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Medicine Unit 3 > Innate Immunology > Flashcards

Innate Immunology Flashcards

1
Q

immune cells

A

leukocytes

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1
Q

where are immune cells produced

A

bone marrow

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2
Q

where are immune chemicals produced

A

by immune cells or damaged cells

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3
Q

what is the immune system

A

collection of cells and chemicals which work together to protect us from disease

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4
Q

innate immunity

A

non-specific
fast

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5
Q

adaptive immunity

A

specific to a pathogen
slower

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6
Q

humoral immunity

A

proteins dissolved in serum, plasma and tissue fluid
complement in innate
antibodies in adaptive

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7
Q

cellular immunity

A

cells which have mechanisms to identify and destroy foreign organisms

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8
Q

pathway to immune memory

A

anatomical barriers
innate humoral (soluble) factors
innate immune cells
adaptive immune cells and antibody
immune memory

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9
Q

cells involved in innate immunity

A

epithelial barriers
complement
phagocytes
natural killer cells
dendritic cells

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10
Q

cells involved in innate immunity

A

B cells
T cells
effector T cells
memory t and B cells

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11
Q

where can microbes enter our bodies

A

respiratory tract
skin
eyes
gastrointestinal tract
genitourinary tract
entrances and surfaces have physical barriers

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12
Q

physical barriers to protect entrances to the body

A

hair
wax
membranes
specialist epithelial cells
air movement
mucus
tears

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13
Q

what do tears contain

A

enzymes such as lysozymes

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14
Q

flow of air and fluid q

A

reduces the chance of micro-organisms attaching

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15
Q

enzymes

A

secretions contain antimicrobial enzymes

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16
Q

low pH

A

restricts which pathogens can survive if ingested

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17
Q

defensins

A

antimicrobial peptides disrupt cell membranes and virus envelopes

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18
Q

normal microbiota

A

outcompete potentially harmful organisms

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19
Q

epithelial cell tight junctions

A

restrict movement of microorganisms deep into tissue

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20
Q

goblet cells

A

produce mucus which acts as a sticky barrier

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21
Q

ciliated cells

A

move mucus along to flush out pathogens

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22
Q

tissue resident immune cells

A

recognise, Engulf/phagocytose and kill pathogens

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23
Q

what happens if the barriers are breached

A

cells are damaged and exposed to the environment
a bump or cut can cause damage and initiate an inflammatory response even without the presence of a pathogen

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24
Q

what is inflammation

A

part of the body response to damage as a way to protect itself
usually localised to the site of damage and involves the immune system
progresses through a series of stages until it is resolved and tissue returns to normal

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25
Q

cardinal signs of inflammation

A

rubor
calor
tumor
dolor
functio laesa

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26
Q

rubor

A

redness

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27
Q

calor

A

heat

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28
Q

tumor

A

swelling

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29
Q

dolor

A

pain

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30
Q

functio laesa

A

loss of function

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31
Q

receptor:ligand interactions

A

way cells give and receive information
receptor binding by its ligand causes signals to be passed through cell to change expression of genes

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32
Q

ligand

A

often a cytokine
e.g. interleukin (IL)

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33
Q

receptor

A

often a cluster of differentiation (CD)

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34
Q

cardinal signs of acute inflammation can be caused by what

A

histamine

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35
Q

histamine

A

released from innate immune cells (mast cells and basophils) and platelets

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36
Q

when histamine binds to histamine receptors what occurs

A

vasodilation and increased blood flow
exudation of fluid from blood into tissue

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37
Q

when no microbes are present

A

fragments of cells are released through damage
contain damage-associated molecular pattern molecules

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38
Q

what do DAMPs include

A

DNA
RNA
proteins
from within the nucleus
bind to receptors to trigger inflammation

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39
Q

what do DAMPs bind to

A

receptors to activate cells
induce inflammatory cytokine release and trigger inflammation

