Q

ways to manipulate the immune system to prevent or treat human disease

A

immunisation
anti-inflammatory and immunosuppressive drugs
cancer immunotherapy

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4
Q

barriers to infection - skin

A

physical barrier - tightly packed, highly keratinised cells,

physiological factors - low pH (5.5), low oxygen tension

sebaceous glands - hydrophobic oils, lysozymes, ammonia

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5
Q

Tell me about mucus

A

Mucous membranes line all body cavities that are in contact with the external environment

Mucus traps bacteria and contains lysozymes and defensins that directly kill invading pathogens

Secretory IgA

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6
Q

tell me about commensal bacteria

A

Compete with pathogens for resources and produce fatty acids and bactericides that stop pathogens growing

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7
Q

What are cytokines

A

Interferons released by virally infected cells signal to neighbouring uninfected cells :

destroy RNA and reduce protein synthesis and undergo apoptosis

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8
Q

What do interferons activate

A

immune cells e.g. NK cells

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9
Q

What are acute phase proteins

A

Proteins produced by the liver whose plasma concentrations increase or decrease in response to inflammation

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10
Q

What are examples of acute phase protiens

A

C3 - complement system protein
MBL - complement system protein
CRP - activates complement via classical pathway

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11
Q

What is transendothelial migration

A

the recruitment of neutrophils to the site of infection/damage during acute inflammation

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12
Q

What are the stages of transendothelial migration

A
  1. Loss of intravascular fluid in the presence of inflammation causes slower blood flow, allowing neutrophils to undergo margination (neutrophils travel close to endothelial cells instead of centre of the vessel)
  2. Neutrophils can then encounter and bind to adhesion molecules expressed by the endothelial cells
  3. Neutrophils migrate across the endothelium via diapedesis
  4. Once in the tissues, the neutrophils travel to the exact site of injury via chemotaxis
  5. Neutrophils are then activated by PAMPs and pro-inflammatory mediators such as TNFa
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13
Q

What are types of killing mechanisms

A

NETs
Phagocytosis
Degranulation

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14
Q

Tell me about NETs

A

neutrophil extracellular traps : release of a net-like structure that traps pathogens, leading to phagocytosis

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15
Q

Tell me about phagocytosis

A

Pathogens release chemical signals that attract neutrophils, which use PRR to bind to and phagocytose these pathogens

Kills internalised pathogens via 2 distinct mechanisms : phagolysosomal killing and ROS-dependent killing

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16
Q

Tell me about degranulation

A

release of anti-bacterial granules leading to direct damage and systemic inflammation

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17
Q

What are the modes of ingestion

A

Receptor mediated endocytosis

Pinocytosis

Phagocytosis

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18
Q

Tell me about receptor mediated endocytosis

A

molecules bound to membrane receptors are internalised

important in the generation of adaptive immunity

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19
Q

Tell me about pinocytosis

A

ingestion of fluid of surrounding cells

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20
Q

Are macrophages a phagocytic cell

A

Yes

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21
Q

what is macrophages phagocytosing bacteria facilitated by

A

opsonization

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22
Q

What is opsonisation

A

the coating of pathogens by soluble factors (opsonins) to enhance phagocytosis

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23
Q

What are the stages of phagocytosis

A
  1. PRRs on macrophages bind to PAMPs on pathogen which signals the formation of the phagocytic cup
  2. Cup extends around the pathogen and pinches off - phagosome
  3. Phagosome fuses with lysosome - phagolysosome
  4. Pathogen killed and contents degranulated n
  5. Debris released into extracellular fluid
  6. Pathogen-derived peptides expressed on special cell surface receptors (MHC-II)
  7. Pro-inflammatory mediators released (TNFa) - acute inflammation
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23
Q

What are examples of opsonins

A

C3b
C-reactive protein (CRP)
IgG/IgM

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24
Q

Are dendritic cells phagocytic cells

A

yes

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25
Q

What do dendritic cells do

A

act as a bridge between the innate and acquired immune system

express antigens on their cell surface and present them to T cells

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26
Q

What are eosinophils associated with

A

allergy

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27
Q

Tell me about basophils

A

Granules contain histamine etc.

act as effector cells in allergic reactions

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28
Q

What do mast cells deal with

A

pathogens too large for phagocytosis

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29
Q

What are mast cells associated with

A

Allergy

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30
Q

What is gene expression

A

Production of new pro-inflammatory substances

e.g. leukotrienes and prostaglandins

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31
Q

What can immune systems be enhanced by

A

antibodies

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32
Q

What is acquired (adaptive immunity)

A

Immunity that is not present from birth

Is specific and slow

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33
Q

What is acquired (adaptive) immunity induced by

A

foreign material

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34
Q

Is acquired immunity able to discriminate between self and non-self

A

Yes

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35
Q

What does acquired immunity include

A

cytokines, antibodies, B and T cells

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36
Q

The complement system, when activated, creates a cascade of chemical reactions that promotes:

A

opsonisation of pathogens

direct pathogen killing

accute inflammation

leukocyte recruitment

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37
Q

Where are low levels of inactive complement system proteins normally found

A

plasma and extracellular fluids

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38
Q

Go and learn the complement system pathways

A

NOW!!!!

