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CMB2004 stage 2 > Lecture 7 -10 > Flashcards

Lecture 7 -10 Flashcards

(54 cards)

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1
Q

Why do we need immunological tolerance?

A

no tolerance = autoreactivity of self = serious pathology

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2
Q

What does negative selection of T cells in the thymus remove?

A

removes T cells expressing TCR with high affinity for self-MHC and self-peptides presented in the thymus

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3
Q

CD4+TH1 T cells are important to activate?

A

macrophages

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4
Q

CD4+ TH17 T cells can be identified by the production of?

A

IL-17

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5
Q

CD4+ TH2 T cells inhibit the responses of?

A

CD4+ TH1 T cells

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6
Q

Once activated CD8+ T cells develop into?

A

cytotoxic effector cells or CTLs

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7
Q

How do iTreg cells differ from nTreg?

A

iTreg cells are generated in LN or periphery whereas nTreg are generated in thymus

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8
Q

What is T cell survival and tolerance based on?

A

TCR affinity

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9
Q

How does B cell tolerance in the bone marrow occur?

A
  1. random Ig gene rearrangement = lead to B cells expressing BCR that recognizes Ag
  2. autoreactive B cells are negatively selected in the bone marrow
  3. negative selection/ rearrangement of the light chain let B cells survive selection
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10
Q

What is the importance of clonal anergy for tolerance?

A

important process in generation of peripheral tolerance = T cells that encounter Ag in the absence of co-stimulation become anergic

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11
Q

What are the steps of anergy that can lead to peripheral tolerance of T cells?

A
  1. bacteria is taken up by macrophage
  2. bacteria can become activated and induce post stimulation
  3. activates T cell which recognises the peptide
  4. anergia T cell can recognise some of the receptors, however they receive signal 1 but not signal 2.
  5. unstimulated marcophage so not deliver a co-stimulatory signals to T cell
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12
Q

What signal do anergia T cells receive?

A

signal 1

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13
Q

What are the other mechanisms of tolerance?

A
  1. immunological ignorance = many AG are not presented at sufficient levels to activate T cells
  2. privileged sites = ]Ag sequestered from immune system (suppressive cytokines also prevalent
  3. many B cell responses are T cell dependent
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14
Q

What are the characteristics for regulatory T cells (Treg)?

A
  • CD4+ T cell subset that suppress immune responses
  • crucial for preventing autoimmune responses
  • arise in thymus from T cells with high affinity receptors for self Ag
  • don’t go through negative selection but do attack cells that should have died but escaped from the thymus.
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15
Q

What is the role of Treg?

A

bind to any cells that have escaped negative selection and turns them off

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16
Q

What is the role of Breg cells?

A

to ensure responses continue only for as long as they areneeded

*to minimize collateral (tissue) damage
*to ensure responses are qualitatively appropriate i.e. right for the specific pathogen

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17
Q

What are the roles of the different CD4+ T cells?

A

CD4+ TH1 —> activation of macrophages, NK cells, cytotoxic T cells

CD4+ TH2 —> promote responses mediated by eosinophils and mast cells; role in antibody responses, especially IgE

CD4+ TH17 (make IL-17) —> promote responses against fungi

CD4+ Treg/B reg —> supress unwanted responses

CD4+ TFH —>specialised TH found in GC to help B cells (can produce TH1,TH2 and TH17 cytokines)

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18
Q

What are the key cytokines in the CD4 TH1 and TH2 response?

A

*IL-12 and IFN-g play a key role in induction of TH1 responses

*IL-4 important for induction of TH2 responses

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19
Q

What are the polarisation of CD4+ T cell responses?

A

TH1 cytokines
–promote commitment to TH1
–inhibit development of TH2, TH17

TH2 cytokines
–promote commitment to TH2
–inhibit development of TH1, TH17

TH17 cytokines
-promote commitment to TH17 cytokines
-inhibit development of Treg

Treg cytokines
- inhibit TH1, TH2, TH17 responses

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20
Q

Why doesn’t the mother reject the baby in terms of Treg?

A

Treg is needed for tolerance of the baby in the mothers womb to not be rejected.

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21
Q

Which cytokines are involved with tipping the immune response to a TH1 and a TH2 predominant response?

A

TH1 = IL2, IFN gamma and TNF beta

TH2 = IL4,5, 10 and 13

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22
Q

What are TLRs and what do they bind?

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A

TLR = Toll like receptors

these are PRRs, 10 in humans- innate and recognise PAMPS such as ssDNA, LPS

23
Q

What is LPS and on what type of bacteria is it present?

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A

Lipopolysaccharide present on gram negatives

24
Q

What kind of infections can Neisseria spp cause?

