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Z MD1 Foundation block > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the 5 major subtypes of T cells

A 
Th1
Th2
Th17
TFH
Treg
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2
Q

What are the cytokines that create Th1, Th2, and Th17 cells

A 
Th1 = IL-12
Th2 = IL-4
Th17 = Il-6
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3
Q

What is the cytokine that create TFH cells

A

IL-6

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4
Q

What is the cytokine that create Treg cells

A

TGF-beta

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5
Q

What major cytokines do Th1 cells produce

A

IFN-gamma

IL-2

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6
Q

What major cytokines do Th2 cells produce

A

IL4,5,13

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7
Q

What major cytokines do Th17 cells produce

A

IL-6,7

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8
Q

what major cytokines do TFG cells produce

A

IL-21 and 17

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9
Q

what major cytokines do Treg cells produce

A

TGF-beta and IL-10

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10
Q

Main roles of Th1 cells

A

promote macrophage recruitment and phagocytosis
promote IgG isotype switch
pro-inflammatory
promote neutrophil activation

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11
Q

main roles of Th2 cells

A

allergy and parasitic infection

  • IgE production
  • eosinophil activation
  • macrophage activation
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12
Q

main roles of Th17 cells

A

neutrophil migration and activation

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13
Q

main roles of TFH cells

A

B cell proliferation and differentiation

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14
Q

what is the order of antibody isotype switching

A

IgM –> IgG –> IgE –> IgA

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15
Q

Which cytokine promotes IgE isotype switching

A

Il-4

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16
Q

which cytokine promotos IgA isotype switching

A

TGF-B

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17
Q

what cytokine promotes IgG isotype switching

A

IFN-gamma

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18
Q

what is the difference between an antigen and a pathogen

A

pathogens cause disease

antigen is a protein that is recognised by the immune system

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19
Q

what does the innate and adaptive immune systems recognise and respond to

A

innate - recognise PAMPs (TLR, DAMPs) by PRRs

adaptive - antigens

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20
Q

which TLRs are intracellular

A

3, 7, 9

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21
Q

which blood cells are from the myeloid progenitor lineage

A 
RBCs
basophils
eosinophils
neutrophils
monocytes - macrophages
dendritic cells
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22
Q

which blood cells are from the lymphoid progenitor lineage

A

T cells
B cells
NK cells

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23
Q

what is the difference between a cytokine and a chemokine

A

cytokine - interacts with and affects the behaviour of nearby cells bearing the appropriate receptors
chemokines - attracts cells bearing the appropriate receptors

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24
Q

what are the two receptors for chemokines

A

CCR

CXCR

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25
Q

where do leukocytes develop

A

primary lymphoid organs

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26
Q

what are the secondary lymphoid organs

A

spleen, lymph nodes, MALT

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27
Q

what stimulates the innate immune system to enter tissues

A

infection and trauma - innate cells enter infected tissues through interactions with endothelial cells -> then bind PAMPs –> activated

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28
Q

where do cells of the adaptive immune system interact with antigens initially

A

in the secondary lymphoid tissues (lymph nodes) –> activated –> proliferated –> blood –> tissues

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29
Q

explain the organisation of lymph nodes

A

cortex - B cells
paracortex - T cels
medulla - macrophages and plasma cells

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30
Q

how do the lymphocytes enter into the lymph node

A

through highly structured endothelial cells (HEV)

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31
Q

function and outcome of neutrophils

A

phagocytosis –> removes EXTRACELLULAR pathogens

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32
Q

function and outcome of monocytes/macrophages

A

phagocytosis and releases cytokines –> removes EXTRACELLULAR pathogens

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33
Q

function and outcome of NK cells

A

binds and kills infected cells, releases cytokines –> removes INTRACELLULAR pathogens

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34
Q

function and outcome of eosinophils

A

binds and kills parasites –> removes parasites

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35
Q

function and outcome of basophils

A

release inflammatory mediators and cytokines –> boosts response, especially for parasites

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36
Q

function and outcome of dendritic cells

A

phagocytoses, presents antigen to T cells and releases cytokines –> stimulates T cells

