Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Molecular Medicine > Immunology > Flashcards

Immunology Flashcards

1
Q

receptors of macrophage

A

TLR

Mannose R

CR R

Fc R

C3a and C5a R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

receptors of neutrophil

A

TLR

CR R

Fc R

C3a and C5a R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

receptors of basophil

A

IgE R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

receptors of mast cell

A

IgE R

C3a and C5a R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

receptors of NK cell

A

MICA stress R

MHC I R

Fc R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

receptors of dendritic cell

A

TLR

Mannose R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cytokines produced by macrophages

A

TNF-alpha

IL6

IL1

CXCL8

IL12.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cytokines produced by neutrophil

A

TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cytokines produced by eosinophil

A

prostaglandins

unspecific cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cytokines produced by basophil

A

histamine IL4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cytokines produced by mast cell

A

histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cytokines produced by NK cell

A

IFN-gamma

perforin

granzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cytokines produced by dendritic cell

A

Co-stimulatory proteins

TNF-alpha

IL6 IL1

IL12

IFN-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Functions of macrophages

A

phagocytosis

inflammation

T-cell activation

tissue repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

functions of neutrophil

A

phagocytosis

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

functions of eosinophil

A

parasitic defense

phagocytosis

allergies

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

functions of basophil

A

inflammation

parasitic defense

allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

functions of mast cell

A

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

functions of NK cell

A

viral control

tumour apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ways in which macrophage work

A

form phagolysosome

APC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ways in which neutrophils work

A
  • form phagolysosme (oxygen independent and dependent)
  • form NET (neutrophil extracellular trap):
  • – toxic granules
  • – chromatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ways in which eosinophils work

A

kill large parasites (by highly toxic granules and ROS)

cause inflammation (prostaglandins and cytokines)

levels increase when TH2 secretes IL5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ways in which basophils work

A

promote TH2 development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ways in which mast cells work

A

C3a and C5a cause histamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ways in which NK cells work

A

Apoptosis (by perforin and grazymes) when:

– Increased stress receptor

– Decreased MHC i

– Cell coated in antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ways in which dendritic cells work

A

form phagolysosome

activated further by IFN-alpha and IFN-beta

Moves (via chemokine gradient) to the nearest lymph node to activate T lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what does TNF-alpha do?

A

enhances endothelium permeability

expression of adhesion molecules

inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does IL6 do

A
  • makes liver produce acute-phase proteins
    • -c reacitve protein
    • -mannose binding lectin
  • fever
  • TH17 differentiation
  • TFH differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what does IL1 do

A

fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what does CXCL8 do

A

recruits neutrophils from bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what does IL12 do

A

activates NK cells causes production of TH1 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does IFN-gamma do

A

activates macrophages

TH1 differentiation

Suppersses TH2

Increases MHC processing

IgG1 and IgG3 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what does IFN-alpha do

A

activates NK cells

activates dendritic cells

increases MHC I production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does IFN-beta do

A

activates dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does IL2 do

A

helps promote cytotoxic t cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What does c reactive protein do

A

acts as opsonin on microbes activates classical complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what does mannose binding lectin do

A

activates mannose binding complement pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does ferritin do

A

binds iron - inhibits microbe iron uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what does fibrinogen do

A

causes coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what does factor VIII do

A

causes coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what does serum amyloid A do

A

recruitment of immune cells to inflammatory sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

steps of ADCC. What does ADCC stand for?

A

stands for Antibodhy dependent cellular cytotoxicity)

1: antibody binds antigens
2: Fc R on immune cells recognise antibody
3: cross-linking of Fc R signals immune cell to kill antigen
4: cell dies by apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the steps of inflammation

A

1- tissue injury

2- release of chemical signals (eg. histamine)

3- dilation of vessels and increased permeability of vessels

4- migration of phagocytes to area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What causes pain when you have inflammation

A

released mediators such as

  1. TNF-alpha
  2. Bradykinin
  3. Histamine

STIMULATE NERVE ENDINGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the functions of inflammation

A

1- prevents spread of damaging agents

2- phagocytosis (eg. cell debris and pathogens)

3- alerts adaptive immune system

4- sets stage for tissue repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the primary lymphoid organs

A

bone marrow

thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What immune cells does the bone marrow produce

A

myeloid cells

NK cells

B and T lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Where do T lymphocytes complete development

