Brainscape's Knowledge GenomeTM

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


See full index

Year 2 > Immunology > Flashcards

Immunology Flashcards

1
Q

MHC class II molecules usually present peptides of what origin?

A

Exogenous

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

Why can MHC class II molecules not bind to peptide in the ER?

A

A protein called the invariant chain in the MHC peptide-binding groove blocks peptides from binding

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

Where are MHC class I and II molecules assembled?

A

Endoplasmic reticulum

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

When is the invariant chain (protein blocking the MHC peptide-binding groove) degraded?

A

Following fusion with the endocytotic vesicle containing antigen

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

What’s involved in antigen processing for MHC class I and II?

A 
MHC class I: proteasome 
MHC class II: proteases within endocytic vesicle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where do MHC class I and II associate with its peptide fragment?

A 
MHC class I: Within the ER 
MHC class II: Within endosomal vesicles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MHC class I molecules usually present peptides of what origin?

A

Endogenous (microbial or self)

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

Where are peptides produced from extracellular antigens/ pathogens?

A

Within enodcytic vesicle

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

Where are peptides produced from viruses or intracytosolic bacteria?

A

Within cytosol

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

What is sequence of class I antigen processing?

A 
Endogenous antigen is degraded in cytosol by proteasome 
Peptides are translocated into the ER 
Peptides associate with MHC class I molecules within ER 
Peptide:MHC complexes move to cell surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is sequence of class II antigen processing?

A 
Exogenous antigen is taken up into cell via endocytic vesicles 
Antigen is degraded in endocytic vesicle by proteases (cathepsin L & S) 
MHC class II produced in ER transported in vesicle to & fuses with endosome 
Peptides associate with MHC class II molecules as invariant chain is degraded 
Peptide:MHC complexes move to cell surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What’s a CTL?

A

cytotoxic T lymphocyte

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

Recognition of virally infected cells by CD8 killer T cells is dependent on what?

A

MHC class I

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

What does CD8 bind to and what is CD8 expressed on?

A 
CD8 binds to MCH class I
CD8 expressed on cytotoxic T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does CD4 bind to and what is CD4 expressed on?

A 
CD4 bind to MHC class II
CD4 expressed on T helper cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are Kupffer cells?

A

Phagocytic cell in liver that lines hepatic sinusoids

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

How may extracellular antigens be presented by MHC class I molecules? And give an example

A

Cross presentation

e.g. Hepatitis C

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

Why would CD4 T cells be expected to be generated in Hepatitis C? And why is this not the case?

A 
Hepatitis C does not infect kupffer cells (macrophage-like cells of liver) - only infects hepatocytes
Kupffer cells therefore acquire viral hepatitis C proteins by phagocytosis/ endocytosis of dying hepatocytes = pathway for MHC class II presentation generating CD4 T cells 
However cross presentation occurs and CD8 T cells are produced instead
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a dendritic cell?

What the difference between an immature and mature/ activated dendritic cell?

A

Dendritic cell: professional antigen presenting cell derived from bone marrow
Immature dendritic cell: take up and process antigens but cannot stimulate T cells
Mature dendritic cell: able to stimulate T cells, present in secondary lymphoid tissue

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

Why are live attenuated vaccines the best way to achieve a cytotoxic T lymphocyte (CTL) response?

A 
Only live viruses have capacity to replicate intracellularly 
Can be presented by MHC class I to CD8 T cells (which are cytotoxic T lymphocytes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the human leukocyte antigen (HLA) system?

A

Group of genes that encode cell surface antigen-presenting proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which HLA genes encode for MHC class I ?

A

HLA A, B and C

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

Which HLA genes encode for MHC class II ?

A

HLA DP, DQ and DR

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

Which cells are MHC class II molecules found on?

A

Immune cells e.g. dendritic cells, B cells, macrophages

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

Which cells are MHC class I molecules found on?

A

All nucleated cells

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

Name 3 professional antigen presenting cells

A

Conventional dendritic cells
B cells
Macrophages

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

What are the differences in structure between MHC class I and II molecules?

A

Class I: only 1 chain crosses the membrane, made of alpha 1, 2, 3 and beta 2 microglobulin domains
Class II: both/ 2 chains cross the membrane, made of alpha 1, 2 and beta 1, 2 domains

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

What do dendritic cells have that increase the chance of the antigen presented on its surface to come into contact with the antigen-specific T cell?

A

Dendrites that sweep large volumes of space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do viruses prevent being killed by CTL/ cytotoxic T lymphocytes (express CD8)?

A 
Viruses down regulate MHC class I molecules on infected cells 
So not recognised by CD8 on CTL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

If infected cells do not present MHC molecules on their surface, how are they disposed of?

