Innate Immunology Flashcards
(105 cards)
1
Q
immune cells
A
leukocytes
1
Q
where are immune cells produced
A
bone marrow
2
Q
where are immune chemicals produced
A
by immune cells or damaged cells
3
Q
what is the immune system
A
collection of cells and chemicals which work together to protect us from disease
4
Q
innate immunity
A
non-specific
fast
5
Q
adaptive immunity
A
specific to a pathogen
slower
6
Q
humoral immunity
A
proteins dissolved in serum, plasma and tissue fluid
complement in innate
antibodies in adaptive
7
Q
cellular immunity
A
cells which have mechanisms to identify and destroy foreign organisms
8
Q
pathway to immune memory
A
anatomical barriers
innate humoral (soluble) factors
innate immune cells
adaptive immune cells and antibody
immune memory
9
Q
cells involved in innate immunity
A
epithelial barriers
complement
phagocytes
natural killer cells
dendritic cells
10
Q
cells involved in innate immunity
A
B cells
T cells
effector T cells
memory t and B cells
11
Q
where can microbes enter our bodies
A
respiratory tract
skin
eyes
gastrointestinal tract
genitourinary tract
entrances and surfaces have physical barriers
12
Q
physical barriers to protect entrances to the body
A
hair
wax
membranes
specialist epithelial cells
air movement
mucus
tears
13
Q
what do tears contain
A
enzymes such as lysozymes
14
Q
flow of air and fluid q
A
reduces the chance of micro-organisms attaching
15
Q
enzymes
A
secretions contain antimicrobial enzymes
16
Q
low pH
A
restricts which pathogens can survive if ingested
17
Q
defensins
A
antimicrobial peptides disrupt cell membranes and virus envelopes
18
Q
normal microbiota
A
outcompete potentially harmful organisms
19
Q
epithelial cell tight junctions
A
restrict movement of microorganisms deep into tissue
20
Q
goblet cells
A
produce mucus which acts as a sticky barrier
21
Q
ciliated cells
A
move mucus along to flush out pathogens
22
Q
tissue resident immune cells
A
recognise, Engulf/phagocytose and kill pathogens
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
24
what is inflammation
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
25
cardinal signs of inflammation
rubor
calor
tumor
dolor
functio laesa
26
rubor
redness
27
calor
heat
28
tumor
swelling
29
dolor
pain
30
functio laesa
loss of function
31
receptor:ligand interactions
way cells give and receive information
receptor binding by its ligand causes signals to be passed through cell to change expression of genes
32
ligand
often a cytokine
e.g. interleukin (IL)
33
receptor
often a cluster of differentiation (CD)
34
cardinal signs of acute inflammation can be caused by what
histamine
35
histamine
released from innate immune cells (mast cells and basophils) and platelets
36
when histamine binds to histamine receptors what occurs
vasodilation and increased blood flow
exudation of fluid from blood into tissue
37
when no microbes are present
fragments of cells are released through damage
contain damage-associated molecular pattern molecules
38
what do DAMPs include
DNA
RNA
proteins
from within the nucleus
bind to receptors to trigger inflammation
39
what do DAMPs bind to
receptors to activate cells
induce inflammatory cytokine release and trigger inflammation
40
when microbes enter the wound
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
41
two classifications of pathogens
intracellular
extracellular
42
examples of extracellular pathogens
bacteria
viruses
fungi
parasites
43
intracellular pathogens
viral replication and assembly
44
extracellular pathogens are tackled by what
humoral parts of immune system
also cells
45
soluble factors
antibodies
actue phase proteins (C reative protein)
complement
46
acute phase proteins
released from liver
serum amyloid protein
C-reactive protein
fibrinogen
mannose-binding lectin
SP-A
SP-D
47
function of serum amyloid protein
48
function of C reactive protein
49
function of fibrinogen
50
function of mannose-binding lectin
51
function of SP-A
52
function of SP-D
53
complement pathway
happens instantly when epithelial barriers are breached
triggered in 3 ways but lead to 3 same outcomes
54
3 outcomes of the complement pathway
opsonisation/phagocytosis
chemotaxis
membrane attack complex