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37
Q

function and outcome of B cells

A

secrete antibodies –> block adhesion of EXTRACELLULAR pathogens

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38
Q

function and outcome of CD8 T cells

A

binds cells infected with INTRACELLULAR pathogens, release cytokines –> kills infected cells

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39
Q

function and outcome of CD4 T cells

A

help macrophages, B cells and CD8T cells, releases cytokines –> better activation of these cells

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40
Q

which PAMPs do mucosal epithelia recognise

A

peptidoglycan
LPS
flagellin

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41
Q

what does the mucosal epithelia do if it recognises PAMPs

A

releases antimicrobial peptides

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42
Q

what are the 6 outcomes of the C’ cascade

A 
Inflammation
chemotaxis
opsonisation
lysis 
MAC
activation of B cells
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43
Q

what are the 3 pathways that can activate C’

A

alternative
lectin
classical

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44
Q

what is the common step of the C’ cascade that is common to all 3 pathways

A

the activation of C3 to C3a and C3b by C3 convertase

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45
Q

what is the action of C3a

A

mediator of inflammation and phagocyte recruitment

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46
Q

what is the action of C3b

A
  • binds with C3a and C4b to form C5 convertase

- powerful mediatory of opsonization of the pathogen

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47
Q

what is the action of C5a

A

mediator of inflammation and phagocyte recruitment

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48
Q

what is the action of C5b

A

binds with C6,7,8,9 –> MAC –> lysis

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49
Q

how is the alternative pathway of C’ activated

A

it isn’t “activated” - it is the result of spontaneous hydrolysis of C3 to C3a and C3b

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50
Q

what activates the classical pathway of C’

A

IgM and IgG bound pathogen –> activates C1 complex

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51
Q

explain the steps of the classical pathway of C’ up to the activation of C3

A

antigen-antibody interaction with C1q activates C1r –> activates C1s –> activates C2 and C4 –> C2a + C4b complex (C3 convertase) –> activation of C3

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52
Q

how is the mannan binding lectin pathway of C’ activated

A

the mannon-binding lectin binds to mannose and other sugars on microbes –> captures MASP-2 –> activates C4 –> activates C2 –> C3 convertase

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53
Q

which outcome does not occur with the MBL pathway of C’

A

MAC formation

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54
Q

the MAC outcome of C’ is essential in the control of which organism

A

Neisseria

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55
Q

what do extracellular TLRs recognise

A

structural components of bacteria (eg. flagellin, LPS, peptidoglycan)

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56
Q

what do intracellular TLRs recognise

A

genomic components of bacteria

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57
Q

what is the major molecule associated with TLR activation and signalling

A

MyD88

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58
Q

what are the inflammatory cytokines produced by macrophages and what are their functions

A 
IL-1 = activates vascular endothelium
TNF-alpha = increases cell migration
IL-6 = increases acute phase proteins
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59
Q

what are the antiviral cytokines produced by macrophages

A

IFN-alpha

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60
Q

what are the stimulatory cytokines produced by macrophages and what are their functions

A 
IL-12 = stimulates T cells and NK cells
GM-CSF = stimulates myeloid cell production
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61
Q

what are the suppressive cytokines produced by macrophages

A

IL-10

TGF-beta

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62
Q

what are the chemokines produced by macrophages

A

CXCL-7 (IL-8)

63
Q

what are the 3 phases of phagocytosis

A

attachment - binding to opsonised organism
ingestion - formation of phagosome
killing - fusion of phagosome-lysosome

64
Q

PAMPs binding to macrophages results in…

A
  • phagocytosis

- chemokine and cytokine release

65
Q

PAMPs binding to DCs results in

A
  • activation
  • chemokine and cytokine release
  • initiation of adaptive immunity
66
Q

what is the first stage of neutrophil migration from blood to tissue

A
  • microbial activation of C’ and macrophages and DC –> induces endothelial receptors such as E selectin and ICAM-1 and release CXCL8
67
Q

what is the 2nd stage of neutrophil migration from blood to tissue

A

CXCL8 attracts neutrophils that express CXCL8-R

68
Q

what is the 3rd stage of neutrophil migration from blood to tissue

A

neutrophils bind to E-selectin on endothelial cells and then LFA-1 of neutrophil binds to ICAM-1