A

Killed by natural killer cells
If there were MHC molecules on the cell, they would bind to inhibitory receptors on NK cells preventing them from killing the cell

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

1) What 2 things are required for activation of a naïve T cell?
2) Why is signal 1 alone not enough to activate T cells?

A

1) Antigen-specific signal
(T cell receptor and its co-receptor CD8/ 4 recognise the peptide:MHC class I/ II complex on the dendritic cell surface)
Co-stimulatory signal
(T-cell co-stimulatory receptor CD28 binds to the B7 co-stimulatory molecule expressed on the dendritic cell)

T cell receptor, CD8/4 and CD28 receptor on naive T cell
peptide:MHC complex and B7 molecule on dendritic cell

2) MHC groove is always filled with peptide e.g. from self proteins sometimes, so should insufficient to activate T cell

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

Once a CD8 T cell is activated, what trigger is required for it to kill cells?

A 
Triggered by MHC class I presented on cell 
(No need for co-stimulatory signal once activated)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which cell is extremely efficient at stimulating naive T cells and why?

A

Dendritic cells - they express a high level of B7

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

How do natural killer cells and cytotoxic T cells kill target cells?

A

Release perforin and granzymes

Causing apoptosis

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

What is the role of Fas within cytotoxic T cell action?

A

CTLs express Fas ligands on their surface
Which binds to Fas molecule on target cell membrane
Activating caspases = apoptosis

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

Which cells do naive CD4 T cells become which are most relevant to viral infection? What do they do and produce?

A

TH1 cells
Exit lymph node, go to site of infection and activate macrophages
Release IL-2 and IFN gamma

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

Which T cells remain within lymph nodes?

A

Follicular helper T cells

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

What is linked recognition?

A

B and T cells can interact as they recognise the same antigen

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

What type of MHC molecule do B cells express?

A

MHC class II

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

How do B cells presenting viral peptides on their MHC II molecules bind to helper T cells?

A

CD40 on B cells bind to CD40 ligand on TH cell

Peptide:MHC II complex binds to T cell receptor

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

What sort of epitopes can B cells recognise?

compared to T cells

A

Protein/ carbohydrate/ lipid/ nucleic acid

T cells only recognise peptide epitopes

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

How do B cells undergo antibody isotype change to increase antibody affinity?

A

Class switching

Somatic hyper-mutation

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

What type of viruses are the majority that infect humans?

A

RNA viruses

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

Name 3 sentinel cells

A

Macrophages
Dendritic cells
Natural killer cells

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

What are the molecular tripwires of the innate immune system?

A

Pattern recognition receptors

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

What do pattern recognition receptors (PRRs) recognise?

A

Pathogen-associated molecular patterns (PAMPs)

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

How are PRRs effective at detective viral infection?

A

Viral nucleic acids detected in cytosol - viruses use host’s machinery for transcription, translation and replication

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

Name 2 important cytoplasmic pattern recognition receptors (PRRs)

A

RIG-1 like receptor

MDA-5

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

What do RIG-1 like receptors (RLRs) bind to?

A

Unusual RNA: double stranded or mRNA without a cap on 5’ end
This binding causes RLR to bind to MAVS (mitochondrial protein)

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

What does RLR binding to MAVS essentially cause?

A

Type I interferon expression

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

What do toll like receptors (TLRs) do?

A

Sense microbial products inside and outside human cells

52
Q

Which toll like receptors (TLRs) are present on endosomes?

A

3, 7, 8 and 9

53
Q

Which toll like receptors (TLRs) are present on plasma membranes?

A

1, 2, 4 and 5

54
Q

Name 3 pyogenic (cause fever) cytokines

A

IL-6
IL-1beta
TNF-aplha

55
Q

How long does immediate innate immunity last?

A

0-4 hours

56
Q

Which defences are involved in immediate innate immunity?

A

Recognition and elimination by preformed soluble and resident effector molecules
Complement system

57
Q

How long does induced innate immunity last?

A

4 hours to 4 days

58
Q

Which defences are involved in induced innate immunity?

A

Recruitment of additional innate effector cells

Inflammation, fever, acute response

59
Q

Which TLRs respond to RNA viruses?

A

TLR 3, 7 and 8

60
Q

Which TLRs respond to DNA viruses?

A

TLR 9

61
Q

What recognises viruses at plasma membranes and endosomes?

A

Pattern recognition receptors (PRR)

62
Q

Which toll-like receptors recognise viral glycoproteins?

A

TLR 1, 2 and 4

63
Q

TLR signals lead to transcription of what?

A

Type I interferons alpha and beta

64
Q

What can interferon response factors (IRFs) initiate once phosphorylated and entered the nucleus?

A

Initiate mRNA synthesis

65
Q

Which cells are capable of producing Type I interferons alpha and beta?

A

Nearly all cells

66
Q

What are 3 actions of interferon response?

