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immu2011 Flashcards

1
Q

What is the difference between dendritic cells in the periphery and dendritic cells in the lymph nodes

A 
Dendritic cells in the periphery:
PRR recognise PAMPs
high phagocytic capacity
process protein antigens onto MHCs
migrate to T cell zones
(in response to danger signals like TNF, they move to the lymph nodes)
Dendritic cells in the lymph nodes:
home to T cell zones, 
express the required surface molecules to naive T cells:
MHC
costimulatory molecules
cytokines
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2
Q

What are 4 main kinds of activatory signals to activate a naive T cell

A

MHC molecules
co-stimulatory molecules
adhesion molecules
cytokines

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3
Q

Where does the CD4 co-receptor bind?

A

on the beta 2 chain on MHC class 2

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4
Q

Where does the CD8 co-receptor bind?

A

on the conserved alpha 3 chain on MHC class 1

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5
Q

What are the functions of CD co-receptors

A

stabilises low affinity binding of TCR to peptide MHC

ensures the appropriate T cell type is activated

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6
Q

What is the function of CD3

A

provide an activation signal transduction via ITAM sequences

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7
Q

LFA-1 receptor

A

ICAM1 is on the APC

LFA1 is on the TC

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8
Q

B7/ CD28

A

B7 is expressed on the DC, and the expression is increased when APC encounters microbial antigen
B7 binds to CD28
Cd28 is found on t cells

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9
Q

CTLA4

A

is structurally similar to CD28
It binds to B7
it is expressed on some T regs

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10
Q

PD-1

A

also structurally related to CD28
found on T cells
binds to PD L1 and PD L2 on APC

They function to terminate responses of these cells

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11
Q

Why are co-stimulators so important

A

Resting APCs, which have not been exposed to microbes or adjuvants, may present peptide antigens, but they do not express costimulators and are unable to activate naive T cells. •T cells that recognise antigen withoutcostimulation may become unresponsive (anergic or tolerant) to subsequent exposure to antigen. •Microbes + cytokines produced during innate immune responses to microbes, induce the expression of costimulators, (e.g. B7 molecules) -The B7 costimulators are recognised by the CD28 receptor on naive T cells, providing signal 2. -In conjunction with antigen recognition (signal 1), this recognition initiates T cell responses. •Activated APCs also produce cytokines that stimulate the differentiation of naive T cells into effector cells (more in our next lecture)

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12
Q

following signalling, which genes are up regulated that are required for T cell proliferation and differentiation

A

The high affinity IL2 receptor (CD25 or IL2-alpha) and the IL2 itself

the naive T cells express a low moderate affinity interleukin called IL-2Rb

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13
Q

What are some markers that identifies regulatory T cells

A

They are CD4+ and may express FoxP3

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14
Q

How does T regs suppress immune responses

A

IL2 binding to CD25 on Tregs induces IL10 production. IL10 is an anti-inflammatory, immune modulating cytokine

They could out compete naive T cells for Dendritic cells and IL2 and suppress T cell proliferation

Function of FoxP3 is not completely clear, but it may cooperate with NFAT to activate CTLA4 transcription

Control inflammation and autoimmunity

and apparently could facilitate tumour escape from immune system

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15
Q

how is Th1 activated

A

bacteria binds to an APC, and the APC would release IFN-gamma and IL12 to the naive T cell to upregulate T bet. This causes it to become Th1

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16
Q

What do Th1 do?

A

They upregulate IFN gamma and upregulate macrophages +classical activation of macrophages and B cell recruitment and cause B cell to class switch to IgG.

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17
Q

How are Th2 activated

A

a protein antigen or helminth binds to an APC. The APC would secrete IL4 which upregulates GATA3 which would upregulate Th2

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18
Q

what do Th2 do

A

they secrete IL4 and IL13

IL4 and IL13 to macrophages would cause them to enhance tissue repair

IL4 to B cells would produce IgG4 in human and IgE. IgE drives mast cell degranulation

Th2 could also secrete IL4 and IL13 which causes intestinal mucosal secretion and peristalsis

IL5 causes eosinophil activation

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19
Q

How are Th17 activated

A

Bacteria causes APC to release TGF beta, Il6 and Il23,

This causes upregulation of Ror-gamma T

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20
Q

What do Th17 do?