A

in the thymus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what initiates extravasion

A

chemokines and expression of adhesion molecules on endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what causes endothelial cells to express cell adhesion moleulces

A

TNF-alpha and C5a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the main cell adhesion molecule used in extravasion

A

P selectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are chemokines

A

molecules that form chemotactic gradient that directs leukocytes to site of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the five steps of extravasion

A

rolling adhesion

tight adhesion

transmigration

breakdown of basement membrane

Cells follow chemokine gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What causes rolling adhesion in the extravasion process

A

Carbohydrate ligands (on pathogen) bind to P selectin molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What causes tight adhesion in the extravasion process

A

IFA integrins on leukocytes are activated by (inside-out) chemokine signalling

Bind to ICAM Receptors on endothelial cells tightly

Stop rolling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What causes transmigration in the extravasion process

A

PECAM proteins present on leukocytes and on junctions between endothelial cells

Enables leukocytes to move through the gap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What causes the break down of the basement membrane in the extravasion process

A

MMP. It is an enzyme produced by leukocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the physical barriers in the immune response

A

MECHANICAL BARRIERS

Mucous secretion and ciliated tract

Secretion of tears

Flushing action of urine

BIOCHEMICAL FACTORS

Lysozyme in tears

HCl of stomach

MICROBIAL FACTORS

Commensal bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What do CR receptors do

A

Complement receptors Recognise 3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What do Fc receptors do

A

Receptor of Fc (constant region) of antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the receptors to recognise PAMP (pathogen-associated moecular pattern)

A

TLR 1 (TLR6=heterodimer): Peptidoglycan

TLR4: LPS

TLR5: Flagellin

TLR 3 (Intracellular): dsRNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Explain the process of phagocytosis

A
  • phagocyte binds via receptor
  • gets engulfed
  • forms phagosome fuses with lysosome
  • phagolysosome gets destroyed via an oxygen-dependent or oxygen-independent pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Describe the process of oxygen-independent phagocytosis

A

Lysosome and basic proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What activates the complement proteins

A

Cutting of complement proteins into fragments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the main complement chemo-attractants

A

C3a and C5a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the main complement opsonins

A

C3b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What forms the MAC

A

C5b6789999

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the functions of effector CD4 T cells

A

activate dendritic cells to increase activation of CD8 T cells (cause production of B7)

Increase activation of macrophages that present peptides on MHC II

Activate B cells to become plasma cells that present peptides on MHC II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are examples of mucosa-associated lympoid tissue

A

Tonsils

Peyers patches

appendix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What determines the function of an antibody

A

the constant region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What causes production of acute phase proteins

A

IL1 and IL6 which stimulate the liver to produce acute phase proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Explain inflammation caused by the complement

A

C3a and C5a

Chemo-attraction recruits cells

Release of histamine by mast cells

Increase permeability by endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Explain the classical complement pathway

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Explain the lectin pathway

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Explain the alternate pathway

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does a mature dendritic cell activate a T cell

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How does a CD8 cell kill an infected cell

A
78
Q

How does a T cell activate a macrophage

A
79
Q

How does a T cell activate a B cell

A

Sends survival signals

80
Q

What two chains does a MHC I consist of

A

Beta2 microglobin

alpha chain

81
Q

What encodes MHC

A

HLA (Human Leukocyte Antigen)

82
Q

How many amino acids is each peptide attached to MHC I

A

8-10

83
Q

Explain antigen processing in a cell expressing MHC I

A
  1. Viral proteins degraded by LMP Proteasome – 8-10 amino acids in length
  2. TAP1 and TAP2 (Transporters associated with antigen processing) translocate peptides from cytosol to ER lumen
  3. MHC I helped by chaperon eproteins due to it being unstable until it binds to protein
  4. MHC I moves through ER, attaches protein, moves through golgi and gets packaged into vesicle to be expressed on surface
84
Q

What are the kinds of MHC I that each person has

A

A maternal and paternal version of:

HLA-A

HLA-B

HLA-C

85
Q

What type of MHC is associated with Ankylosing Spondylitis

A

HLA-B27

86
Q

What type of MHC is associated with recovery from lethal malaria

A

HLA-B53

87
Q

What two protein chains are associated with MHC II? What forms the peptide binding cleft