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A

Meningitis and gonnorhea

25
Which type of bacterial infections can the MAC be particularly useful in killing the pathogen?
Gram negative that are dividing, eg Neisseria meningitidis
26
What are examples of gram negative and gram positive bacteria?
Gram positive = Staphylococcus aureus, Streptococcus spp. Gram negative = Campylobacter, Salmonella, Shigella, Haemophilus, Neisseria
27
What is the difference between gram positive and gram negative bacteria?
gram positive = thick peptidoglycan layer gram negative - lipopolysaccharide
28
What are the roles of TLRs?
Promote inflammation Promote dendritic cell maturation Influence differentiation of T cells Activate B cells (TI-1 antigens) = second signal needed to stimulate B cells.
29
Which MHC molecule would present processed peptides from extracellular microorganisms?
MHC II APCs because we need to endocytose the pathogen to present the extracellular antigen
30
What are the type I interferons and what is their function?
IFN-alpha and IFN-beta Prevents viral nucleic acid production/replication by the production of interferons
31
What is the type II interferon and what is their function?
IFNgamma = secreted by activated T cells and by NK cells Inhibits TH2 response (antibodies) and promotes TH1 (cell killing)
32
What is the role of natural killer cells?
releases lytic granules that kill som virus-infected cells
33
What are the two receptors on NK cells and what do they recognise?
1. activating receptors = recognise carbohydrate ligands = triggers killing 2. inhibitory receptors = recognises MHC class I molecules but do not bind
34
What are the 2 mechanisms used by cytotoxic T cells?
1. secretion of cytotoxic granules: perforin = polymerises in membrane granzymes = proteases enter cell 2. Fas ligand on T cell interacts with Fas on target = causes cell that is infected to die
35
What are the roles of CTLs?
- secrete IFNgamma - inhibits viral replication - upregulates MHC class I and II expression and antigen presentation - increases macrophage phagocytosis of dead cells - promotes NK cell killing activity
36
How does HIV infect?
Attacks specific immune system Targets CD4 T cell, macrophages and dendritic cells
37
List 4 ways that a pathogen can evade an effective immune response
1. concealment of antigens 2. antigenic variation 3. immunosuppression 4. interference with effector mechanisms
38
What are the examples of antigenic variation?
1. large number of antigenic types = streptococcus 2. mutation (antigenic drift) = influenza, polio, HIV 3. recombination (antigenic shift) = influenza 4. gene switching = trypanosomes
39
What is the difference between antigenic drift and antigenic shift?
antigenic drift = minor genetic changes antigenic shift = major genetic changes, virus hybrid from cross species
40
What type of genetic rearrangement causes major flu pandemics?
antigenic shift = major genetic changes
41
What type of bacteria is Streptococcus Pneumoniae?
gram positive = thick polysaccharide capsule
42
What are the two types of Streptococcus Pneumonia vaccines and what is the difference between the two?
1. Pneumovax = polysaccharide vaccine which contains all 23 capsules = not suitable for children under 2 = just B cell IgM response which generates a T independent response 2. Prevnar 13 = conjugate vaccine which contains 13 capsule = T cell and B cell response
43
Trypanosoma brucei (African sleeping sickness) undergoes gene rearrangement of which protein to curb full clearance of the pathogen from the host?
variant-specific glycoprotein (VSG) that keeps changing
44
What can happen if you get mass macrophage activation around the body following sepsis?
macrophaes are very good at producing cytokines, could end up with a cytokine storm- can lead to lots of changes
45
What are the two forms of immunosuppression?
1. infection of immune cells e.g HIV attacks T cells 2. induction of regulatory T cells
46
What type of bacteria is H. Pylori?
gram-negative bacteria
47
What are the characteristics of the measles virus?
- an RNA virus - disease associated with a rash and respiratory symptoms - shown to infect dendritic cells = increased apoptosis, decreased stimulation of T cells
48
What are the examples of interference with effector mechanisms?
1. molecules interfering with antibody function 2. molecules interfering with complement 3. molecules binding cytokines 4. subvert responses by producing molecules with cytokine activity 5. inhibition of phagocytic killing
49
What are the different subgroups of vaccines?
1. inactivated 2. attenuated 3. subunit 4. toxoid 5. conjugate
50
What is a conjugate vaccine?
something with low antigenic property covalently bound to something with high antigenic property (eg Streptococcus pneumonia + diphtheria) can alter the immune response to get TH cells involved and switch to a T dependent immune response.
51
What is an adjuvant?
a substance administered with an antigen to promote the immune response
52
What are the characteristics of passive immunity?
- short lived - Hypogammaglobulinaemia in infants as maternal IgG declines - IVIgG every 2-4 weeks
53
What is an adjuvant?
a substance administered with an antigen to promote the immune response
54
How can adjuvants act?
- activate dendritic cells via TLR or NLR - cause release of endogenous danger signals - promote antigen uptake by dendritic cells - stimulate release of cytokines - promote cross-presentation of exogenous antigens by class I

CMB2004 stage 2 (2 decks)

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