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MIMM214 > Innate immunity > Flashcards

Innate immunity Flashcards

1
Q

How do pathogens cause infection?

A

they enter the body by breaching an epithelial or mucosal barrier

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2
Q

name 4 epithelial surfaces providing first barrier of defence against infection

A

skin, gut epithelium, respiratory epithelium, mucosal membranes

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3
Q

name 2 protective substances that epithelial layers produce?

A

acidic pH, antimicrobial peptides

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4
Q

name the 4 major categories of innate immunity cellular elements

A

granulocytes (neutrophils)
monocytes & macrophages
dendritic cells
NK and ILCs (innate lymphoid cells)

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5
Q

name the 4 main stages of an infection and its response

A
  1. pathogens adhere to epithelium
  2. local infection, penetration of epithelium
  3. local infection of tissues
  4. adaptive immunity
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6
Q

name the 3 types of cells mediated by phagocytes

A

macrophages, neutrophils, immature dendritic cells

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7
Q

what can dendritic cells and macrophages do through phagocytosis (other than removing pathogens)?

A

generation of antigenic peptides for presentation to T cells

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8
Q

what are called soluble proteins bound to microbial surfaces for pathogen recognition? what do they do?

A

opsonins or soluble pattern-recognition proteins
enhance phagocytosis (opsonization)

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9
Q

give an example of opsonins

A

antibodies

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10
Q

what are called membrane protrusions that extend from phagocytes?

A

pseudopodia

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11
Q

what are called large membrane-enclosed endocytic vesicles?

A

phagosomes

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12
Q

what do phagosomes fuse with? what does that form?

A

they fuse with lysosomes to form phagolysosomes

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13
Q

what happens in phagolysosomes to kill microbe?

A

acidification and acquiring of antimicrobial peptides and enzyme

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14
Q

what 4 things are contained in phagolysosomes that kill microbes?

A

antimicrobial proteins and peptides, low pH, hydrolytic enzymes, oxidative attack

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15
Q

What’s an oxidative attack?

A

phagocytes generate ROS with their NADPH oxidase enzyme complex. ROS increase oxygen consumption causing a respiratory burst

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16
Q

what does DAMPs stand for and what does it signal

A

damage-associated molecular patterns -> signal dying cell

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17
Q

what does CD47 signal? what type of cells express a LOT of CD47?

A

healthy erythrocytes (inhibits phagocytosis)
tumour cells

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18
Q

what type of innate immune cells are neutrophils?
where do they reside?
what can they produce?

A

phagocytes
reside in the circulation
produce extracellular matrix NETs

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19
Q

what are microglia also called?
what are they responsible for?
what do they recognize?

A

macrophages of the brain: important for establishing proper neuronal connections
recognize DAMPs

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20
Q

what are the 4 main stages of phagocytosis?

A
  1. PRRs recognize DAMPs and pseudopodia appear
  2. bacterium injested in phagosome
  3. fusion with lysosome = phagolysosome
  4. bacterium is killed and digested by enzymes
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21
Q

describe complement system

A

soluble proteins that cooperate with the innate and adaptive immune system to eliminate pathogens.
mainly proteases

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22
Q

what are the 3 main functions of complements?

A

increase vascular permeability and chemotaxis, destroy pathogen cell membrane, opsonization

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23
Q

what do complements start as?

A

inactive pro-proteases

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24
Q

what does proteolytic cleavage of pro-proteases generate?

A

small fragment: a; specific function
large: b; proteolytic activity (cascade)

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25
Q

name the 2 C3 convertases

A

C4b2a and C3bBb

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26
Q

what are lectins? what PRRs trigger the lectin activation pathway?

A

lectins: circulating PRRs
Mannose-binding lectin MBLs or Ficolins

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27
Q

lectin pathway and classical pathway activation

A

C4b2a (C3 convertase) cleaves C3 into C3a and C3b. happen on pathogen surface

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28
Q

what does C1q binds to? what does it trigger?