A

alpha and beta chains

alpha-1 and beta-1 form the peptide binding cleft

88
Q

What are the types of MHC II in humans

A

Materal and Paternal copies of:

HLA-DP

HLA-DQ

HLA-DR

89
Q

How many amino acids does each MHC II bind

A

Bind peptides of 13-17 amino acids in length

90
Q

What is different between the way that MHC I binds peptides and the way that MHC II binds peptides

A

MHC I - attached at one site

MHC II - attached along entire length

91
Q

Explain the antigen processing in MHC II

A
  1. MHC II is made on ER
  2. Invarient chain binds to prevent cytoplasmic peptide binding and travels to endosome in vesicle
  3. Acid proteases cleave invarient chain. Leaves CLIP blocking the peptide groove
  4. Protein HLA-DM swops CLIP for pathogen peptides
  5. Packaged into vesicle
  6. Expressed on cell membrane
92
Q

Which MHC is associated with Coeliac disease? What is coeliac disease?

A

HLA-DQ2 and HLA-DQ8

Coeliac disease is Gluten Sensitive Enteropathy

93
Q

What is the structure of a TCR

A
94
Q

What type of recombination does an alpha chain undergo (of a T cell)

A

V-J recombination

95
Q

What type of recombination does a beta chain undergo (of a T cell)

A

V-D-J recombination

96
Q

What enables TCR diversity

A
  • Ingeritence of multiple germline genes
  • somatic recombination
  • Junctional diversity: imprescise joining and insertion of small sets of nucleotides at the junctions
  • Random selection of alpha and beta chains
97
Q

Explain the process of positive selection

A
  1. MHC I and MHC II come into contact with developing T cells (thymocytes)
  2. CD4 == MHC I. CD8 == MHC II
  3. If they don’t bind, they die by neglect
98
Q

Explain the process of negative selection

A
  1. Rare pepulation of thymic cells generally expressed outside the thymus make AIRE (autoimmune regulator) which is:
    1. Transcription factor
    2. Enables expression of proteins which are only produced in specific cells (E.g. insulin)
  2. If a thymocyte binds too strongly to this, they die by apoptosis
99
Q

Where does positive selection of T cells happen

A

In the cortex of the thymus

100
Q

Where does negative selection of T Cells happen

A

In the medulla of the Thymus

101
Q

What do effector CD4 cells secrete

A

IL12 – promotes CD8 cell proliferation

102
Q

What cytokines do CD8 T cells secrete

A

IL2

103
Q

How does the extrinsic pathway of the CD8 T cell work

A

FAS ligand binds to FAS

104
Q

How does the intrinsic pathway of the CD8 T cell work

A

Perforin and Granzyme are secreted which cause apoptosis of the antigen

105
Q

What determines the differentiation of a CD4 T cell?

What are the associated cytokines with each CD4 T cell?

A

What kind of cytokines are present when it is differentiating

  • IFN-gamma + IL12 = TH1
    • IL4 = TH2
  • TGF-beta + IL6 = TH17
  • IL6 = TFH
  • TGF-beta + IL2 = TReg
106
Q

What cytokine does TH1 secrete

A

IFN-gamma (activates macrophages)

107
Q

What does TH1 activate? How does it do this?

A

Macrophages

Via a CD40 + CD40-L synapse

108
Q

What is the main role of TH1

A

to destroy microbes that persist in macrophage vesicles

109
Q

What cytokines do TH2 secrete

A

IL4 and IL5

These recruit granulocytes

110
Q

what is the main function of TH2

A

to destroy extracellular parasites

111
Q

What happens if TH2 is activated inappropriately?

A

Allergies in most cases

112
Q

What is the first effector helper cell to be generated in the presence of IL6 and TGF-beta

A

TH17

113
Q

What cytokine does TH17 secrete? What is its function?

A

IL17

Causes fibroblasts and epithelial cells to secrete IL6, CXCL8, G-CSF

114
Q

What is the main role of TH17

A

amplifies the acute inflammatory response by the innate emmune system. It’s main role is to recruit neutrophils important in fighting extracellular bacteria and fungi.

115
Q

Where are TFH located?

