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Study Notes - Principles > *Immunology 2 (lectures 3 and 4) > Flashcards

*Immunology 2 (lectures 3 and 4) Flashcards

1
Q

What are the 2 distinct mechanisms of communication in the immune system?

A 
Direct contact (receptor: lingered interactions)
Indirect (production and secretion of cytokines)
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2
Q

Do immune cells have receptors or ligands on them?

A

Receptors

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3
Q

What cells tend to produce and secrete cytokines?

A

Injured tissue cells

Activated immune cells

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4
Q

What is an autocrine signal?

A

A signal that acts back on the same cell that produced it

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5
Q

What are the physiological symptoms of acute inflammation? (4)

A

Rubor
Calor
Tumor
Dolor

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6
Q

What are the 3 phases involved in innate immune cells recognising and responding to pathogens?

A

Recognition
Activation
Effector

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7
Q

What happens in the recognition phase of innate immune cells recognising and responding to pathogens?

A

Pathogens express signature molecules not found on human cells called |”pathogen associated molecular patterns” -PAMPS (common to many different types of pathogens)
innate immune cells (and some other cell types) express specific receptors for these PAMPS called “pattern-recognition receptors” (PRRs) - found on cell surface and intracellular (detect extra- and intra- cellular pathogens)

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8
Q

Example of PAMPs and PRRs on gram negative bacteria?

A 
PAMPs = lipopolysaccharide (LPS)
PRRs = Toll-like receptor 4 (TLR4) - extracellular
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9
Q

Example of PAMPs and PRRs for fungi?

A 
PAMPs = beta-glucans
PRRs = dectin 1 (extracellular)
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10
Q

Example of PAMP and PRR for TB?

A 
PAMP = muramyl dipeptide
PRR = NOD2 (intracellular)
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11
Q

Example of PAMP and PRR for viruses?

A 
PAMP = ssRNA
PRR = toll-like receptor 7 (intracellular)
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12
Q

What role do macrophages play in the homeostasis of the skin?

A

Induction of programmed cell death (apoptosis)

Specific recognition and removal of dying cells by phagocytes e.g. macrophages

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13
Q

How are apoptotic cells cleared by tissue-resident macrophages? (5)

A

Apoptotic cells release “find-me” signals to attract and activate macrophages
Macrophages recognise specific “eat-me” signals expressed on the surface of apoptotic cells
Macrophages rearrange their cytoskeleton to internalise apoptotic cells
Digestion of the ingested “cargo”
Secretion of anti-inflammatory mediators e.g. IL-10

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14
Q

What happens when physical barriers are breached by pathogens?

A

PAMPs of pathogens are recognised and injured tissue cells release “danger” signals
This activates macrophages, mast cells and NK cells
This causes the pathogens to be killed, infected tissue cells killed, production of inflammatory mediators

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15
Q

What happens when macrophages digest a pathogen compared to apoptotic cell debris?

A

Pro-inflammatory mediators are released compared to anti-inflammatory mediators

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16
Q

How do macrophages kill pathogens? (2)

What enhances its killing ability?

A

Phagolysosome (acidification, lysosomal hydrolases)
Production of toxic reactive oxygen and nitrogen species
(killing ability (and other functions) are enhanced by pro-inflammatory cytokines e.g. IFN gamma

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17
Q

How do pro-inflammatory cytokines enhance macrophages pathogen killing? (3)

A

Produced by NK cell (and some T cells) e.g. IFN gamma
Increased production of toxic reactive oxygen and nitrogen species
Increase microbicidal activity
Boost antigen presentation capability

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18
Q

How do mast cells aid in the killing of pathogens?

A

They produce inflammatory mediators that enhance killing response

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19
Q

Where do mast cells reside?

A

In tissues and protect mucosal surfaces (play a key role in defence against parasites)

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20
Q

What happens when a pathogen binds to a PRR on a mast cell?

A 
Degranulation occurs (release of pre-formed pro-inflammatory mediators)
Gene expression = production of new pro-inflammatory mediators
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21
Q

What is the purpose of NK cells?

A

They specifically kill virally infected cells and abnormal cancer cells

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22
Q

How do NK cells recognise cells infect with intracellular pathogens or cancer cells?

A 
If they have an MHC class 1 then the NK cells binds and doesnt attack
If there is no MHC class 1 (virus or cancer cell), the NK cell attacks it and releases pro-inflammatory mediators
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23
Q

What 3 cells produce inflammatory mediators as part of the innate immune response?

A

Macrophages
mast cells
MK cells

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24
Q

What are some examples of inflammatory mediators produced by macrophages, mast cells and NK cells?