A

They release IL17 and IL22 on tissue cells.
IL17 causes inflammation and neutrophil response, and the production of antimicrobial peptides. IL22 causes tissue cells to have increased barrier functions

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21
Q

Th1 host defense against

A

intracellular microbes

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22
Q

Th2 host defense against

A

helminthic parasites

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23
Q

what kind of disease happens if Th1 is not appropriately controlled

A

autoimmune diseases; tissue damage associated with chronic infections

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24
Q

What kind of disease happens if Th2 is not properly controlled

A

allergic diseases

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25
Q

What happens to activated CD8+ T cells

A

it leads to an upregulation of integrins, selectin ligands and chemokine receptors

the endothelial cells at the site of infection are induced by cytokines such as TNF and IL 1 to express selectins and ligands for integrins

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26
Q

what do granzymes do

A

They cleave caspases and induce apoptosis

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27
Q

what do perforin do

A

create holes in plasma membrane and facilitates entry of granzymes into target cell

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28
Q

Fas ligand

A

binds to fas or CD95 on infected cell

binds to Fas which triggers caspase activation

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29
Q

what are the light chains made of?

A

1 constant domain and 1 variable domain

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30
Q

what are heavy chains made of

A

1 variable and 3 to 4 constant domains

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31
Q

what is the hinge region of the antibody

A

it basically allows variable regions to come closer together or further apart to bind epitopes close together or far apart on an antigen

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32
Q

Where are follicular B cells found

A

through the follicles of secondary lymphoid organs

They make up the bulk of T dependent, class-switched and high affinity antibody responses

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33
Q

Where are marginal B cell zones located?

A

In the peripheral region of the splenic white pulp

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34
Q

Where are B-1 cells found?

A

mucosal tissues and peritoneum

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35
Q

What are features of both B cells and B-1 cells

A

marginal zone B cells and B-1 cells express antigen receptors of limited diversity
They respond largely to polysaccharide and lipid antigens
They make predominantly T independent IgM responses

IgM antibodies produced spontaneously by B-1 cells, are sometimes called natural antibodies
they help clear apoptotic cells and may provide protection against some bacterial pathogens

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36
Q

How do naive Th cells make it to the t cell zones

A

Naive T cells express CCR7, and it allows them to home to CCL19 and CCl21 in the T cell zones.

Activated effector T cells lose CCR7 and upregulate other chemokine receptors that allow them to home to the periphery

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37
Q

what do naive B cells express to allow them to migrate to B cell follicles

A

They express CXCR5 which may allow them to migrate towards CXCL13 expressed in B cell follicles

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38
Q

How do newly activated B cells move to T cell zones

A

newly activated B cells lose CXCR5 and up regulate CCR7

the same chemokine expressed by naive T cells
this enables B cells to home to the T cell zones by migrating towards CCL19 and CCL21

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39
Q

How is the affinity often expressed?

A

Kd
The concentration of antigen required to occupy half the available antibody molecule in a solution.

The lower the Kd, the higher the affinity

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40
Q

outline the processes that make B cells mature (stages of humoral immunity)

A

1) extrafollicular response

2) the germinal centre response

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41
Q

Where does somatic hypermutation take place?

A

germinal centres

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42
Q

What happens in the dark zone and light zone of the germinal centre reaction

A

darkzone
does not contain any FDC or T cells
It is densely packed with rapidly proliferating B cells,

in the light zone
the small non-dividing progeny of B cells migrate to the B cells
They come into close contact with the process of the abundant Follicular dendritic cells and T follicular helper cells

(somatic mutation and affinity maturation/isotype switching happens in the light zone)

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43
Q

Where are follicular dendritic cells found?

