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Basic Immunology- Module 1 > Cell Death and immunological implications > Flashcards

Cell Death and immunological implications Flashcards

1
Q

What are the functions of cell death in normal circumstances?

A

tissue homeostasis; embryogenesis; cell turn-over

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2
Q

What is type I cell death?

A

apoptosis

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3
Q

What characterises apoptosis?

A

nuclear fragmentation; shrinkage and membrane blebbing

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4
Q

what is type II cell death?

A

autophagy

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5
Q

What are the features of autophagy?

A

extensive cytoplasmic vacuolization and lysosomal degradation

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6
Q

What is type III cell death?

A

necrosis

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7
Q

What is necrosis?

A

an accidental death that causes damage

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8
Q

What are the features of necrosis?

A

passive; accidental:trauma; infections; swelling and loss of membrane integrity; evidence of inflammation

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9
Q

When may apoptosis cause inflammation?

A

end-stage apoptosis can have membrane pore formation and thus inflammation

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10
Q

What is seen in early apoptosis?

A

membrane relatively intact, exposure of phophatidylserine

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11
Q

what is karyorrhexis?

A

chromatin condensation

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12
Q

What is pyknosis?

A

nuclear fragmentation

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13
Q

What are hte morphological characteristics of apoptosis?

A

plasma membrane blebbing; mitochondrial depolarisation; nuclear and cytoplasmic condensation; apoptotic bodies

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14
Q

What is a biochemical marker of apoptosis?

A

phosphatidylserine flipping- changes from inner to outer leaflet of hte plasma membrane

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15
Q

How can DNA fragmentation be measured in the lab ?

A

DNA laddering- electrophoresis; DNA strain breaks by TUNEL assay

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16
Q

What is the difference between the caspase induced in intrinsic vs extrinsic pathways?

A

intrinsic pathway: caspase-9 and caspase 3; extrinsic pathway- caspase 8

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17
Q

What is necroptosis?

A

caspase-independent cell death

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18
Q

What protein does necroptosis rely on?

A

RIP1 kinase 3 (receptor interacting protein)

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19
Q

What receptors trigger necroptosis?

A

death receptors eg TNFR1

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20
Q

What events can trigger necroptosis?

A

inflammation; ischaemia-reperfusion injury; thrombosis

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21
Q

What is the inflammasome?

A

a pro-inflammatory protein formed after stimulation of NOD-like receptors, production of an active caspase in the complex processes cytokine proproteins into active cytokines

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22
Q

What triggers ferroptosis?

A

intracellular pertubation notably lipid peroxidation

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23
Q

Waht is ferroptosis characterised by?

A

iron dependent production of reactive oxygen species

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24
Q

Does ferroptosis rely on caspases?

A

no

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25
Q

What process in ferroptosis invovled in?

A

glutamate toxicity on neuron

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26
Q

What is pyroptosis characterised by?

A

cellular swelling and plasma membrane permeabilisation due to gasdermin protein family

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27
Q

What are the similarities and differences between pyroptosis and necrosis?

A

both are very inflammatory however pyroptosis is controlled and the cell doesn’t burst

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28
Q

When doe spyroptosis arise?

A

after canonical and non-canonical activation of hte inflammasome (caspase 1, 3, 4 and 11)

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29
Q

What is found in the cytoplasmic domains of cytokine receptors?

A

JAKs

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30
Q

What transcription factors bind to phosphorylated JAKs on cytokine receptors?

A

STatS

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31
Q

What changes in the neutrophil are associated with NETosis?

A

chromatin decondensation; nuclear membrane disintegration

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32
Q

What is NET formation associated iwth?

A

bacterial clearance; thrombosis; sepsis and SLE

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33
Q

What antimicrobial peptides and released in NET?

A

LL37; human neutrophil peptide

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34
Q

What are NETs composed of?

A

nuetrophil DNA with associated histone; nuetrophil proteases

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35
Q

What is NET formation?