69
Q

what is the 4th stage of neutrophil migration from blood to tissue

A

migration of neutrophil through the endothelial cells and into the tissue –> chemotaxis to site of inflammation

70
Q

what cells are cytotoxic cells

A

NK cells
eosinophils
macropahges

71
Q

what is the major cytokine released by NK cells

A

IFN-gamma

72
Q

what is the difference between epitope and antigen

A

epitope = part of the antigen that binds the TCR or BCR
antigen = the target of an immune response
(one antigen may have many epitopes)

73
Q

what is the difference between the conformation of epitopes that T and B cells recognise

A

T cells only recognise linear epitopes

B cells can recognise both linear and discontinuous epitopes

74
Q

what part of the B cell recognises antigen

A

the BCR/antibody/Ig

75
Q

what are the 2 forms of antibody

A 
surface antibody (IgG or IgM) - the B cell Receptor
secreted/soluble antibody
76
Q

what part of the antibody is involved in binding of the antigen

A

the variable region of the H and L chains

77
Q

what is the importance of the constant region of the antibody

A

determines whether the Ab is IgM, IgG, IgA, IgD or IgE

78
Q

what are the functions of the constant region of the antibody

A
  • mediate effector function
  • activation of classical C’ cascade
  • delivery of Abs
79
Q

where are our antibodies made

A

in the bone marrow during B cell development

80
Q

what are the 4 main stages of antibody diversity production

A
  1. V region
  2. junctional diversity
  3. Combinatorial diversity
  4. somatic hypermutation
81
Q

explain the variable regions of the heavy and light chains of an Ab

A

heavy - has 3 regions: variable, diversity and joining regions (VDJ)
light - has 2 regions: variable and joining regions (VJ)

82
Q

explain the 1st step of antibody diversity (V region)

A

RANDOM SOMATIC GENE REARRANGMENTS
heavy chain gene rearrangements in B cells
- D onto J and the DJ onto V
light chain gene rearrangements in B cells
- J onto V
- kapp and gamma rearrangment

83
Q

what is gene rearrangement during antibody diversity mediated by

A

RAG enzymes

84
Q

explain the junctional diversity stage of antibody diversity

A

during the joining process of the V region gene segments, deletions and insertions of nucleotides occur - mediated by TdT

85
Q

explain the combination diversity stage of antibody diversity

A

join a particular heavy chain with a particular light chain

86
Q

what gives the multipotent progenitor cell for haemopoietic cells the signal to transform into the common lymphoid progenitor cell

A

Flt3L expressed by bone marrow stromal cells tells the MPC to differentiate into CLP

87
Q

what is the role of IL-7 in B cell development

A

helps the process along

- if you dont have IL-7 - you dont have development

88
Q

explain the 4th step of antibody diversity production (somatic hypermutation)

A

after antigen binds to B cell in secondary lymphoid tissue –> genomic mutation occurs to help increase affinity

89
Q

what are the two fates of B cells

A

plasma cells –> pump out Ig (no longer have surface Ig)

memory B cells

90
Q

what are the 3 processes that underpin vaccination

A
  • stronger and faster proliferation of B cells
  • affinity maturation - stronger and more powerful
  • isotype switching
91
Q

which enzyme helps facilitate isotype switching

A

AID

92
Q

where does isotype switching occur

A

in secondary lymphoid tissues only after B cells have been stimulated

93
Q

what determines isotype switching

A
  • dependent on T cell help

- cytokines released (microenvironment)

94
Q

which Ig are more specialised for neutralisation

A

IgG and IgA

95
Q

which Ig are more specialised for opsonization

A

IgG1>IgG3>IgG4=IgA

96
Q

which Ig are more specialised for ADCC

A

IgG1=IgG3

97
Q

which Ig are more specialised for degranulation

A

IgE

98
Q

which Ig are more specialised for C’ activation

A

IgM»IgG1=IgG3>IgG2=IgA

99
Q

explain what neutralisation by Abs is

A

Ab binding to, and blocking proteins that are essential for attachment to the host cell –> blocking infection

