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mimm 214 midterm > Innate Immunity > Flashcards

Innate Immunity Flashcards

Basics, Phagocytosis, Complement, Cell Migration, PRR & Signaling, Inflammatory Cytokines, ILCs & NK cells

1
Q

Where do pathogens enter from?

A

Mucosal and epithelial surfaces

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2
Q

What surfaces provide the first barrier against infection?

A

Epithelial surfaces such as skin, gut epithelium, respiratory epithelium and mucosal membranes

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3
Q

What are some mucosal membranes?

A

Saliva, hair, mucus, tears

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4
Q

What protective substances do epithelial layers produce?

A

Acidic pH, antimicrobial peptides

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5
Q

Which cells are part of the innate immunity?

A

Neutrophils, granulocytes, monocytes, macrophages, dendritic cells, NK cells and ILCs

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6
Q

What are some key molecules?

A

Antimicrobial enzymes/peptides and complement

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7
Q

What are the stages of a response to an infection?

A

Pathogens adhere to epithelium
Local infection of tissues
Adaptive immunity

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8
Q

What is phagocytosis?

A

Engulfment and internalization of pathogens or their components upon their binding to receptors on the cell surface of phagocytes

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9
Q

Which phagocytes mediate phagocytosis?

A

Macrophages, dendritic cells, neutrophils

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10
Q

What does phagocytosis lead to?

A

Removal of pathogens, clearing debris, generation of peptides for presentation to T cells

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11
Q

True or false: All PRRs induce phagocytosis

A

False, many receptors that mediate phagocytosis are PRRs

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12
Q

How does phagocytosis occur indirectly?

A

Opsonization via opsonins (soluble pattern-recognition proteins)

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13
Q

What are the steps of phagocytosis?

A
  1. Receptors interact with ligand
  2. Membrane protrusions (pseudopodia) extend
  3. Bacterium is ingested and produces phagosome
  4. Phagosome fuses with lysosome and produces phagolysosome
  5. Phagolysosome acidifies, acquires antimicrobial peptides and enzymes to kill pathogens
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14
Q

What do neutrophils contain?

A

Primary and secondary granules

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15
Q

What do phagolysosomes contain?

A

Low pH, hydrolytic enzymes, oxidative attack (ROS and RNS), antimicrobial peptides

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16
Q

What is the purpose of oxidative attack on phagocytosed pathogen?

A

ROS damages microbial membranes and generates NADPH oxidase enzyme complex to increase O2 consumption and lead to respiratory burst

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17
Q

How do phagocytes clear cells that have undergone apoptosis?

A

DAMPs are recognized by PRRs

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18
Q

What is a result of dead and dying neutrophils?

A

Pus

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19
Q

What are NETs?

A

Neutrophil extracellular traps that capture microorganisms and prevent spread

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20
Q

What is a complement?

A

Group of soluble proteins that cooperate with both the innate and adaptive immunity to eliminate pathogens

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21
Q

What is a protease?

A

Enzyme that performs proteolysis

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22
Q

What characterizes a protease?

A

C followed by a number, “factor” followed by capital letter

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23
Q

Where are complement proteins produced?

A

Liver

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24
Q

What are the key mechanisms of action of the complement system?

A

Inflammation, destroying pathogen cell membranes, opsonization

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25
Q

How does complement get activated?

A

3 ways: Classical, lectin and alternative pathways

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26
Q

What does proteolytic cleavage generate?

A

One small fragment (a) with specific function, one large fragment (b) with proteolytic activity

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27
Q

What are the two C3 convertases and what are their role?

A

C4b2a and C3bBb
Cleave C3 into C3a and C3b

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28
Q

What are the functional categories of complement proteins?

A

Initiators and convertase activators

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29
Q

What are the downstream effects of the complement system?

A

Opsonins, MAC, anaphylatoxins

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30
Q

What triggers lectin pathway?

A

PRRs such as lectins (MBL and ficolins)

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31
Q

What do the lectins do?

A

They bind to the surface of pathogens and trigger signaling cascades
C3 convertase is generated (C4b2a) and cleaves C3

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32
Q

What triggers classical pathway?

A

C1q binds to pathogen surface and also to antibodies that are bound to pathogen surface

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33
Q

True or false: The classical pathway can connect adaptive to innate

A

True

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34
Q

What happens when C1q binds?

A

Triggers signaling cascade on pathogen surface
C3 convertase is generated (C4b2a) and C3 is cleaved

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35
Q

What are C3a and C3b involved in?

A

C3a: inflammation
C3b: opsonization and C5 convertase (C5a and C5b)

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36
Q

In which pathway are factor B and protease factor D required?

A

Alternative pathway

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37
Q

What happens in the alternative pathway when C3b has been produced?

A

Amplification loop for C3b formation that requires factor B and protease factor D
C3bBb is generated (C3 convertase)

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38
Q

When there is a high concentration of C3…

A

C3 undergoes spontaneous hydrolysis, which also involves factor B and D

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39
Q

What stabilizes C3bBb?

A

Factor P secreted by neutrophils

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40
Q

Which complement proteins promote inflammation?

A

C3a and C5a

41
Q

What do C3aR and C5aR on granulocytes do?

A

They stimulate release of proinflammatory cytokines and granule components from basophils, eosinophils, neutrophils and mast cells

42
Q

How is increased phagocytosis made possible?

A

Phagocytes have receptors for C3b

43
Q

Which complement factors are involved in the formation of MAC?

A

C5b directly and C3b indirectly (C5 convertase)

44
Q

What does MAC do?