A

release of mitochondrial DNA- host defence mechniams with stimulation of adaptive immune system

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36
Q

What is NETsosi?

A

nuclear collapse with release of nuclear DNA- danger signal triggering inflammation

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37
Q

What is the difference in the mrophology between NET formation and NETosis?

A

NET formation- net-like structure; NETossi- cloud

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38
Q

What is NETotic cell deaht?

A

ROS dependent RCD restricted to haematopoietic cells

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39
Q

What is autophagy?

A

basic catabolic mechanism that involves cell degradation of cellular components through the activation of lysosomes

40
Q

whati sh te function of autophagy?

A

promotes cellular survivla during starvation

41
Q

What is a marker of autophagy?

A

lipidation of LC3

42
Q

Waht disease is autophagy heavily implicated in?

A

Alzheimers

43
Q

What is immunogenic cell death?

A

form of RCD sufficient to activate an adaptive immune response through release of DAMPs

44
Q

What are examples of DAMPs?

A

calreticulin; HMBB1; type I IFN

45
Q

What is cellular senescence ?

A

cells permanently lose their proliferative capacity but are still viable

46
Q

What are the characteristics of cellular senescence?

A

altered chromatin structure; vacuolization; can secrete immunomodulatory proteins

47
Q

Where are lupus autoantigens concentrated?

A

on the surface of apoptotic blebs and bodies

48
Q

What is found on apoptotic bodies?

A

nucleosomes; RO; La; Sm; MUMA; PARP

49
Q

What is found on apoptotic blebs?

A

Ro; ribosomal P; calreticulin; Jo-1

50
Q

What degrades NETs?

A

DNase I

51
Q

What are the completely physiological forms of RCD generally referred t oas?

A

programmed cell death

52
Q

What are apoptotic bodes?

A

formation of intact small vesicles taken up by neighouring cells with phagocytic activity and degraded within lysosomes

53
Q

What is anoikis?

A

specific variant of intrinsic apoptosis initiated by the loss of intergin-dependent anchorage

54
Q

What is autosis?

A

specific instance of autophagy-dependent cell death that critically relies on the plasma membrane Na/K ATPase

55
Q

What is efferocytosis?

A

mechanism whereby dead cells and fragments thereof are taken up by phagocytes and disposed

56
Q

What can inhibit ferroptosis?

A

iron chelators and lipophilic antioxidents

57
Q

What are causes of intrinsic apoptosis?

A

grwoth factor withdrawal; DNA damage; ER stress; ROS overload; replication stress; microtubular alteractions of mitotic defets

58
Q

What is endo-stage apoptosis generally followed by?

A

copmlete breakdown of the plasma membraen and acquisition of a necrotic morphocyte (secondary necorisis)

59
Q

What has end-stage apoptosis linked to?

A

pore-forming activity of gasdermin E

60
Q

What is the critical step for intrinsic apoptosis?

A

irreversible and widespread mitochondrial outer membrane permeabilisation (MOMP)

61
Q

Which BCL2 proteins mediate apoptosis in repsonse to apoptotic stimuli?

A

BAX and BAK

62
Q

Which BLC2 family membrers are able to form pores across the outer mitochondrial membrae?

A

BOK; BAX and BAK

63
Q

What does BID stand for?

A

BH3 interacting domain death agonist

64
Q

What BLC2 proteins antagonise apoptosis?

A

BLC2; BLCxl; MCL1; BCL-W and BFL-1

65
Q

How do the anti-apoptotic proteins oppose apoptosis?

A

by directly binding pro-apoptotic members and preventing their oligomerization and pore-forming activity

66
Q

What does the interaction between pro- and anti-apoptotic proteins rely on?

A

hydrophobic binding groove (mainly)

67
Q

Give examples of BCL2 proteins which bind to anti-apoptotic proteins and limit their availability (sensitisers)

A

BAD; BMF and HRK

68
Q

How is CASP3 invovled in PS flipping?