39
Q

Where do B cells mature

A

in the bone marrow

40
Q

What are B cells important in

A

humoural immune response

41
Q

What do B cells produce

A

antibodies that attack pathogens circulating in the blood and lymph

42
Q

B cells play a key role in defence against …

A

extracellular pathogens

43
Q

What do B and T cells normally circulate around

A

their primary lymphoid tissue (site of development) in their inactive form

44
Q

What activates the B and T cells and where

A

Antigen presentation in the secondary lymphoid tissue (lymph nodes, spleen, MALT)

45
Q

B cell activation : what do membrane-bound antibodies on the B cells bind to

A

target antigen IgM (or IgD)

46
Q

Why are neutrophils much better killers than macrophages

A

Because they have a 2nd way to kill internalised pathogens

47
Q

How many signals to B cells require to become fully active

A

2

48
Q

Once activated, what do B cells become

A

plasma cell (antibodies) or a memory B cell

49
Q

What is generated in B cell activation

A

IgM and IgG

50
Q

Tell me about the transport of lymphocytes

A

Lymph and Lymphocytes leave lymph node, medullary sinus, efferent lymphatic vessels, blood circulation via lymphatic ducts at the subclavian vain

51
Q

What is Ig

A

immunoglobin

52
Q

What are antibodies made up of

A

2 light chains and 2 heavy chains

53
Q

Where are membrane bound antibodies located

A

surface of B cell

54
Q

what is agglutination

A

the action of an antibody when it cross-links multiple antigens producing clumps of antigens

55
Q

what does agglutination do

A

enhance phagocytosis
prevents viruses from binding to and infecting host cells

56
Q

What is the first antibody to be made in an infection

A

IgM

57
Q

When is IgM a monomer/pentamer

A

Monomer when bound to B cell membrane

Pentamer when released into plasma

58
Q

What are the functions of IgM

A

B cell activation, agglutination, complement system activation through classical pathway

59
Q

What is the most abundant antibody in the plasma

A

IgG

60
Q

Is IgG a monomer or pentamer

A

Monomer

61
Q

What are the functions of IgG

A

foetal immunity (placental transfer)

62
Q

What is the second most abundant antibody

A

IgA

63
Q

What are the functions of IgA

A

neonatal defense (found in breastmilk)

64
Q

What are IgE produced in

A

allergic response

65
Q

Where to T cells mature

A

thymus

66
Q

What can T cells recognise

A

peptide antigens

67
Q

What are regulatory T cells involves in

A

lymphocyte suppression

68
Q

What are memory T cells involved in

A

the adaptive immune response

69
Q

Tell me about CD4+ Helper T cells

A

activate B cells and stimulate production of memory B cells

70
Q

Tell me about CD8+ killer T cells

A

kill infected cells

71
Q

What can T cells only recognise

A

peptide antigens that are presented to their TCR by MHC molecules

72
Q

Tell me about Class I MHC

A

expressed on all nucleated cells

present peptide antigens to CD8+ killer T cells

73
Q

Tell me about Class II MHC

A

expressed only on antigen presenting cells (e.g. dendrites, macrophages), present peptide antigens to CD4+ helper T cells

74
Q

What are hypersensitivity reactions

A

Immune response that results in bystander damage to the self

usually exaggeration of normal immune mechanisms

75
Q

Type 1 hypersensitivity reaction

A

immediate hypersensitivity

76
Q

Type 2 hypersensitivity reaction

A

direct cell effects

77
Q

Type 3 hypersensitivity reaction

A

immune complex mediated

78
Q

Type 4 hypersensitivity reaction

A

delayed type hypersensitivity

79
Q

Are most complex diseases one or a combination of the types of hypersensitivity

A

combination

80
Q

what is a classical type of type 1 hypersensitivity (immediate)

A

allergy, mediated by the inappropriate production of specific IgE antibodies to harmless antigens

81
Q

What are the cells involved in type I hypersensitivity reactions

A

Mast Cells, B Cells, Eosinophils

82
Q

Children who produce more Th2 …

A

are more likely to develop allergens than children who switch to producing Th1

83
Q

take a minute to breath

A

a whole minute!!!

84
Q

Tell me about the management of IgE mediated allergic disorders

A

Avoidance of allergen

Block mast cell allergen - medication

Prevent effects of mast cell activation - anti-histamines

Anti-inflammatory agents - removes Th2 cells

Adrenaline - epi-pen

85
Q

What is type II hypersensitivity reactions (direct cell effects) mediated by

A

IgM/IgG antibodies bind to antigens present on cell surfaces or ECM. this marks the cell for destruction

86
Q

Type IIa reactions

A

destruction of antigen-positive cells

87
Q

Type IIb reactions

A

stimulation of cell surface antigens

88
Q

Tell me the summary table (because you lazy) of the 4 types of hypersensitivity reactions

A

Type 1 - antibody mediated immunity, IgE, Fast response (minutes), allergic reactions, asthma/allergic rhinitis

Type 2 - antibody mediated immunity, IgG/IgM, Intermediate, body cells directly attacked by antibodies, Rheumatic heart disease

Type 3 - antibody mediated immunity, IgG/IgM, intermediate, complex accumulation and destruction, rheumatoid arthritis

Type 4 - cell mediated immunity, Th1, late response (48-72 hours), cell mediated cytotoxicity, transplant rejection/contact dermatits

89
Q

Tell me about resolution

A

normal immune response

pathogen cleared

tissure repair

90
Q

Tell me about the response to a latent infection

A

normal immune response

pathogen controlled

infection can re-occur

91
Q

Tell me about the response to chronic infection

A

Defective immune response

Pathogen not cleared or controlled

92
Q

What are primary immunodeficiencies a result of

A

genetic defects

93
Q

What are secondary immunodeficiencies caused by

A

environmental factors, such as HIV or malnutrition

94
Q

What does SPUR stand for - PRIMARY IMMUNE DEFICIENCY

A

Serious infections, persistent infections, unusual infections, recurrent infections

95
Q

Are serious infections responsive or unresponsive to oral antibiotics

A

unresponsive

96
Q

What are other features that suggest primary immune deficiency

A

Weight loss
severe skin rash
chronic diarrhoea
cancer
family history

Foundations (10 decks)

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