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Immunology > 2. Innate Immunity > Flashcards

2. Innate Immunity Flashcards

1
Q

aim of innate immune response

A

limit spread, eliminate microorganisms and repair damage

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2
Q

aim for adaptive immunity

A

to clear pathogens and produce a memory response

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3
Q

Cells of the innate immune system

A

Phagocytes (neutrophils, monocytes, macrophages, mast cells, eosinophils), antigen presenting cells (monocytes, macrophages and dendritic cells) and other immune cells (NKCs, ILCs, NKTCs)

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4
Q

four main types of defensive barriers/features

A

anatomical, physiological/chemical, phagocytic/endocytic, inflammatory

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5
Q

examples of anatomical defence barriers

A

skin, mucosa

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6
Q

how is skin used as a defence barrier

A

sloughing of dead skin, acidic (pH3-5), commensal microflora that secrete bacteriocins

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7
Q

how are mucosal surfaces used a defence barriers?

A

cilia propulsion, entrapment, flow of secretions, competition by commensal bacterial, tight junctions

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8
Q

examples of physiological/chemical defences

A

temperature (fever), low pH (stomach, skin), chemical mediators/antimicrobial proteins

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9
Q

Protein examples

A

Lysozyme, Lactoferrin, Psoriasin, Surfactant P

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10
Q

lysozyme

A

found in tears/saliva that cleaves peptidoglycans of bacterial cell walls

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11
Q

Lactoferrin

A

Binds to essential nutrients, inhibiting bacterial and fungal growth

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12
Q

S100 proteins e.g. Psoriasin

A

secretions and on skin, Disrupts microbial cell membranes

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13
Q

Surfactant Proteins

A

respiratory tract, block bacterial surface components

by binding to them, have a lubricating function

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14
Q

Peptide examples

A

Defensins, Cathelicidins, Histatin, Dermicidin

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15
Q

Defensins

A

bind negatively charged microbial structures, Aggregate to form pores in cytoplasmic membrane, activate complement pathway, found in neutrophil granules

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16
Q

Cathelicidins

A

disrupt microbial membranes

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17
Q

what did Metchnikoff use to study phagocytosis?

A

daphnia and starfish larvae

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18
Q

examples of endocytosis

A

Pinocytosis
Macro-pinocytosis
Receptor-mediated endocytosis
Phagocytosis

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19
Q

which type of endocytosis is used by most cells?

A

pinocytosis and receptor-mediated

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20
Q

pinocytosis

A

Cell drinking. aids osmoregulation. non-specific

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21
Q

Macro-pinocytosis

A

larger gulps of cell drinking. Aids in processing of Antigens for an immune response

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22
Q

Receptor-mediated endocytosis

A

specific uptake of ligand, growth factor, hormone, immune complex via a receptor. clathrin associated

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23
Q

Phagocytosis

A

internalise, kill/destroy/digest particulate matter

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24
Q

phagocytic cell types

A 
Monocytes/Macrophages
Neutrophils
Dendritic cells 
Eosinophils
B cells/Mast cells
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25
Q

stages of phagocytosis

A 
1- Recognition
2- Ingestion
3- Digestion
4- Exocytosis –
also presentation 
and storage
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26
Q

direct recognition

A

non-opsonic - Pattern Recognition Receptors (PRRs) on phagocytes bind to Pathogen Associated Molecular
Patterns (PAMPs) or to Damage Associated Molecular Patterns (DAMPs) on particles/microbes

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27
Q

indirect recognition

A

opsonic - Receptors on phagocytes bind to opsonins coating the surface of particulate matter/microbes

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28
Q

examples of PAMPs

A

bacteria - cell wall components, flagella. viral glycoproteins, fungi

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29
Q

examples of DAMPs

A

necrosing cells (ssRNA release), short-chain fatty acids in diet, apoptosing cells (PS, RNA, vitronectin)

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30
Q

C type lectin receptors

A

Mannose Receptor, Dectin-1, DC-SIGN

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31
Q

Mannose Receptor

A
  • Binds to mannose/fucose/α mannan
  • On surface of most Mφs and DCs
  • Has 8 extracellular domains and cytoplasmic tail
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32
Q

Dectin-1

A
  • Binds β1-3 glucan on fungi and bacteria

* Expressed on a wide variety of myeloid lineage cells

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33
Q

DC-SIGN

A

• Binds mannans on bacteria, fungi and parasites

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34
Q

Scavenger receptors

A

SR-A and B

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35
Q

SR-A

A

• Found on all macrophages & some endothelial cells, binds modified low-density lipoprotein e.g. oxidised LDL

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36
Q

SR-B

A

• Includes CD36 found on endothelium, DC, platelets, MC & MF
• Binds variety of altered ‘self’ molecules such as
oxidised LDL or vimentin on the surface of apoptotic cells
• Also recognise some PAMPs

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37
Q

Toll-like receptors

A

Toll gene identified in

Drosophila, Leucine rich repeats of external domain,

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38
Q

intracellular TLRs

A

detect DNA/RNA associated with viruses
and strongly induce type I interferons –
cytokines with antiviral effects

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39
Q

extracellular TLRs

A

expressed mainly by immune cells and are strongly

associated with bacterial/fungal infections

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40
Q

which cell types express all TLRs?