A

C1q binds to pathogen or to antibodies on pathogen
Triggers signalling cascade of classical pathway or links to adaptive immunity

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29
Q

what are C3a and C3b functions?

A

C3a = inflammation
C3b = opsonization; is a C5 convertase

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30
Q

describe the alternative pathway

A

factor B and protease factor D:
amplification loop of C3b (C3bBb)
C3 spontaneous hydrolysis

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31
Q

what factor stabilizes C3 convertase C3bBb from the alternative pathway?

A

properdin (factor P) secreted by neutrophils
stabilizes by binding to microbial surfaces

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32
Q

what’s C3 convertase’s role?

A

cleave C3

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33
Q

which complements trigger inflammation? and what else do they do?

A

C3a and C5a recruit phagocytes

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34
Q

what happens if there is too much C3a and C5a?

A

anaphylactic shock

35
Q

how do C3a and C5a promote inflammation?

A

bind to C3aR and C5aR on granulocytes to stimulate proinflammatory cytokines and granule release from basophils, eosinophils, neutrophils and mast cells

36
Q

which complements are involved in membrane attack?

A

C5b (directly involved) and C3b (indirectly involved)

37
Q

negative regulation of complement

A

complement-regulatory proteins prevent appearance and promote disappearance of C3 convertase

38
Q

what complement-regulatory protein inhibits MAC formation?

A

protectin (CD59)

39
Q

what does PAMPs stand for

A

Pathogen-Associated Molecular Patterns

40
Q

what cells express PRRs?

A

myeloid white blood cells (neutrophils, basophils, eosinophils, granulocytes, mast cells, macrophages)
T cells, B cells, NK cells

41
Q

name groups of PRRs

A

toll-like r, NOD-like r, RIG-like r, C-type lectin r, ficolins, MBL, ..

42
Q

how do TLRs work?

A

bind PAMPs with adaptor proteins -> signaling cascade -> phosphorylation -> activates TFs -> transcription of innate immune/pro-inflammatory genes

43
Q

Name the key adaptor proteins and TFs that work with TLRs

A

adaptor proteins = MyD88 & TRIF
transcription factors = IRF3/7, NF-kB, AP-1

44
Q

describe C-type Lectin receptors

A

membrane receptors that bind carbohydrates on pathogen and allergens

45
Q

describe the CLRs signaling cascad

A

binding -> activates tyrosine kinase -> CARD adaptor protein -> IRF5 activation -> MAPK pathway -> AP-1 and NF-kB(TF) activation

46
Q

describe RIG-I-like receptors RLRs

A

cytosolic PRRs that binds viral dsRNA -> activates mitochondrial signaling protein MAVS -> activates IRFs and NF-kB (TFs)

47
Q

describe NOD-like receptors NLRs

A

(NOD = nucleotide oligomerization domain)
cytosolic PRRs that recognize peptidoglycan from bacteria cell wall & triggers NF-kB, AP-1, and IRF signaling and activates caspase-1 protease -> triggers pro-inflammatory cytokines release (post-translational modification)

48
Q

name the cytokines produced from PRR signaling involved in inflammation

A

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

49
Q

name the cytokines produced by PRR signaling that have antiviral effect

A

Type 1 IFN (IFN-alpha, IFN-beta)

50
Q

what are 2 costimulatory molecules who’s expression is increased through PRR signaling and what do they do

A

B7.1 (CD80), B7.2 (CD86); do 2nd signal of t cell activation

51
Q

how does PRR signaling help moving stuff around the cell

A

enhance migration to secondary lymphoid organs (targets DCs to lymphoid tissue) and upregulates adhesion molecules

52
Q

how do type 1 interferon work

A

PRR signal = IFN secretion = triggers more signaling = more transcription of genes that help kill virus

53
Q

name the transcription factors that get activated through PRR signaling

A

NF-kB, IRFs, AP-1

54
Q

which interferon deficiency leads to severe Covid-19?

A

Type 1 IFN

55
Q

summary what are the 6 effects of PRR signaling?

A

cytokine secretion, chemokine secretion, receptor expression, migration, costimulation, expression of other genes

56
Q

where are adhesion molecules located?