A 
NO
Prostaglandins/ leukotrienes
Histamines
Cytokines e.g. TNFalpha, IL-1, IL-6, IFNgamma
Chemokines
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25
Q

What systemic effect do cytokines have (IL-1, IL-6, TNFalpha)? (3)

A

Cause the release of prostaglandins from the hypothalamus causing fever
Cause the release of acute phase response proteins from the liver
Cause creased neutrophil production (leukocytosis) in the bone marrow)

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26
Q

What is the acute phase response?

A

A group of physiological processes that occur soon after the onset of infection due to the release of a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation (this is stimulated by IL-2, IL-6 and TNFalpha) causing the alteration in protein synthesis in the liver

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27
Q

What are examples of acute phase proteins? (7)

A 
CRP
Serum amyloid protein (SAP)
Complement proteins
Fibrinogen
Haptoglobin
Manganese superoxidase dismutase
Proteinase inhibitors
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28
Q

What biological role does CRP, SAP and complement proteins have?

A

Preventing the spread of infection

Diagnostic marker

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29
Q

What role does fibrinogen have?

A

Coagulation

Wound healing

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30
Q

What role does CRP, haptoglobin, manganese superoxidase dismutase and proteinase inhibitors have?

A

Preventing systemic inflammation

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31
Q

How many subunits is CRP made up of?

A

5 identical subunits

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32
Q

What does high levels of CRP mean?

A

There is inflammation/ infeciton

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33
Q

How does CRP enhance phagocytosis?

A

CRP opsonises bacteria, facilitating their clearance by phagocytes

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34
Q

What are the 3 purposes of CRP?

A

Diagnosis
Enhance phagocytosis
Complement system activation

35
Q

What anti-inflammatory cytokine is produced when apoptotic cells are phagocytes by macrophages?

A

Anti-inflammatory IL-10

36
Q

What are the 3 tissue resident innate immune cells that are involved in the early responses to pathogens?

A

Macrophages
NK cells
Mast cells

37
Q

What role does macrophages have in the early innate immune reopens to pathogens? (2)

A

Phagocytosis and pathogen killing

Pro-inflammatory cytokines (TNFalpha, IL-1, IL-6)

38
Q

What role does NK cells have in the early innate immune response to pathogens?

A

Release of pro-inflammatory cytokines (IFNgamma) which enhances macrophage killing ability
Specific killing of virally infected tissue cells

39
Q

What role do mast cells have in the early innate immune response to pathogens?

A

Release of pro-inflammatory cytokines

40
Q

What effects do nitric oxide, prostaglandins, leukotrienes and histamines have? (4)

A

Cause vasodilation
Increase vascular permeability
Cause smooth muscle contraction
Cause pain

41
Q

What local effects do cytokines released from macrophages, mast cells and NK cells have?

A

Increase vascular permeability

Endothelial cell activation

42
Q

What is released from macrophages that causes increased vascular permeability? (3)

A

TNF alpha
IL-1
Nitric oxide

43
Q

What is released from mast cells that causes increased vascular permeability? (4)

A

Histamine
TNF alpha
Leukotrienes
Prostaglandins

44
Q

What is released from macrophages that causes vasodilation?

A

TNF alpha

45
Q

What is released from mast cells which causes vasodilation?

A

Histamine

46
Q

What is released from macrophages that causes endothelial cell activation (expression of cell adhesion molecules)? (2)

A

TNFalpha

IL-1

47
Q

What cell adhesion molecules are express on the epithelium?

A

Selectins (receptors)

ICAM-1, VCAM-1 (ligands)

48
Q

What is released from mast cells that causes endothelial cell activation in the vasculature?

A

Histamine

49
Q

How do neutrophils get out of the vasculature during inflammation and to the damaged cells?
What other cells do this? (5)

A

Transendothelial migration and chemotaxis of neutrophils
Monocytes
NK cells
Basophils
Eosinophils
T cells (during the adaptive immune response)

50
Q

What releases chemokines causing chemotaxis of neutrophils?

A

Macrophages

Mast cells

51
Q

When do neutrophils stop rolling along the endothelial wall?

A

When they come into contact with ICAM or VCAM

52
Q

What on the neutrophil allows it to bind to selections and ICAM/ VCAM?

A

Integrins

53
Q

What is the name for the movement or passage of blood cells, especially white blood cells, through intact capillary walls into surrounding body tissue?

A

Diapedesis

54
Q

What is the purpose of neutrophils once inside infected tissue?

A

To find and kill pathogens

55
Q

What is another name for neutrophils?