A

Induce resistance to viral replication in all cells
Increase expression of ligands for receptors in NK cells
Activate NK cells to kill virus-infected cells

67
Q

Why can naive T cells only be activated by professional antigen presenting cells?

A

Because only professional APCs have B7 for co-stimulatory signal

68
Q

How does CMV (cytomegalovirus) try to block peptide entry to ER?

A

Inhibits peptide loading

69
Q

How does TLR (toll like receptor) triggering relate to activation of naïve CD8 T cells?

A

TLR triggering leads to up regulation of co-stimulatory ligands B7 on dendritic cells

70
Q

What if the T and B cell interacting recognise different epitopes of the viral particle?

A

As long as both epitopes are from the SAME COMPLEX this is fine

71
Q

In hepatitis B infection, what order are the antibodies produced?

A

Core before surface

72
Q

How can immunity against hepatitis B by vaccination be distinguished from by natural infection?

A

Natural infection: core antibodies present as well as surface
Vaccination only contains surface antigens so only surface antibodies present in blood afterwards

73
Q

How can chronic hepatitis B infection be differentiated from acute?

A

Acute: IgM
Chronic: IgG
(core antibodies present in blood in both)

74
Q

What are the 4 possibilities with the following serology results:
HBsAg - negative
anti-HBs - negative
anti-HBc - positive

A

Resolved infection - most common
False-positive anti-HBc
Low level chronic infection
Resolving acute infection

75
Q

Where are the primary lymphoid tissues and what do they do?

A

Bone marrow and thymus

Lymphocyte development and maturation occurs here

76
Q

Where are the secondary lymphoid tissues and what do they do?

A

Lymph nodes, spleen and mucosal-associated lymphoid tissue

Acquired immune responses initiated here

77
Q

Why vaccinate asplenics and people with sickle cells disease and severe coeliac disease with pneumococcal conjugate vaccine?

A

sickle cells disease = functional asplenia
severe coeliac disease damages the spleen

asplenia = decreased clearance of encapsulated bacteria (e.g. Hib, E. coli, salmonella, pneumococcus, neisseria meningitidus) from bloodstream
APC migrate to spleen via bloodstream as no lymphatic supply - secondary lymphoid tissue

78
Q

Which TLRs recognise single stranded viral RNA?

A

7 and 8

79
Q

Which TLRs recognise double stranded viral RNA?

A

3

80
Q

Which immunoglobulins are present in milk and can cross the placenta?

A

Milk - IgA

Placenta - IgG

81
Q

Explain generally how pattern recognition receptors (PRRs) work within the innate response

A

PRR detect PAMPs
Activates IRFs
that are phosphorylated and enter the nucleus
to cause interferon synthesis
Interferons binds to interferon receptors
Triggering transcription of hundreds of interferon stimulated genes (ISG)

82
Q

What do interferon stimulated genes (ISGs) do?

A

Suppress:
Viral entry
Viral replication
Alter cellular metabolism to generate anti-viral state

83
Q

What increases proteasome and macrophage efficiency?

A

IFN gamma

released by NK cells

84
Q

What is the primary role of conventional dendritic cells?

A

Activation of naïve T cells

85
Q

What is the primary role of plasmacytoid dendritic cells?

A

Production of interferons upon virus exposure

86
Q

What do plasmacytoid dendritic cells express high levels of and what does this allow?

A

TLR 7 and 9

Detection of viral infection

87
Q

What can be given for hep B and C viral infections?

A

Recombinant interferon a

88
Q

Which cytokines activate natural killer cells?

A

Interferon alpha and beta
IL-12
TNF-alpha

89
Q

What are the 3 waves of defence against viral infection?

A

1st: cytokines (IFN-alpha and beta, TNF-alpha ans IL-12)
2nd: natural killer cells
3rd: T-cells

90
Q

When are cytokines/ NK cells/ T cells produced and when do their numbers peak during viral infection?

A

Cytokines until day 5, peak at day 2
Natural killer cells until day 6, peak at day 3
T-cells from day 2, peak at day 7

91
Q

Why do subcutaneous and intramuscular injections produce good immune responses?

A

Both areas well served with conventional dendritic cells

subcut more likely to trigger side effects

92
Q

Why does injecting into the buttocks not produce a good immune response?

A

Adipose tissue poorly vascularised and poorly served by DCs

93
Q

How do conventional dendritic cells transport antigens from infection site to the secondary lymphoid tissue?

A

TLR signalling
Causes CCR7 receptors to be expressed on DC
They bind to CCL21 (chemokine produced by lymphoid tissue)
So DC migrates to lymphoid tissue
Antigen presenting function also enhances
So activate naïve T cells in lymphoid tissue

94
Q

How does CMV down regulate MHC class I?