A

Cell lysis

45
Q

What prevents complement activation?

A

Complement-regulatory proteins

46
Q

Which cells have PRRs?

A

All types of myeloid white blood cells and lymphoid cells

47
Q

Cytosolic sensors of viral nucleic acids are expressed by which cells?

A

All cells of the body

48
Q

Where are PRRs located?

A

Cell surface, intracellular or secreted

49
Q

Where are TLRs located?

A

Cell surface and intracellular

50
Q

What do extracellular and intracellular TLRs recognize?

A

Extracellular: bacteria
Intracellular: virus

51
Q

What events do the adaptor proteins that TLRs recruit lead to?

A

NF-kB transcription factor, IRF transcription factor, AP-1 transcription factor from MAP kinase pathway

52
Q

What are the adaptor proteins involved in TLRs?

A

MyD88 & TRIF

53
Q

What is a key event in the activation of transcription factors?

A

Phosphorylation

54
Q

What are the steps of a signal transduction?

A

Ligand-induced receptor dimerization, recruitment of adaptors, second messengers, activation of TFs, changes in gene expression, post-transcriptional or post-translational modifications, functional response

55
Q

Where are CLRs located?

A

Cell surface

56
Q

What do CLRs bind?

A

Carbohydrates on pathogens and some allergens

57
Q

What triggers CLR signaling cascades?

A

Activated tyrosine kinases (CARD adaptor protein, IRF5 activation, MAPK pathways activation)

58
Q

What transcription factors are produced from CLRs?

A

AP-1 and NF-kB

59
Q

What do the activated tyrosine kinases induce?

A

Expression of inflammatory cytokines

60
Q

Where are RLRs located?

A

Cytosol

61
Q

What do RLRs recognize?

A

Viral double-stranded RNAs and certain structured single-stranded RNA

62
Q

What triggers signaling pathways in RLRs?

A

MAVS

63
Q

What transcription factors are produced by RLRs?

A

IRFs and NF-kB

64
Q

Where are NLRs located?

A

Cytosol

65
Q

What do NLRs recognize?

A

Peptidoglycan from bacterial cell wall

66
Q

What TFs are produced from NLRs?

A

AP-1, NF-kB and IRFs

67
Q

Which protease cleaves IL-1beta/IL-18 into active forms?

A

Caspase-1

68
Q

True or false: Caspase-1 is not involved in a post-translational modification

A

False, it is

69
Q

What does ubiquitination involve?

A

Attachment of ubiquitin to a target protein, which can mediate their formation for further signaling

70
Q

What are the effects of PRR signaling?

A

Cytokine production and chemokine production, increased expression of costimulatory molecules, enhanced migration to secondary lymphoid organ

71
Q

Which cytokines are responsible for inflammation?

A

IL-1, IL-6, IL-18, TNF-alpha, IL-12

72
Q

Which cytokines are responsible for potent antiviral effects?

A

Type I IFN

73
Q

Which chemokines are produced in PRR signaling?

A

CC and CXC chemokines

74
Q

What is the role of costimulatory molecules?

A

Providing SIGNAL 2 to T cells in lymphoid tissue

75
Q

What is the result of type I IFN signaling?

A

Transcription of genes, leading to inhibition of viral replication

76
Q

How do monocytes migrate to the site of infection?

A

They bind to adhesion molecules

77
Q

What are the families of adhesion molecules?

A

Selectins, integrins, immunoglobulin superfamily

78
Q

What are the steps of migration?

A

Rolling adhesion, tight binding, diapedesis, migration

79
Q

What is diapedesis?

A

Cell crossing from the lumen of a vessel

80
Q

Cytokines affect the behavior of…

A

Autocrine, paracrine and endocrine cells

81
Q

What are the biological functions of cytokines?

A

Activation, proliferation, differentiation and survival of target cells

82
Q

What is cascade induction?

A

The action of a cytokine on a target cell induces that cell to produce one or more additional cytokines

83
Q

What are the five major groups of cytokines?

A

IL, IFN, TNF, growth factors, chemokines

84
Q

Explain the complex network of cytokines

A

One cytokine can be produced by many cells and each cell type can produce different cytokines

85
Q

What is cell-mediated immunity directed to?

A

Viral infections

86
Q

What is humoral-mediated immunity directed to?

A

Extracellular bacteria

87
Q

What is the role of TNF-alpha?

A

Inflammation

88
Q

What does TNF-alpha stimulate?

A

Migration of innate cells, dilating blood vessels and increasing clotting

89
Q

What does SEPSIS stand for?

A

Systemic infection and inflammation

90
Q

What induces the acute phase response?

A

Proinflammatory cytokines

91
Q

What characterizes the acute phase response?

A

Increased synthesis or secretion of antimicrobial proteins from the liver

92
Q

What does a fever caused by IL-1beta, IL-6, TNF-alpha bring about?

A

Increased body temperature

93
Q

True or false: NK cells share a common progenitor with B and T cells

A

True

94
Q

How many types of ILC exist?

A

Three

95
Q

What is the difference between ILCs and NK cells?

A

ILCs contribute to the defense against certain pathogens
NK cells directly kill cells

96
Q

NK cells express receptors for self proteins that can be induced by…

A

Infections, malignant transformations, other stresses

97
Q

What kind of receptors do NK cells have?

A

Activating and inhibitory

98
Q

What do NK cell receptors recognize?

A

MHC class I and MHC class I-like molecules on target cells

99
Q

How do NK cells trigger apoptosis?

A

Granules via signaling from the receptor

mimm 214 midterm (3 decks)

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