A

cleaves XKR8 which interacts with BSG and neuroplastin to form a phospholipid-scarmbling complex responsible for PS exposure

69
Q

What else is required for flipping PS aside from hte XKR8:BSG/NPTN complex?

A

ATPase phosphlipid transporting 11a and 11c

70
Q

what other role do executioner caspases carry out, aside from activating CAD?

A

positively or negatively regulate the emission of multiple DAMPs

71
Q

What does death receptor ligation cause?

A

assmebly of a multiprotein complex at the intracellualr tail of the receptor: DISC

72
Q

What does DISC stand for?

A

death-inducing signallign complex

73
Q

What is the function of DISC?

A

molecular platform to regulate the activation and functions of CASP8

74
Q

What drives DISC assmebly in Fas ligation?

A

FADD

75
Q

What is the adaptor in TNFr1 signalling?

A

TRADD

76
Q

What initiates MPT-driven necrosis?

A

severe oxidative stress and cytosolic calcium overload

77
Q

What does the term MPT refer to?

A

abrupt loss of the impermeability of hte IMM to small solutes leading to osmotic breakdown of both mitochondrial membranes and RCD

78
Q

What initiates necroptosis?

A

perturbations of the extracellular or intracellualr microenvironment detected by specific receptors

79
Q

What death receptors are involved in necroptosis?

A

FAS; TNFR1; TLR3 and TLR4

80
Q

What does necroptosis rely on at a molecular level?

A

RIPK3 and MLKL

81
Q

What is the function of phosphorylation of MLKL by RIPK3?

A

MLKL forms oligomers that bind phosphatidylinositol and trigger plasma membrnae permeabilisationand PS exposure

82
Q

What does RIPK3 activation rely upon?

A

formation of a RIPK1 and RIPK3 amyloid like signalling complex:necrosome

83
Q

What is the main regulator of ferooptosis?

A

GPX4- limits lipi peroxidation

84
Q

What pro-inflammatory cytokines is pyroptosis associated with?

A

IL-1b and IL18

85
Q

What is a major trigger for pyroptosis?

A

cytosolic LPS from invading gram negative bacteria

86
Q

What is the difference between anergy and senscence?

A

anergy is introduced during priming due to absence of costimulatory signals whereas senscence is growth arrest after extensive proliferation

87
Q

When do exhausted T cells arise?

A

cells which initially gained effector function but become gradually silenced due to continuous TCR stimulation from persistent antigen

88
Q

Give examples of infections where exhausted T cells arise?

A

HIV; LCMV; HBV; HCV; HTLV1

89
Q

What happens to mice with impeded T cell exhaustion?

A

develop severe spontaneous AI diseases and succumb to fatal CD8 T cell-mediated immune pathologies during early LCMV infection

90
Q

What are the characteristics of exhaustion?

A

continuous enhancement of T cell dysfunction due to persistent antigen exposure, an increased expression of multiple inhibitory receptors; progressive loss of effector cytokine secretion; altered cell metabolism and different transcriptional profile

91
Q

Do all T cells undergo exhaustion during chronic diseases or cancer?

A

it is not uniform- specfiic subsets with different memory-like or proliferative potentials emerge upon exposure to persisting antigen

92
Q

How does CTLA-4 work?

A

coutneracts the positive signal mediated by CD28 by competeting for the sam ligands- CD80/86 with higher affinity ; and can entrp its ligands by trans-endocytosis followed by degradation

93
Q

What is the function of CTLA-4?

A

dampens T cell activation; decreases the efficacy of APCs to activate T cells and augments Treg mediated immune suppression

94
Q

What is sustained PD-1 cell surface expression a characteristic marker of?

A

T cell exhaustion

95
Q

What happens to severely axhausted T cells?

A

not maintained and die off

Basic Immunology- Module 1 (31 decks)

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