A

Blocks peptide entry to ER

Inhibiting peptide loading

95
Q

Where are B cells stored?

A

Lymph node

Migrate to bone marrow as plasma cells

96
Q

What does Activation-Induced Cytidine Deaminase (AID) do?

A

Catalyses somatic hypermutation of Ig genes leading to affinity maturation of antibodies in B cells

Catalyses class switching of Ig constant regions leading to isotype-switching of antibodies

97
Q

How is the complement system involved in immediate innate immune response?

A

Mannose-binding lectin is a PRR

98
Q

How do the most pathogenic viruses prevent the body from entering an antiviral state?

A

Shut off interferon supply

99
Q

When does the adaptive immune response take over? Which defences are involved in adaptive immunity?

A 
From 4 days
Virus-reactive T and B Cells are 
identified in draining lymph node, 
proliferate and differentiate to
become effector cells
100
Q

Which TLR do conventional dendritic cells express?

A

All but TLR 9

101
Q

How does whooping cough infection prevent infected individuals from clearing their lungs leading to a cough?

A

Cytotoxin protein produced by B. Pertussis stops cilia from beating

102
Q

What causes whooping cough?

A

Bordetella pertussis bacterium

103
Q

What is the incubation period of whooping cough?

A

6-20 days

104
Q

If the whole cell pertussis vaccine produces more efficient and longer lasting immunity than the acellular vaccine, why do we use the latter?

A

Whole cell vaccine is reactogenic (seizures, high fever and permanent brain damage (extremely rare)

105
Q

When should mothers be injected with DTaP?

A

3rd trimester of each pregnancy

106
Q

What is the incubation period for mumps?

A

15-24 days

107
Q

How is mumps diagnosed?

A

Parotitis (90% of patients with symptomatic mumps have one or both swollen parotid glands) Anti-mumps specific IgM in the saliva 7 days after onset of parotid swelling

108
Q

How are primary and secondary vaccine failures different?

A

Primary: no seroconversion after vaccination (no vaccine-specific antibody response)
Secondary: loss of immunity after seroconversion (memory waning).

109
Q

What sort of diseases is herd immunity ineffective against?

A

Diseases that are not transmitted from person to person e.g. tetanus

110
Q

What type of pathogen is Hib?

A

Facultatively anaerobic gram-negative bacterium (makes ATP by aerobic respiration if oxygen is available but capable of switching to anaerobic respiration if oxygen is unavailable)

111
Q

Why is encapsulation a major cause of virulence?

A

Can prevent efficient complement fixation by the alternative pathway
Requires high affinity IgG to overcome encapsulation

112
Q

What does Hib cause?

A

Pneumonia (not influenza)
Epiglottitis
Meningitis

113
Q

How is Hib diagnosed?

A

Hib isolated from STERILE site (cerebrospinal fluid or blood)
as Hib is a commensal organism in the nasopharynx

114
Q

What type of vaccine is Hib?

A

Conjugate

115
Q

How do conjugate vaccines elicit a greater immune response?

A

Polysaccharides on their own elicit weak T-cell independent immune responses as only peptides stimulate TCR
Conjugate vaccines recognised by B and T cells
Ensures T cell help is made available

116
Q

Which region of the MHC molecule does class switching affect?

A

Constant region of heavy chain

does not change the VDJ region and the light chain so antigen specificity is maintained

117
Q

Where is IgM found? Where is IgM produced?

A

Found circulating in blood and lymph

Made principally by plasma cells resident in the lymph nodes, spleen and bone marrow

118
Q

Which immunoglobulin is favoured for Hib immunity?

A

Hib is an encapsulated bacteria

So IgG2 favoured as very effective at binding to the polysaccharide coats of encapsulated bacteria

119
Q

What are examples of encapsulated bacteria?

A 
Hib
E. Coli
Salmonella
Pneumococcus
Neisseria meningitidus
Klebsiella pneumoniae
120
Q

Which HPV strains cause genital warts on the skin around the anus and vagina (low risk of cancer)?

A

HPV 6, 11

121
Q

Which HPV strains cause cells in throat or cervix to undergo dysplasia making them more likely to become cancerous?

A

HPV 16, 18

122
Q

What type of vaccines are diphtheria and tetanus?

A

Toxoid

123
Q

What do IL-1 beta and TNF-alpha do?

A

Increase vascular permeability to allow effector cells to enter infected tissues

124
Q

What does C reactive protein do?

A

Binds to pathogens
Acts as an opsonin
Triggering classical pathway of complement fixation in the absence of antibodies

125
Q

What causes measles?

A

Morbillivirus of paramyxovirus family

126
Q

What causes mumps?

A

Rubulavirus of paramyxovirus family

127
Q

What causes rubella?

A

Rubivirus of togavirus family

Year 2 (13 decks)

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