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40
Q

when microbes enter the wound

A

release chemicals which are viewed as foreign
can trigger inflammation
some are pathogenic and can grow within tissue, causes more damage to ells
some can enter cells living inside of them

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41
Q

two classifications of pathogens

A

intracellular
extracellular

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42
Q

examples of extracellular pathogens

A

bacteria
viruses
fungi
parasites

43
Q

intracellular pathogens

A

viral replication and assembly

44
Q

extracellular pathogens are tackled by what

A

humoral parts of immune system
also cells

45
Q

soluble factors

A

antibodies
actue phase proteins (C reative protein)
complement

46
Q

acute phase proteins

A

released from liver
serum amyloid protein
C-reactive protein
fibrinogen
mannose-binding lectin
SP-A
SP-D

47
Q

function of serum amyloid protein

A
48
Q

function of C reactive protein

A
49
Q

function of fibrinogen

A
50
Q

function of mannose-binding lectin

A
51
Q

function of SP-A

A
52
Q

function of SP-D

A
53
Q

complement pathway

A

happens instantly when epithelial barriers are breached
triggered in 3 ways but lead to 3 same outcomes

54
Q

3 outcomes of the complement pathway

A

opsonisation/phagocytosis
chemotaxis
membrane attack complex

55
Q

opsonisation/phagocytosis

A

phagocytes recognise C3b through complement receptor and “eat” microbe

56
Q

chemotaxis

A

C3a and C5a recruit phagocytic cells and promote inflammation

57
Q

membrane attack complex

A

C3b sets off a pathway regulating in disruption of the cell membrane

58
Q

3 pathways of complement pathway

A

alternative
classical
lectin

59
Q

alternative pathway

A

spontaneous
binding of C3b to microbe

60
Q

classical pathway

A

antibody activated

61
Q

lectin pathway

A

recognise sugars on pathogens

62
Q

DAMPs

A

damage associated molecular patterns
bind receptors to make innate immune cells aware of tissue damage

63
Q

PAMPs

A

pathogen associated molecular patterns
bind receptors to make innate immune cells aware of infection

64
Q

what do PAMPs and DAMPs bind to

A

pattern recognition receptors PRRs

65
Q

common pathogen PAMPs

A

RNA viruses
DNA viruses
gram positive bacteria
gram negative bacteria
fungi
protists

66
Q

families of PRR

A

external: toll like receptors, phagocytic receptors
internal:
cytoplasmic- NOD and RIG-like receptors
endosomal- toll like receptors

67
Q

phagocytic receptor

A

induce uptake of pathogens into endosomes and killing of the pathogen

68
Q

phagocytic receptor examples

A

complement receptor
scavenger receptor
mannose receptor
Fc receptor
C-type lectin receptor

69
Q

complement receptor

A

recognises C3b complement protein bound to pathogen surfaces

70
Q

what does TLR4 bind t o

A

LPS

71
Q

what does TLR5 bind to

A

flagellin

72
Q

what does TLR1 2 and 6 bind to

A

lipoproteins

73
Q

what does TLR9 bind to

A

CpG DNA

74
Q

what do TLR7 and 8 bind to

A

ssRNA

75
Q

what does TLR3 bind to

A

dsRNA

76
Q

scavenger receptor

A

recognises lipoproteins in bacterial cell walls

77
Q

mannose receptor

A

recognise mannose on the surface of some bacteria

78
Q

Fc receptors

A

recognises antibody bound to pathogen surfaces

79
Q

C-type lectin receptors

A

recognises beta-glucan sugar in fungal cell walls

80
Q

TLR signalling

A
  1. PAMP binds to PRR, sends signal to nucleus
  2. adaptors containing TIR domains (MyD88) transmit the message in the cytoplasm
  3. protein transcription factor called NFkB assembles and binds to DNA
  4. Instructs the cells to produce new proteins which initiate the next stage of the immune response
81
Q

how do immune cells communicate

A

cell to cell contact
release of chemicals (cytokines)