A

They are only found in the lymphoid follicles

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44
Q

How are follicular dendritic cells different to normal dendritic cells

A

They present antigen on MHC to T cells

I think this is a typo, FDCs should only be presenting to B cells

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45
Q

Follicular Dendritic cells role

A

involved in displaying antigens for the selection of germinal centre B cells

They present the antigen bound antibody complex

They provide survival signals to the B cells withich would outcompete others for binding to the antigen being presented. B cells that receive no signal die.

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46
Q

What is the most common kind of white blood cell in the blood

A

neutrophils, accounting for 40 to 60%

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47
Q

how do immunologists identify immune cells

A

cell morphology

expression of surface molecules

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48
Q

Do mast cells have a myeloid progenitor

A

no, they enter tissues as immature mast cell progenitors

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49
Q

Where are mast cells found and what do they do

A

They are found in peripheral tissues exposed to environment and degranulate cytokines/histamine

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50
Q

What do eosinophils fight

A

parasites and helminths

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51
Q

Where are eosinophils found

A

mucosal linings of respiratory, gastrointestinal and genitourinary tracts

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52
Q

how are basophils different to mast cells

A

usually not found in peripheral tissues

and has to be recruited,

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53
Q

neutrophils

A 
not normally found in tissues,
infiltrate inflamed peripheral sites
phagocytosis
cytokines that promotes inflammation and recruitment of other cells
promotes phagocytosis by macrophages

can kill bacteria by entrapping them in extracellular structures called NETs

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54
Q

innate lymphoid cells

A

like T cells, they can provide early defense against infections and interact with adaptive immune system

ILC1 provides defense against viruses
ILC2 promote allergic inflammation

ILC3 provide intestinal barrier function

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55
Q

NK cells

A

if microbes breach epithelia

they can play a very important role in antiviral and tumour immunity

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56
Q

What are the 2 only primary lymphoid tissues

A

bone marrow and thymus

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57
Q

what happens in the primary lymphoid tissues

A

lymphocytes first express antigen specific receptors

lymphocytes attain functional maturity

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58
Q

What happens in the secondary lymphoid tissues

A

lymphocyte response to antigen initiated and developed

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59
Q

In adults where do most blood cells come from

A

flat bones

60
Q

What happens in the bone marrow for B cells

A

B cell maturation
gains antigen specific receptors

plasmablasts (mature antibody secreting B cells) also come back to the bone marrow

61
Q

What happens in the thymus?

A

cortex-contains dense T cells
medulla-T cells, DCs and macrophages

central tolerance is acquired for T cells.
There are cells called MECs which express autoimmune regulators that cause the clonal deletion of reactive T cells

62
Q

what happens in the spleen

A

blood recirculation, lots of blood borne antigens are trapped. Lots of phagocytes as well

63
Q

the spleen architecture

A

t cell rich, b cell rich, red pulp, white pulp

The B cell zones are further away from the blood vessel of the T cell zone.

64
Q

What happens in the marginal zone

A

marginal sinus, has a few dendritic cells.
Transit zone. Cell moving from blood to white pulp.
We have macrophages

65
Q

adaptations of the epithelium that helps us

A 
stratification adds cellular layers
Keratinisation hardens uppermost layer
mucus secretion
cilia
tight junctions
antimicrobial peptides
66
Q

alpha and beta defensins

A

alpha defensins
small cationic proteins that could basically activate immune signalling or directly kill stuff

alpha is produced by antimicrobial cells like paneth cells or leukocytes

mucosal epithelial cells generally secrete beta

67
Q

structure of defensins

A

cationic, beta sheet rich

68
Q

TLR structure

A

leucine rich repeat ectodomain

for ligand binding.