A

Stay in the follicles of secondary lumphoid organs (lymph nodes and spleen)

116
Q

What cytokines do TFH secrete

A

IFN-gamma

IL4

TGF-beta

117
Q

What is the main role of TFH

A

to activate B cells:

  • To somatic hypermutate the variable region
  • To class switch to produce new antibodies
  • To become plasma cells
118
Q

How does TFH activate B cells

A

Makes a CD40 + CD40-L immunological synapse

119
Q

In the presence of ___, B cells produce ___

A
  1. IFN-gamma; IgG1 and IgG3
  2. IL4; IgE
  3. TGF-beta; IgA
120
Q

What enables memory T cells to block the apoptotic death of some lymphocytes

A

Expression of BCL2

121
Q

What are the two types of Tregs

A

Natural Tregs

Adaptive Tregs

122
Q

Where do natural tregs develop

A

thymus

123
Q

What do natural tregs secrete

A

IL10 and TGF-beta

Inhibit T cell proliferation. Prevents dendritic cell from secreting IL12, thus preventing CD4 differentiation into TH1

124
Q

Where do adaptive tregs develop

A

in the periphery

125
Q

What do adaptive tregs secrete

A

IL10

IL4

TGF-beta

126
Q

What does a lack of adaptive tregs result in

A

autoimmune disease in gut

inflammatory bowel disease

127
Q

Where do B cells develop? Where is its receptor made

A

In the bone marrow

128
Q

Describe a BCR

A

2 heavy and 2 light chains

Heavy chains: variable and constant region

Light chains: variable and constant region

Disulphide bonds join them

129
Q

Explain the recombination of the B cell heavy chain

A

V-D-J recombination

Variable region is attached to the first constant region mu.

If mRNA is produced and cannot be translated into functional protein, other chromosome is recombined instead.

130
Q

Explain the recomination of the B cell light chain

A

V-J recombination

Two gene coding loci:

  • Kappa (attempted first) — 2x as many
  • Lambda
131
Q

Explain the process of negative selection of BCR

A

If BCR binds too strongly to antigen - undergoes apoptosis

132
Q

Where does a naive B cell recieve its survival signals from?

A

From the lymph node when it is circulating

133
Q

How long does a naive B cell survive

A

3 days

134
Q

Where in the lymph node is a B cell found

A

In the primary lymphoid follicle

135
Q

Explain the process of activation of a B cell

A
  • BCR binds to antigen on Follicular Dendritic Cell and presents them on MHC II after endocytosing antigen.
  • TFH cell recognises peptide and activates B cell
  • Some B cells are activated to proliferate and become plasma cells that secrete IgM
  • Class switching and Somatic hypermutation happen due to the TFH binding
136
Q

What are the factors that lead to diversity of the BCR repertoire

A
  1. Combined Diversity (VDJ)
  2. Junctional diversity (addition of nucleotides)
  3. Combination of heavy and light chain
  4. Somatic hypermutation
137
Q

How does class switching occur

A
  1. Change in the constant region of the heavy chain in a gene. This requires preceding constant regions to be removed as first is always selected. This results in excised DNA segment
  2. Results in a different antibody

THE ANTIBODY IS DETERMINED BY THE CYTOKINES THAT ARE PRESENT

138
Q

What is the variable region of an antibody also called

A

Fab (Fragment antibody binding)

139
Q

What is the constant region of an antibody also called?

A

Fc (Fragment constant)

140
Q

What are the different antibody constant regions? What isotype/class do they produce?

A

mu = IgM

delta - IgD

gamma = IgG

epsilon = IgE

alpha = IgA

141
Q

What is the structure of IgM

A

Pentamer == 4 constant regions

142
Q

How long does an IgM last

A

5 days

143
Q

What is the structure of an IgG

A

Monomer == 3 constant domains

144
Q

What is the function of IgG

A

Fixes complement

145
Q

Which cells recognise IgG

A

macrophages, neutrophils and dendritic cells

146
Q

How long does IgG last

A

23 days

147
Q

What is the structure of IgA

A

Dimer == 3 constant regions

148
Q

What is the function of IgA

A

Primarily acts as a neutralising agent

149
Q

How long does IgA last

A

6 days

150
Q

How does IgA get into the hollows of organs

A

Secreted by plasma cells in MALT

Binds to receptor and is internalised

Carried through cytoplasm of epithelial cell to lumen

Cleaved enzymatically at lunial surface which results in the release of IgA with part of receptor (secretory component) attached

151
Q

What is the structure of IgE

A

Monomer

152
Q

What is the function of IgE? How does it work?