A

different locations! some only on activated endothelium, some are everywhere

57
Q

what are the adhesion molecules that slow down leukocytes on vascular epithelium?

A

selectin

58
Q

what can severe or chronic inflammation cause?

A

arthritis or loss of function

59
Q

what are the 4 steps of migration

A

rolling adhesion, tight binding, diapedesis, migration

60
Q

what kind of molecules are cytokines?

A

small mostly soluble heterogeneous glycoproteins

61
Q

what is cytokine’s main role?

A

cellular communication

62
Q

in what 3 ways can cytokines act?

A

autocrine, paracrine, endocrine

63
Q

name 4 examples of function of cytokines?

A

change adhesion molecules/chemokine receptors expression
increase/decrease enzyme activity
activate B and T cells
cascade induction

64
Q

what are the 5 major cytokines groups?

A

interleukins, interferons, tumor necrosis factors TNF, growth factors, chemokines

65
Q

what is pleiotropism?
what is redundancy?

A

Pleiotropism: one molecule (ex cytokine) may be produced by many different cell types and have effects on many different cell types
Redundancy: different molecules (ex cytokines) may have the same effect

66
Q

what is synergy?
what is antagonism?

A

Synergy: many (cytokines) work togther to induce an effect
Antagonism: one (cytokine) can inactivate the effect of another

67
Q

how are cytokines related to adaptive immune response?

A

they tell which adaptive immune response to use (cell-mediated or humoral)

68
Q

describe cell-mediated immunity

A

mostly directed to viral infections and intracellular pathogens
is characterized by macrophage and cytotoxic T lymphocyte activation

69
Q

describe humoral immunity

A

mostly directed to extracellular pathogens/bacteria
is characterized by B cell activation and antibody production

70
Q

What is the main cytokine involved in inflammation? what secreted it? how does it work? what 2 diseases is it involved in?

A

TNF-alpha
- secreted by macrophages
- stimulates vasodilation, clotting, innate cells migration
- involved in Rheumatoid arthritis and Crohn’s disease

71
Q

what is sepsis?

A

systemic infection and inflammation caused by TNFalpha

72
Q

what happens with a systemic infection?

A

macrophages are activated in the liver and spleen -> TNF-alpha secreted in bloodstream -> decreased blood volume -> vessels collapse -> spreaded coagulation -> wasting, organ failure -> death

73
Q

describe acute phase response

A

increased production and secretion of antimicrobial proteins from liver, such as MBL, complement, C-reactive protein
- induced by pro-inflammatory cytokines working synergically

74
Q

what can C-reactive proteins do?

A

can opsonize bacteria and induce complement classical pathway activation

75
Q

what is special about natural killer cells?

A

they share a common lymphoid progenitor with B and T cells but are innate lymphoid immune cells

76
Q

what is unique to ILCs and NK cells compared to other lymphoid myelage cells?

A

they are not antigen specific

77
Q

where are ILCs?
How do they get activated?
what do they do?

A

they reside in tissues (and lymphatic vessels lwk).
they are activated by cytokines (no PRRs) produced by other innate cells or DCs.
they contribute to defense against specific pathogens by secreting cytokines.

78
Q

where are NK cells?

A

mainly in circulation, sometimes in tissue

79
Q

what activates NK cells?

A

infection, malignant transformations, other stresses

80
Q

what can NK cells do?

A

kill altered self cell, or produce cytokines that induce adaptive responses against altered self cell

81
Q

describe NK cell’s receptors

A

Germline encoded
Inhibitory (prevent NK activation) or activating
Recognize MHC class 1

82
Q

what binds to NK cell’s inhibitory receptor?

A

MHC class 1 (present on healthy cells)

83
Q

what are the 2 ways how NK cells can kill altered self cell

A

via granules that trigger apoptosis, or express a TNF that gets recognized by target cell receptor and triggers apoptosis

84
Q

what induces acute phase response?

A

proinflammatory cytokines (IL-1, IL-6, TNFalpha)

MIMM214 (5 decks)

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