A transmembrane domain for anchoring

and toll interleukin 1 receptor for cytosolic signalling

69
Q

In flies, tlr has

A

developmental roles and immune roles

70
Q

what is the TLR signalling pathway

A

TLR=>TIR
recruits adaptor proteins such as MAL and MyD88 which cleaves IKKa to p65 and p50 which then go activates the nucleus (NFkB pathway)

can also activate TRIF/TRAm pathway for IRF3

71
Q

What does NOD1 sense

A

mesodiaminopimelic acid
mainy gram negative bacteria

NOD1 is expressed in gut epithelia

72
Q

NOD2

A

senses mostly muramyl dipeptide
gram -ve and gram positive bacteria

typically expressed by leukocytes and specialised immune cells

73
Q

RIPK2

A

phosphorylate stuff to activate NFkB

74
Q

body guard concept

A

you could have these nod like receptors activate innate immune system like NOD receptors

They use the same is LRR

75
Q

NFkB

A

IKK complex formed.

This then phosphorylate IKb subunit and then release p50 and p65.

76
Q

homing definition

A

blood to specific site

77
Q

migration or recruitment

A

general leukocyte movement from blood into tissues

78
Q

recirculation

A

blood into secondary lymphoid organs into blood

79
Q

What does TNF and IL1 do to endothelial cells

A

They stimulate endothelial cells to rapidly express E selectin and P selectin, and this causes leukocytes which express selectin ligand to roll. Leukocytes therefore then express integrins which further causes the cells to roll

80
Q

How do leukocytes bind to High endothelial venules

A

HEVs have addressins such as PNAd -a ligand for L selectin

81
Q

how do naive T cells return to blood anatomically

A

efferent lymphatics,
through the lymphatic vasculature
finally into the superior vena cava or subclavian vein

82
Q

How do naive T cells find their way into lymph nodes?

A

L selectin receptor on HEV binds to L selectin on naive T cells

Naive T cells express a CCR7 receptor

that is attracted to CCL19/21 expressed by HEV

T cells express LFA1 integrin that can also bind to ICAM 1 on HEV

83
Q

chemokine common functions

A

+ve charge so they could bind to extracellular matrix and remain localised near secreting cells

they create a chemokine gradient

84
Q

general features of tumour necrosis factors

A

trimeric complexes
membrane bound and soluble forms

cytokine ligands are expressed as membrane bound proteins and released by proteolytic cleavage

85
Q

What is TNF a

A

a powerful pro inflammatory cytokine

86
Q

What are the main producers of TNF a

A

macrophages

87
Q

What do TNF a bind to

A

TNFR1 most mammalian cells

or TNFR2 restricted to immune cells

88
Q

TRADDs

A

TNF receptor associated death domain-activates caspase pathway

89
Q

TRAFs

A

TNF receptor associated factors

activate NFKB transcription factors that can cause survival and cytokine expression

90
Q

Interferon function

A

up regulate genes that protect neighbouring host cells from infection like
proteases and nucleases

they can activate immune cells-kill me signal

they can upregulate antigen presentation to T lymphocytes

91
Q

interleukins

A

communicate between leukocytes.

signal through receptors and jak stat pathway

92
Q

What are the hallmarks of the innate immune system

A 
speed
duration
repetitive
interactive
non-reactive
93
Q

haustoria

A

feeding structures of stuff like rust which do not penetrate through plasma membrane

94
Q

PTI

A

weak immune response that commonly involves callose deposition, production of antimicrobial compounds and defence proteins

95
Q

ETI

A

rapid/robust and causes the hypersensitive reaction also known as programmed cell death

96
Q

gene for gene hypothesis

A

if the antigen is avirulent and the host is resistant, there is low immunocompatibility and the host could be infected.

avr1avr1 is the virulent strain

97
Q

Why is the gene to gene hypothesis important?

A

a low IT (incompatible) suggest the presence of at least one pair of either the avirulence and resistance genes in the host and pathogen

98
Q

resistance exists on a continuum

A

host
intermediate host
intermediate nonhost
nonhost

99
Q

Complementarity determining region

A

where the antigen binds

100
Q

how many different kinds of light chains are there?

A

kappa and lambda, they differ in constant domain

101
Q

how are different epitopes of protein antigens recognised?