A

Polymorphonuclear cells

56
Q

What are neutrophils?

A

Phagocytic cells that circulate in the blood and are rapidly recruited into inflammatory sites by cytokines and other pro-inflammatory mediators

57
Q

What are the functions of neutrophils? (2)

A

To kill extracellular pathogens

To produce pro-inflammatory cytokines e.g. TNFalpa

58
Q

Characteristic features of neutrophils?

A

Intracellular granules

Multi-lobed nucleus

59
Q

What are the 3 possible neutrophil killing mechanisms?

A

Phagocytosis
Degranulation
NETs

60
Q

What are the 2 possible killing mechanisms that neutrophils use once they have encapsulated the pathogens in phagosomes?

A

Anti-microbial proteins

NADPH oxidase-dependent mechanisms

61
Q

What are examples of anti-microbial proteins in the granules of neutrophils that are used i phagocytosis? (4)

A

Cathepsins
Defensins
Lactoferrin
Lysozyme

62
Q

What is another name for NADPH oxygenate-dependant killing mechanisms?

A

The respiratory burst

63
Q

How does the respiratory burst kill pathogens?

A

Through the production of toxic reactive oxygen species e.g. superoxide, hydrogen peroxide, NO

64
Q

What type of killing mechanisms do neutrophils use to kill extracellular pathogens (bacteria and fungi)?

A

Degranulation - causes tissue damage and systemic inflammation

65
Q

What does NETs stand for?

A

neutrophil extracellular traps

66
Q

How do NETs work?

A

They are released by activated neutrophils into the extracellular environment and immobolise pathogens (prevents them from spreading, facilitates their phagocytosis)

67
Q

Are neutrophils long or short lived?

A

Short (die by apoptosis and are phagocytes by macrophages)

68
Q

What is pus made up from?

A

Neutrophils, NETs, dead bacteria, cellular debris

69
Q

Why is pus fellow/ green?

A

Lactoferrin binds iron, iron is green

70
Q

What pathological consequences does excess amounts of TNF alpha have?

A

Ailments suc as IBD, psoriasis, autoimmune conditions, rheumatoid arthritis, asthma and cancer are linked to too much of this

71
Q

As well as leukocytes, what else leaks out of the vasculature during inflammation?

A

Complement proteins (kinins, coagulation factors, fibrinolytic system)

72
Q

How many complement proteins are there?
Where are they produced?
Where are they found?

A

Approx. 30
Liver
Circulate in blood and are recruited into infected and inflamed tissues

73
Q

What activates complement proteins?

A

Pathogens

74
Q

What is an acute acute phase protein that is synthesised during early events of inflammation?
What is it cleaved to?
What pathways activate the cleaving of this?

A 
C3
C3b and C3a
Classical pathway
Mannose-binding lectin pathway
Alternative pathway
75
Q

What does activation of downstream complement proteins cause?

A

Pathogen killing
Pathogen opsonisation
Leukocyte recruitment and inflammation

76
Q

What is the mannose-binding lectin pathway of complement activation?

A

Mannose-binding lectin (an acute phase protein) binds to mannose on bacterium
This causes C4b joined to C2a to convert C3 to C3a and C3b stimulating downstream events

77
Q

What is the alternative pathway of complement activation?

A

C3 spontaneously breaks down to C3a and C3b
C3b is then either rapidly degraded or binds to bacterium via ligands
Factor B then binds to the C3b attached to the bacterium which then causes factor D to join on too
This then causes more C3 to breakdown in an amplification loop leading to downstream events

78
Q

What does C3b do?

A

Converts C5 to C5b and C5a (C5a causes killing, etc. whist C5b assembles on the surface of the pathogen with C6, C7, C8 and C9 to form the membrane attack complex)
This causes osmotic cell lysis

79
Q

What complement protein acts as an opsonin?

A

C3b

80
Q

What are C3a and C5a also known as?
Why?
How do they do this?

A

Anaphylatoxins
Act directly on blood vessels causing increased permeability
Act on mast cells causing release of pro-inflammatory mediators and chemokines

81
Q

What type of complement proteins are active?

A

Cleaved complement proteins

82
Q

Half life of cleaved complement proteins?

A

Very short

83
Q

What do dendritic cells act as?

A

The bridge between the innate and adaptive immune systems?

84
Q

What do dendritic cells do?

A

Present in peripheral tissues in an immature state
Phagocytose antigens, cell debris, particles, mature and migrate into secondary lymphoid tissues where they play a key role in antigen presentation

Study Notes - Principles (39 decks)

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