55
opsonisation/phagocytosis
phagocytes recognise C3b through complement receptor and "eat" microbe
56
chemotaxis
C3a and C5a recruit phagocytic cells and promote inflammation
57
membrane attack complex
C3b sets off a pathway regulating in disruption of the cell membrane
58
3 pathways of complement pathway
alternative
classical
lectin
59
alternative pathway
spontaneous
binding of C3b to microbe
60
classical pathway
antibody activated
61
lectin pathway
recognise sugars on pathogens
62
DAMPs
damage associated molecular patterns
bind receptors to make innate immune cells aware of tissue damage
63
PAMPs
pathogen associated molecular patterns
bind receptors to make innate immune cells aware of infection
64
what do PAMPs and DAMPs bind to
pattern recognition receptors PRRs
65
common pathogen PAMPs
RNA viruses
DNA viruses
gram positive bacteria
gram negative bacteria
fungi
protists
66
families of PRR
external: toll like receptors, phagocytic receptors
internal:
cytoplasmic- NOD and RIG-like receptors
endosomal- toll like receptors
67
phagocytic receptor
induce uptake of pathogens into endosomes and killing of the pathogen
68
phagocytic receptor examples
complement receptor
scavenger receptor
mannose receptor
Fc receptor
C-type lectin receptor
69
complement receptor
recognises C3b complement protein bound to pathogen surfaces
70
what does TLR4 bind t o
LPS
71
what does TLR5 bind to
flagellin
72
what does TLR1 2 and 6 bind to
lipoproteins
73
what does TLR9 bind to
CpG DNA
74
what do TLR7 and 8 bind to
ssRNA
75
what does TLR3 bind to
dsRNA
76
scavenger receptor
recognises lipoproteins in bacterial cell walls
77
mannose receptor
recognise mannose on the surface of some bacteria
78
Fc receptors
recognises antibody bound to pathogen surfaces
79
C-type lectin receptors
recognises beta-glucan sugar in fungal cell walls
80
TLR signalling
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
how do immune cells communicate
cell to cell contact
release of chemicals (cytokines)
82
what can cytokines do
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
examples of proinflammatory cytokines
tumour necrosis factor TNFa
interleukin 6 IL-6
interleukin 1beta
84
examples of anti-inflammatory cytokines
Interleukin 10 IL-10
transforming growth factor beta
85
effects of pro-inflammatory cytokines on the local tissue
tight functions open
more fluid exit
diapedesis (monocyte squeeze through interstitial space)
antimicrobial chemicals exit
86
phagocytes function
ingest microbes by phagocytosis or pinocytosis
87
pinocytosis
take in fluids and some solutes
88
how do macrophages kill the pathogen
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
what does a lysosome contain
antimicrobial peptides,ezymes and reactive oxygen species
90
where will immune cells move to to find the pathogen
to where the chemokine concentration is the highest
91
what do neutrophils do when they arrive
phagocytosis
apoptosis
netosis
92
netosis
93
what occurs if the pathogen isn't cleared
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
intracellular pathogens
can't be tackled by humeral parts of the immune system
relies on a cellular response
95
how do cells recognise the intracellular microbes
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
intracellular bacteria
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
what are the most common intracellular pathogens
viruses
98
what is the difference between bacterial and viral endosomal TLR signalling
in viruses the interferon response factors IRF assemble and bind to DNA
99
interferons that lead to antiviral response
IRF 3
interferon beta
type 1 interferons
100
type 1 interferons
INFa and INF beta
increase viral defences and reduce viral replication cytokines make by infected cells
101
preventing the virus from replicating itself
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
sacrificing the infected cells
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
how do NK cells kill
IFNy and TNFa activate other immune cells
granules containing perforin and granzyme lead to apoptosis
104
how do NK cells know which cells to kill when none are foreign
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