A

sequence of amino acids

3D shape of protein antigen-conformational epitopes

102
Q

affinity

A

strength of binding between one antigen binding site on an antibody molecule and its corresponding epitope

Affinity is often expressed as the dissociation constant
The lower the Kd, the higher the affinity

103
Q

avidity

A

overall strength of the interaction between the antibody and its antigen
depends on both the affinity and valency of interactions.

cross reaction

104
Q

how many valencies does have IgA have

A

4?

105
Q

What affects avidity

A

valency
affinity of antibody for the epitope
structural arrangement of the parts that interact.

106
Q

rheumatic fever

A

some people are infected with strep throat

after such infections, individuals produce anti-strep throat antibodies that cross react with an antigen in heartmuscle
and this may cause an inflammatory disease called rheumatic fever.

Other individuals making anti-streptococcal antibodies that deposit in kidney glomeruli causes post streptococcal glomerulonephritis

107
Q

in what ways are the T cell receptors for antigen similar to BCR

A

membrane bound, constant regions

variable regions

108
Q

What unique features of the TCR make it different to BCRs

A

two chains, alpha and beta chains

no heavy and light chains. Slow on rate, slow off rate.

109
Q

How are DCs activated

A

after sensing TNF or IL1, the DC migrate from the periphery to draining lymph nodes

110
Q

What are the steps in which lymphocytes are activated?

A

1) recognition of peptide and MHC
2) Co-receptors
3) adhesion molecules like LFA1 and ICAM1
4) positive costimulation

111
Q

where are follicular B cells found

A

in secondary lymph nodes in follicles

they are t dependent

112
Q

where are marginal b cells found

A

in the peripheral region of the splenic white pulp

113
Q

what are B1 cells

A

B cells that are responsive to mostly polysaccharide and lipid

mostly express IGm and are found in mucosal tissues and peritoneum

114
Q

how do T cells move towards periphery

A

activated effector T cells lose CCR7 and up regulate other chemokine receptors that allow them to home to the periphery: they respond to either CCL19 or CCL21

They upregulate CXCR5 which basically gets them to move closer to CXCL13 expressed in B cell follicle

115
Q

What do activated B cells express to make them move towards the margin

A

activated b cells lose CXCR5 and upregulate CCR7. The same chemokine expressed by naive T cells
This enables B cells to home to the T cell zones by migrating towards either CCL19 or CCL21

116
Q

What is the effect of the upregulation of CD40 on activated B cells?

A

allows the B cells to receive additional help from the already activated T cells

T cell provides CD40L TO cd40 on b cells causing class switching and shit to happen

117
Q

similarities and key differences between marsupial with monotremes(platypus) and eutherian mammals (like humans)

A

similarities: bone marrow, spleen, lymph node, MALT

key differences: thymuses, spleen, timing of immune development

118
Q

Thymus differences between polyprotodont marsupials (like devil and opossum) against diprotodont marsupials (like wallaby and wombat)

A

polyprotodont have thoracic thymus vs

diprotodont which have a cervical and thoracic thymus.

119
Q

thymus of different animals with us and rats

A

basically the same thing,
cervical and thoracic thymus structurally and functionally similar to eutherians

mature thymus-cortex/medulla and Hassal’s corpuscles

T lymphocyte development:
gene expression studies
thymectomy-lymphocyte depletion and delayed antibody response

120
Q

Development of the immune system between monotremes, marsupials and eutherians

A

marsupials are immunonaive at birth and the immune system develops within non-sterile pouch
born early developmental stage

mammals are born at a late developmental stage
immunocompetent and birth
immune system develops within sterile uterus

121
Q

Development of marsupial immune system in more detail

A

1 month: thymus and bone marrow

3 months: spleen and lymph node

4-5 months: MALT

122
Q

how are marsupial newborns protected in the pouch

A

They are protected via passive immunity by milk
which transfers IgA in the first phase

Then they start getting IgG transfer.

123
Q

protection in the pouch

A

expansion of antimicrobial peptide genes in marsupials and monotremes.
e

124
Q

are immune cell populations in marsupials and monotremes same as mammals

A

yup pretty much exactly same. Have CD4, CD4 and CD8.

They do have different antibody markers.