82
Q

what can cytokines do

A

inform cells there is danger, turn on inflammation which is a pro inflammatory cytokines

inform cells there is no danger, keeps cells inactive and turn off inflammation which are anti-inflammatory cytokines

83
Q

examples of proinflammatory cytokines

A

tumour necrosis factor TNFa
interleukin 6 IL-6
interleukin 1beta

84
Q

examples of anti-inflammatory cytokines

A

Interleukin 10 IL-10
transforming growth factor beta

85
Q

effects of pro-inflammatory cytokines on the local tissue

A

tight functions open
more fluid exit
diapedesis (monocyte squeeze through interstitial space)
antimicrobial chemicals exit

86
Q

phagocytes function

A

ingest microbes by phagocytosis or pinocytosis

87
Q

pinocytosis

A

take in fluids and some solutes

88
Q

how do macrophages kill the pathogen

A
  1. pathogen recognised by PRR, macrophages are activated and phagocytosis is induced
  2. pathogen is internalised in a phagosome, fuses with lysosome
  3. activated macrophages make pro-inflammatory cytokines which attract and activate other immune cells
  4. pathogen is killed by oxidative burst and digested enzymes

2 and 3 occur at the same time

89
Q

what does a lysosome contain

A

antimicrobial peptides,ezymes and reactive oxygen species

90
Q

where will immune cells move to to find the pathogen

A

to where the chemokine concentration is the highest

91
Q

what do neutrophils do when they arrive

A

phagocytosis
apoptosis
netosis

92
Q

netosis

A
93
Q

what occurs if the pathogen isn’t cleared

A

continued release of pro-inflammatory cytokines can be damaging and have systemic effects
damaged blood vessels produce bradykinin which increase vascular permeability, stimulate nerves to cause pain
inflammation may become chronic

94
Q

intracellular pathogens

A

can’t be tackled by humeral parts of the immune system
relies on a cellular response

95
Q

how do cells recognise the intracellular microbes

A

DAMPs recognised by PRR
PAMPS
infected cells hold up flags to show immune system they’re infected
pathogens recognised outside of cells at certain times in their life cycle

96
Q

intracellular bacteria

A

extracellular bacteria recognised by receptors and phagocytosed by cells
phagocyte will try and kill bacteria by acdification and enzymatic digestion
some bacteria thrive in acidic conditions and survive
others can penetrate the cell from outside or escape from phagosomes in cytoplasm
when in cytoplasm bacterial products can be recognised by intracellular PRRS
cytokines released to activate NK cells and adaptive immune cells

97
Q

what are the most common intracellular pathogens

A

viruses

98
Q

what is the difference between bacterial and viral endosomal TLR signalling

A

in viruses the interferon response factors IRF assemble and bind to DNA

99
Q

interferons that lead to antiviral response

A

IRF 3
interferon beta
type 1 interferons

100
Q

type 1 interferons

A

INFa and INF beta
increase viral defences and reduce viral replication cytokines make by infected cells

101
Q

preventing the virus from replicating itself

A

type 1 interferon antiviral response
IFN alpha and beta bind to IFNa receptor
outcome is activation of genes which degrade viral RNA and halt protein synthesis needed to make viral capsules
also activate natural killer cells

102
Q

sacrificing the infected cells

A

natural killer cells kill the virus infected cells and cancer cells by apoptosis
virally infected cells and cancer cells are very similar and killed by the same mechanisms

103
Q

how do NK cells kill

A

IFNy and TNFa activate other immune cells
granules containing perforin and granzyme lead to apoptosis

104
Q

how do NK cells know which cells to kill when none are foreign

A

recognsie altered self
molecules are up or down-regulated when cells are damaged
cancerous and virally infected cells express less inhibitory and more activating ligands

Medicine Unit 3 (28 decks)

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