100
Q

explain what opsonization by Abs is

A

Ab bind to and coat pathogen –> targets them for phagocytosis

101
Q

explain the process of NK cell killing of a cell

A
  • Ab binds to target cell via variable region
  • Ab binds to NK cell
  • cross linking of FcR triggers NK cell killing
102
Q

which Ig is associated with mucosal lymphoid tissue

A

IgA

103
Q

what is affinity maturation

A

the process by which a B cell increases its affinity for a particular antigen as the immune response progresses through somatic hypermutation
- as the infection continues, only high affinity surface Ig are selected for survival (clonal selection)

104
Q

what do you need for activation of T cells

A

presentation of the peptide antigen by the MHC

105
Q

which cells are the professional Antigen presenting cells (APCs)

A

dendritic cells
macrophages
B cells

106
Q

what is different between the antigens presented to B and T cells

A
  • Antibodies bind to epitopes in whole protein complexes

- T cells recognize short linear epitopes only that have to be presented by MHC

107
Q

explain the T cell R

A
  • has alpha and beta chains
  • -> alpha has V, J and C gene segments
  • -> beta has V, J, C and D regions
108
Q

what protein do all T cells have

A

CD3

109
Q

what is the difference in roles between CD8 and CD4 T cells

A

CD8 - kill tissues infected with IC pathogens and neoplastic cells
CD4 - produce cytokines that augment and specialise adaptive and innate responses

110
Q

where are MHC class 1 and 2 molecules found

A

1 - on almost all nucleated cells of the body

2 - on antigen presenting cells only

111
Q

which 3 molecules do MHC class 1 and 2 molecules have

A

1 - HLA A, B and C

2 - HLA DR, DP and DQ

112
Q

why is the antigen diversity larger for MHC class 2

A 
because the binding cleft is open and therefore can fit longer peptides in there
(MHC class 1 has a cleft with closed ends - can only fit small peptides)
113
Q

how are antigens held in the cleft of MHC molecules

A

held in place by specific anchor residues

114
Q 
polymorphism:
which genes within MHC class 1 and 2 vary most between different individuals
A 
MHC class 1 - the alpha 1 and alpha 2 chains
MHC class 2 - the alpha 1 and beta 1 chains
115
Q

how many alleles are there for MHC

A

6

116
Q

the polymorphism of MHC confers what property

A

different specificities for peptide

117
Q

what are the 2 pathways to get antigen presented on MHC

A 
cytosolic pathway --> MHC class 1
endosomal pathway --> MHC class 2
118
Q

explain the stages of the cytosolic pathway to get an antigen presented on MHC

A
  • protein in the cytoplasm (endogenous) -> through proteosome –> peptides
  • peptides actively transported to ER by TAP
  • MHC class 1 loaded onto peptide in ER = stabilisation of MHC
  • transported to Golgi –> expressed on cell surface
  • recognised by CD8 T cells
119
Q

explain the stages of the endosomal pathway to get an antigen presented on MHC

A
  • uptake of peptide by endocytosis (exogenous)
  • synthesis of MHC class 2 in ER –> cytoplasm with a stabilisation chain
  • MHC and peptide intersect in endosome
  • expressed on cell surface
  • recognised by CD4 T cell
120
Q

how can exogenous antigens find their way into the cytosolic pathway

A

cross presentation

121
Q

why are superantigens special

A

they do not need to be processed by the cell and presented via MHC

122
Q

how do superantigens activate the immune system

A

they bind directly to conserved regions of MHC Class 2 Beta1 chains together with the variable-beta chain of many T cell receptors
(they cross link the MHC of APC to CD4 T cells) –> large number of T cells activated –> significant pathology

123
Q

what “activates” DCs

A

the recognition of PAMPs or DAMPs by the PRR

124
Q

explain the early maturation events of DCs

A

signalling via TLRs results in:

  • loss of anchor molecules
  • increase in chemokine receptor expression (CCR7) –> migration to lymph nodes
  • increase in secretion of cytokines - to attract precursor DC and monocytes to infected site for more antigen uptake
125
Q

explain the late maturation events of DCs

A
  • increased surface expression of MHC class 2
  • increased antigen processing
  • increased adhesion molecules
  • secrete new chemokines
  • loose ability to capture angtigen
  • expression of costimulatory molecules
  • secrete cytokines
126
Q

which costimulatory molecules do mature DCs express

A

CD80 and CD86 - signal two for T cell activation

127
Q

explain the early events of DC to T cell interaction

A
  • initial adhesion involves LFA-1 (T cell) adhesion to ICAM-1 (DC)
  • stabilised when T cell R binds to peptide in MHC (signal 1) –> conformational change in LFA-1 to increase binding affinity
128
Q

what is signal 2 of Tcell-DC interaction

A

CD28 (T cell) to CD80/86 (DC)

129
Q

without costimulation (signal 2) - what happens to the t cell

A

in becomes anergic (inactivated)

130
Q

what is signal 3 of T cell-DC interaction

A

cytokines produced by DC - directs the differentiation of T cells

131
Q

which B cell responses are NOT dependent on T cells

A
  • activation by polysaccharides and most lipids
132
Q

explain the antibodies produced by T cell independent activation of B cells

A
  • exclusively IgM
  • low affinity
  • no memory
133
Q

what molecule expressed by T cells is essential for T cell dependent B cell activation and differentiation

A

CD40L

134
Q

when do T cells express CD40L

A

when they are activated by APCs

135
Q

what happens if you dont have CD40L

A

B cells cannot differentiate and therefore you are stuck with IgM

136
Q

where does the activation of B cells by T cells occur

A

in the paracortex/follicle junction in lymph nodes

137
Q

what is in the germinal centres of lymph nodes

A

sites of intense B cell proliferation and affinity maturation

138
Q

what are follicular dendritic cells

A

they are resident cells of the lymphoid follicle that capture immune complexes and drive B cell activation and affinity maturation (somatic hypermutation) by presenting the antigen all the time
(long term antigen depot)

139
Q

CD8 T cells require an additional activator (aside from the DC signal 1,2,3) - what it is

A

needs help by CD4 T cells - must recognise the same antigen

140
Q

how are CD8 T cells activated via CD4 T cells

A

CD4 T cells interact with the APC via CD40L and therefore allow the DC to induce CD8 T cell activation

141
Q

what are the two pathways for Cytotoxic T lymphocyte killing

A
  • granule exocytosis –> activation of caspases –> apoptosis
  • FasL-Fas mediated target cell apoptosis
142
Q

CD8 T cells kill tissues recognition of antigen in which MHC molecule

A

class 1

143
Q

how are B cells activated via C’

A

activated via the complement receptor CR2 (CD21)

- further boosted by T cells

144
Q

which cytokines by macrophages promote

  • increased vascular endothelial permeability
  • increased neutrophil migration
  • chemokines
A
  • vascular endothelial permeability = IL-1
  • increased neutrophil migration = TNF-alpha
  • chemokines = CXCL-8
145
Q

what are the steps of IC pathogens activating NK cells

A
  • pathogen interacts with PRR on macrophages –> inflammatory cytokines
  • interact with IC PRR in infected epithelial cells and macrophages –> IFN –> blocks neighbouring cells translation of viral mRNA
  • upregulate Class 1 MHC
  • induce influx and activation of NK cells –> kill infected cell
146
Q

when do APCs present CD80/86

A

only when activated by recognition of PAMPs/DAMPs by PRRs

147
Q

two outcomes of the failure of CD28-CD80/86 interaction

A
  • anergy of T cells

- binding of alternate T cell ligands to CD80/86 following activation may lead to suppression of T cell proliferation

148
Q

what alternate T cell ligands (other than CD28) can CD80/86 bind to, and when are they expressed

A

CTLA-4 - only expressed when the T cell has already been activated –> T cell suppression

149
Q

where do long lived plasma cells live

A

in the bone marrow

150
Q

which cytokine is essential for CD4 T cell proliferation

A

IL-2

151
Q

how does cyclosporine affect the immune system

A

inhibits IL-2 production –> therefore no T cell proliferation

152
Q

how does rapamycin affect the immune system

A

blocks signalling through IL-2R –> inhibits T cell proliferation

153
Q

which has the stronger interaction with CD80/86?

- CD28 OR CTLA-4

A

CTLA-4

Z MD1 Foundation block (7 decks)

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