A

Binds to FC-epsilon-R on mast cell and eosinophil

Remains on surface of mast cells, waiting for second exposure to antibody.

If an antibody binds a large mulivalent pathogen again, IgE is cross-linked on mast cell surface which results in degranulisation

153
Q

How long does IgE last

A

6 hours

154
Q

Which antibody is important in allergies

A

IgE

155
Q

What does JAK-STAT signalling regulate

A

Cellular responses to cytokines and clood cell growth factors (poeitins):

haemopoeisis

Immune development

Immune activation

156
Q

What results from the dysregulation of JAK-STAT signalling

A

Inflammatroy disease

Erythrocytosis

Immune deficiency

Leukaemias and Myeloproliferative disorders

157
Q

Explain the process of JAK-STAT signalling

A
  1. Cytokine binds to tyrosine receptor and causes it to dimerise
  2. JAK (on the tyrosine receptor) phosphorylates the tyrosine receptor. This causes it to attract STAT
  3. JAK phosphorylates STAT which then leaves the receptor
  4. STAT dimerises, enters nucleus and acts as a transcription factor
158
Q

What are the types of cytokines that are most commonly used in JAK-STAT signalling

A

IL2, IFN-gamma, Erythropoeitin, GH

159
Q

Explain the process of TCR Signalling

A
  1. TCR + CD4 complex binds to MHC II
  2. LCK (tyrosine kinase) phosphoryates part of the TCR
  3. The phosphorylated TCR results in activation of ZAP-70 (tyrosine kinase)
  4. ZAP-70 phosphorylates LAT and SLP-76 (both scaffold proteins)
  5. Scaffold proteins are held together by GADs (adaptor proteins). Phosphorylation of the scaffold proteins results in activation of PLC-gamma (phospholipase C)
  6. Remain steps follow that of the Gq signalling pathway
160
Q

Explain the process of BCR signalling

A

BCRs are cross-linked by an antigen

This stimulates SRC Tyrosine Kinases inside of the cell to be activated

161
Q

What is a NF-kappa-B

A

A transcription factor

162
Q

What does NF-kappa-B simulate the production of

A

cytokines

acute phase proteins

apoptotic regulators

163
Q

Explain the NF-kappa-B family

A

Class

Protein

Aliases

I

NF-kappa-B1

P105 – P50

NF-kappa-B2

P100 – p52

II

Rel A

P65

Rel B

C-Rel

164
Q

Explain the significance of having Class I and Class II NF-kappa-B. Also explain the difference thereof.

A

Class I need to be bound to class II

Class I: large precursors are converted into mature proteins (by degradation of the C terminal)

Class II are ready to activate the gene due to having TAD (Transactivation domain)

Class I has no TAD. Results in suppression of gene unless bound to Class II

165
Q

What are the parts of NF-kappa-B that binds to DNA

A

N-terminal Rel homologous domain

166
Q

What are cytokines and receptors that work together to activate the NF-kappa-B

A

TNF-alpha via TNFR

IL1 VIA IL1 R.

BCR and TCR also activate pathways

167
Q

Explain the process of NF-kappa-B signalling

A
  • I-kappa-B naturally inhibits dimerisation of the pathway
  • IKK-beta is in a complex with IKK-alpha and NEMO
  1. Cytokine binds to a Receptor
  2. TAK1 gets activated, through adaptor proteins, by the TNF Receptor
  3. TAK1 phosphorylates IKK-beta and activates it
  4. This phosphorylated IKK-beta phosphorylates I-kappa-B with tags it for polyubiquination
  5. Heterodimer is now able to form
168
Q

What are the different receptors used in NK-kappa-B signalling? What are their functions?

A

BCR/TCR –> Adaptive immune response

TLR –> Innate immune response

TNF-beta and IL-1R1 –> Inflammatory response

169
Q

What are the diseases that have an effect on the NF-kappa-B pathway? What do they do?