A

monocytes, macrophages, dendritic cells

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41
Q

which type of TLR do B cells, T cells and granulocytes express?

A

TLR4

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42
Q

NOD-like receptors (NLRs)

A
  • Family of 23 members divided into 3 main groups (B,C and P)
  • Interact with intracellular PAMPs and DAMPs
  • Activate the NFkB pathway and autophagy
43
Q

RIG-like receptors

A
  • Bind viral dsRNA and so detect viral replication

* Initiate anti-viral cytokine (type 1 interferons)

44
Q

AIM2–like receptors (ALRs) and cGAS/STING

A

• Bind DNA molecules from bacteria and viruses
• Induce production of anti-viral and inflammatory
cytokines

45
Q

inflammasome

A

NLRs and ALRs clump together to initiate pro-inflammatory cytokine production

46
Q

pyroptosis

A

self-death by pro-inflammatory cytokines

47
Q

pro-inflammatory cytokines

A

Interleukin-1 and 18

48
Q

examples of opsonins

A

IgG (antibody), fragments of Complement & lectins

49
Q

antibody receptors

A

Fc. Recognise the constant region

(i.e. not antigen binding) of antibodies

50
Q

complement receptors

A

Bind to components of the classical, alternative and lectin complement
pathways

51
Q

examples of complement receptors

A

CR1, CR2, CR3, CR4, C3a/4a and C5aR

52
Q

process of phagocytosis

A

pseudopodia form & surround particle, fuse
engulfing particle in membrane-bound vesicle. requires energy and cytoskeletal rearrangement (surface receptors need to cluster)

53
Q

Oxygen Independent digestion

A
  • Acidification
  • Lysozyme
  • Other enzymes
  • Defensins
  • Lactoferrin
  • Cathelicidins
  • S100 proteins
54
Q

Oxygen Dependent digestion

A

• Reactive oxygen
intermediates
• Reactive nitrogen
intermediates

both lead to respiratory burst

55
Q

Other oxygen independent Enzymes

A

• Acid hydrolases: phosphatases, sulphatases, glycosidases,
deoxyribonucleases
• Lipases: eg phospholipase A2
• Neutral proteases: collagenases, elastase, cysteine proteases

56
Q

examples of free radical scavengers

A

Catalase, superoxide dismutase and glutathione

57
Q

what can ROI and RNI damage?

A

proteins, lipids, DNA and cell membranes

58
Q

how does ROI cause respiratory burst?

A

Rapid increase in O2 consumption, surge of targeted activity in phagosomes and
phagolysosomes, free radical reactive to microbial components

59
Q

how does RNI cause respiratory burst?

A

inducible Nitric oxide synthase (iNOS)
activated by microbial products and some
cytokines, expression in vasculature and neurones, argenine oxidised to citrulline and nitric oxide within phagocytes

60
Q

professional phagocytes

A

macrophages, monocytes and neutrophils

61
Q

where are ROI/RNI found in professional phagocytes?

A

macrophages/monocytes - lysosomes

neutrophils - primary and secondary granules

62
Q

what happens to pathogens that escape digestion stages?

A

undergo pyroptosis or autophagy by intracellular PRR recognition

63
Q

what happens to products of phagocytosis?

A

Heavy metals tend to be
‘stored’ and PAMPs and DAMPs once processed are often presented to the adaptive
immune response

64
Q

5 hallmarks of inflammation

A

rubor (redness) et tumor (swelling) cum calor (heat) et dolor
(pain), & loss of function (functio laesa)

65
Q

purpose of inflammation

A 
increasing 
blood flow, permeability of 
vasculature – allowing leukocyte 
migration
to aid limiting the spread of 
infection, tissue damage and to 
promote healing
66
Q

NETs

A

Neutrophil Extracellular Traps

67
Q

immune cells that produce inflammatory mediators

A

Mast cells, Basophils and Macrophages

68
Q

examples of inflammatory mediators

A 
• Prostaglandins, Leukotrienes,
• Histamine
- thromboxanes
• Cytokines
• Chemokines
69
Q

Cytokines

A

movement of cells

70
Q

interleukin

A

communication/messaging between white blood cells

71
Q

Chemokines

A

movement towards a

chemical

72
Q

interconnected mediator producing

systems

A

kinin, clotting, fibrinolytic and complement

73
Q

examples of cytokines

A

Interleukin-1, 6, 8, 10, 12 (IL-1, IL-6 etc), Tumour
necrosis factor a (TNF-a), Transforming growth factor β (TGF-β)
and interferon γ (IFNg)

74
Q

alarm cytokines

A 
IL-1, IL-6 and TNFα
- causing local 
and systemic activation of fever, 
increased vascular permeability, 
production of acute phase 
proteins and increased 
adhesion molecule expression
75
Q

anti-inflammatory cytokines

A

IL-10 and transforming growth factor beta (TGF-β)

- down-regulate responses

76
Q

IL-12 and IL-18

A

induce the differentiation of pro-inflammatory subset of T

cells

77
Q

IL-8

A

potent chemokine for neutrophils

78
Q

IFNγ

A

contributing to chronic inflammation

by recruiting Mφs to sites of damage/infection

79
Q

(IFNa and b)

A

have antiviral properties within

infected cells

80
Q

protein structure of chemokines

A

4 cysteine residues & sequence of amino

acids involving first two of these

81
Q

Chemotaxis

A

migration & activation of

range of cells towards the source (along a concentration gradient)

82
Q

Eicosanoids

A

unsaturated fatty acids derived from
arachidonic acid
- e.g. Prostaglandins, Leukotrienes and Thromboxanes

83
Q

Kinin system

A

• Hageman factor (Factor XII) activated following tissue injury
• Activates pre-kallikrein to form kallikrein which cleaves kininogen
to form Bradykinin
• Bradykinin = basic protein that increases vascular permeability,
causes vasodilation, pain and contraction of smooth muscle

84
Q

Clotting system

A

• Hageman factor activated following
tissue injury
• Activated by damage to blood vessels
and leads to large amounts of Thrombin
• Thrombin then acts on soluble fibrinogen….fibrin and clot
formation and fibrinopeptides which increase vascular
permeability and neutrophil chemotaxis

85
Q

Fibrinolytic system

A

• Triggered by damage to endothelial cells and
activation of Hageman factor
• Removes clots from the injured tissue
• Active end product = plasmin
• Plasmin is a potent proteolytic enzyme which
breaks down the fibrin clots into degradation
products which are chemotactic for neutrophils
• Also contributes further to inflammation by activating
the classical complement pathway
• Important to block leakage & repair, must maintain
circulation – fibrinolytic system

86
Q

3 activation pathways of complement cascade

A

classical, lectin and alternative

87
Q

3 major outcomes of complement cascade

A 
Opsonise particles to increase 
phagocytosis
Regulate inflammatory & 
immune responses
Lyse target cells and 
microorganisms
88
Q

MAC and its components

A

membrane attack complex - C5b, C6, C7, C8 and polyC9

89
Q

activation of classical pathway

A

Antibody (IgG or IgM) or c reactive protein (CRP) binds to antigen and attracts C1

90
Q

what metal ion is needed in complement cascades?

A

Mg2+

91
Q

what stabilises C3bBb?

A

properdin

92
Q

activation of alternative pathway

A

spontaneous cleavage of C3 - autohydrolysis due to being an unstable inactive precursor

93
Q

activation of lectin pathway

A

mannose binding leptin associated with serine proteases

94
Q

ILC1 + NKs

A

secrete pro-inflammatory TH1-like cytokines (IFNg and TNFa)

95
Q

ILC1

A

immunity to

extracellular pathogens

96
Q

NKs

A

immunity to intracellular pathogens and tumour cells

97
Q

ILC2

A

immunity to worms, wound healing, secrete TH2

type cytokines that activate eosinophils

98
Q

ILC3

A

lymphoid tissue development, intestinal health,
immunity to extracellular bacteria and fungi, secrete
regulatory cytokines

99
Q

3 mechanisms of target cell killing

A
  1. kill targets using perforins
  2. express Fas ligand to induce apoptosis
  3. antibody dependent cellular cytotoxicity
100
Q

how do eosinophils kill target cells?

A

Granules contain Cationic peptides, Major
basic protein and Peroxidase all of which
can be released directly onto the surface
of extracellular pathogens (worms) - do not phagocytose

101
Q

g/d T cells

A

Important in gut antigen recognition of bacterial antigens (particularly
lipids) through non MHC restricted means (CD1)

102
Q

B1 cells

A

B cells expressing CD5 - Mainly produce low affinity antibody (IgM) mostly against
bacterial antigens (particularly carbohydrates) and are called
natural antibodies

103
Q

receptors for opsonins

A

antibody receptor (Fc region), complement receptors - mainly CR1,3,4

104
Q

acute phase protein examples

A

c-reactive protein, mannose binding lectin, serum amyloid a

Immunology (9 decks)

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