125
Q

functional difference between mammal and marsupials/monotremes

A

the level of response differs
mouse=800
platypus=30

126
Q

difference between marsupial and monotreme TCR

A

they have a fifth TCR chain-mu
this is unique to marsupials and monotremes
we don’t have a gene that produces mu
mu gene has no vdj recombination.

2 isofroms of mu TCR in marsupials and only 1 isoform in monotreme

127
Q

difference between eutherian and (marsupial and monotreme TLRs)

A

they have the same TLR repertoire as eutherians except TLR1 and TLR6 could not be identified

Unique TLR1/6 like not found in eutherians

Ancestral gene
Duplicated and evolved into TLR1 and TLR6

tlr1 and tlr6 basically combined.

128
Q

difference in mhc

A

mhc class 1 gene UT only found in marsupials and monotremes. They are highly duplicated

MHC genes for marsupials and monotremes dispersed everywhere. For monotremes some are located on sex chromosomes

129
Q

difference between immunoglobulins

A

marsupials don’t have IgD.
montremes have the same as humans

Diversity in the other animals are lower:
marsupials have limited heavy chain diversity so the light chain compensates

The platypus have limited heavy and light chain diversity

130
Q

DFTD

A

clonal cell line
arose from a schwann cell in a female devil

we know its from a female because it has genes normally found on x chromosome and no sry gene

131
Q

Why is DFTD not recognised?

A

hypothesis 1: DFTD is seen as self because devils lack diversity at MHC genes

hypothesis 2: DFTD evades the immune system by down regulating MHC expression

132
Q

is MHC diversity low

A

yup they gone through lots of bottlenecks and lots of alleles have been lost. Lots of Devils are like clones, very limited pool of MHC

3 population crashes in european arrival.

133
Q

What devils are more susceptible

A

angiogenesis

134
Q

skin graft histology

A

allograft rejected even though MHC of the 2 devils were almost identical
lymphocyte infiltration-immune activation and rejection of foreign cells

they have functional MHC diversity and can distinguish self from non-self

135
Q

DFTD downregulates MHC1 expression

A

MHC 1 and genes essential for antigen loading and presentation (TAP 1, TAP2 and B2M) show low/no expression in DFTD.

it basically acetylate the chromatin on these cells

136
Q

devil immune system and age

A

lymphocytes in devils decline with age
lower anti cancer response

TCR diversity declines with age

137
Q

NK cells DFTD

A

devil NK cells may require anti DFTD antibodies for activation resulting cytotoxic response. So no anti DFTD means that there may be no NK cell response

138
Q

DFTD immunotherapy

A

DFTD-treat DFTD cells with interferon gamma which induces MHC 1 expression and makes stuff visible to the immune system. Testing in captive and reintroduced devils the antibody response.

current formulations require multiple injections and trapping is difficult
devils are elusive and trap shy.

139
Q

why is DFTD so difficult to treat

A

it could evolve
are DFTD functionally different? nope
Is DFTD more or less aggressive. Double the amount of genetic material-slows tumour development, increase in polymorphism, and masks deleterious mutations

slow growing tumour more aggressive

140
Q

insurance program

A

intensive program
free range closure
peninsula islands
genetic

141
Q

controlling plant diseases

A

cultural practices
breeding
fungicides

142
Q

what is wheat

A

a hexaploid: A, B, and D
aabbdd
3 hybridisation events

143
Q

Sr26

A

gene for stem rust resistance gene.
Sr26 is transgenic…
cultivated from a different cultivar.

144
Q

How do breeders select how to breed stuff

A

breeders want resistance that is easy to select, minimise yield loss and is durable

do it by phenotyping.
basically you infect them with rust then phenotyping.

backcrossing/germplasm
iterative resistance gene try to get into the plants.

145
Q

multigenic resistance

A

massive populations reached

this is done by genetic engineering
genome sequencing
pull out eti and stick them together.
isolate 5 resitsance genes and then reinsert them as basically one large glued chunk into the wheat genome

it is considered cisgenic, because it is a gene from the same kind of plant.

immu3102 (12 decks)

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