A
  • Viruses
    • HIV Proteins
      • Binding sites for NF-kappa-B controls expression of the viral gene
    • Yersina Pestis (causes plague)
      • Secretes YopP that prevents ubiquination of I-kappa-B which causes blockage of the person’s immune response
  • Cancers
    • Inappropriate activation of NF-kappa-B
  • Inflammatory diseases
    • Exploit this pathway
170
Q

Regarding monoclonal antibodies, what can be conjugated to them

A

Fluorochromes and Enzymes

171
Q

What are examples of in-vitro diagnostic agents

A

ELISA

Flow Cytometry

Immunohistochemistry

Western Blotting

172
Q

Explain the process of Indirect ELISA

A

Detects antibody in serum

  1. The well is coated with antigen
  2. Serum is added and the antibodies bind
  3. Well is washed and antibodies are added that are anti-human
  4. Washed again and a substrate is added that changes colour
173
Q

What is the major difference between Direct and Indirect ELISA

A

Indirect ELISA - Detects antibody in serum

Direct ELISA - Detects antigen in serum

174
Q

What are the properties that can be tested for using flow cytrometry

A

Particle/cell size (forward scatter - a shadow)

Particle/cell complexity (side scatter - granules, nuclear lobes)

Surface or intracellular markers (fluorochromes linked to MoAB)

175
Q

In flow cytrometry, what are the antigens that are targetted by fluorochrome labelled monoclonal antibodies

A

B-cells –> CD19, CD20, CD22

T-cells –> CD3, CD4, CD8

Myeloid Cells –> CD13, CD33

176
Q

What are all the things required for cell cytrometry?

A
  1. Cells need to be in single file.
    1. In sheath fluid (a special solution)
    2. Hydrodynamic focusing: Uses energy to focus small particles to centre
  2. Laser
  3. Optics –> mirrors and Filters
  4. Electronic detection system
  5. Computer software
177
Q

What do you use to sample and identify components of a solid tumour

A

Immunohistochemistry

Stain with monoclonal antibodies with associated colour change

178
Q

Explain the process of western blotting

A
  1. Separate proteins using gel elctrophoresis
  2. Stain separated proteins with antibodies to see which ones they are

(helps in detection of HIV)

179
Q

What is the difference between monoclonal and polyclonal antibodies

A

Polyclonal = Many antibodies that are different that recognise the same antigen

Monoclonal = Antibodies that are identical (come from same B cell)

180
Q

How are monoclonal antibodies produced using mice

A
  1. Mouse injected with antigen
  2. Reinject mouse later to get a greater secondary immune response
  3. Take lymph nodes and spleen and put into tube to get B lymphocytes
  4. Add myeloma cells:
    1. live long
    2. some form hybridomas with B lymphocytes
  5. Need to select for hybridoma cells
181
Q

Explain the selection for hybridomas

A
  • B cells
    • short-lived and die in a few days
  • Myeloma cells
    • no enzymes for salvage pathway
    • De Novo pathway blocked
  • Screening and purication of most appropriate antibodies from the most appropriate hybridome
    • You need one type of hybridoma in one plating well in order to select hybridoma secreting correct antibody
182
Q

Explain the selection of Fab (variable region) using bacteriophages in creating monoclonal antibodies

A
  1. Isolate populations of genes encoding antibody variable regions
  2. Construct fusion protein of V region with a bacteriophage coat protein
  3. Cloning a random population of variable region gives rise to a phage-display library
  4. Selection of phage with desired V region occurs by specific binding of antibody to antigen
183
Q

What are the examples of drugs that use monoclonal antibodies? What do they do?

A

Trastuzumab: Inhibits growth factor receptor found on surface of some breast cancer cells

Infliximab: Targets TNF-alpha in inflammatory diseases

Abciximab: Targets an integrin, preventing activated platelets from aggregating

184
Q
A
185
Q

What does IL5 do?

A

Recriuts and activates eosinophils

B cell proliferation

186
Q

What does IL4 do

A

Recruits and activates mast cells

Recruits and activates basophils

Proliferation of TH2

IgE production

Inhibits TH1 development

187
Q

What does G-CSF do

A

Recruits granulocytes (neutrophils, eosinophils, basophils)

188
Q

What does erythropoeitin do

A

increases RBC production

189
Q

What does Thrombopoein do

A

Increases production of platelets

190
Q

What does IL10 do

A

Supresses the immune system

191
Q

What does IL17 do

A

activates fibroblasts

activates endothelial cells

proinflammatory

recruits neutrophils

192
Q

What does TGF-beta do

A

IgA production

TH17 differentiation

Promotes Treg

Inhibits immune system

Molecular Medicine (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions