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CMB2004 stage 2 > Lecture 7 -10 > Flashcards

Lecture 7 -10 Flashcards

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?

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?

A

Lipopolysaccharide present on gram negatives

24
Q

What kind of infections can Neisseria spp cause?

A

Meningitis and gonnorhea

25
Q

Which type of bacterial infections can the MAC be particularly useful in killing the pathogen?

A

Gram negative that are dividing, eg
Neisseria meningitidis

26
Q

What are examples of gram negative and gram positive bacteria?

A

Gram positive = Staphylococcus aureus, Streptococcus spp.

Gram negative = Campylobacter, Salmonella, Shigella, Haemophilus, Neisseria

27
Q

What is the difference between gram positive and gram negative bacteria?

A

gram positive = thick peptidoglycan layer
gram negative - lipopolysaccharide

28
Q

What are the roles of TLRs?

A

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
Q

Which MHC molecule would present processed peptides from extracellular microorganisms?

A

MHC II APCs because we need to endocytose the pathogen to present the extracellular antigen

30
Q

What are the type I interferons and what is their function?

A

IFN-alpha and IFN-beta

Prevents viral nucleic acid production/replication by the production of interferons

31
Q

What is the type II interferon and what is their function?

A

IFNgamma = secreted by activated T cells and by NK cells

Inhibits TH2 response (antibodies) and promotes TH1 (cell killing)

32
Q

What is the role of natural killer cells?

A

releases lytic granules that kill som virus-infected cells

33
Q

What are the two receptors on NK cells and what do they recognise?

A
  1. activating receptors = recognise carbohydrate ligands = triggers killing
  2. inhibitory receptors = recognises MHC class I molecules but do not bind
34
Q

What are the 2 mechanisms used by cytotoxic T cells?

A
  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
Q

What are the roles of CTLs?

A
  • 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
Q

How does HIV infect?

A

Attacks specific immune system

Targets CD4 T cell, macrophages and dendritic cells

37
Q

List 4 ways that a pathogen can evade an effective immune response

A
  1. concealment of antigens
  2. antigenic variation
  3. immunosuppression
  4. interference with effector mechanisms
38
Q

What are the examples of antigenic variation?

A
  1. large number of antigenic types = streptococcus
  2. mutation (antigenic drift) = influenza, polio, HIV
  3. recombination (antigenic shift) = influenza
  4. gene switching = trypanosomes
39
Q

What is the difference between antigenic drift and antigenic shift?

A

antigenic drift = minor genetic changes

antigenic shift = major genetic changes, virus hybrid from cross species

40
Q

What type of genetic rearrangement causes major flu pandemics?

A

antigenic shift = major genetic changes

41
Q

What type of bacteria is Streptococcus Pneumoniae?

A

gram positive = thick polysaccharide capsule

42
Q

What are the two types of Streptococcus Pneumonia vaccines and what is the difference between the two?

A
  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
Q

Trypanosoma brucei (African sleeping sickness) undergoes gene rearrangement of which protein to curb full clearance of the pathogen from the host?

A

variant-specific glycoprotein (VSG) that keeps changing

44
Q

What can happen if you get mass macrophage activation around the body following sepsis?

A

macrophaes are very good at producing cytokines, could end up with a cytokine storm- can lead to lots of changes

45
Q

What are the two forms of immunosuppression?

A
  1. infection of immune cells e.g HIV attacks T cells
  2. induction of regulatory T cells
46
Q

What type of bacteria is H. Pylori?

A

gram-negative bacteria

47
Q

What are the characteristics of the measles virus?

A
  • an RNA virus
  • disease associated with a rash and respiratory symptoms
  • shown to infect dendritic cells = increased apoptosis, decreased stimulation of T cells
48
Q

What are the examples of interference with effector mechanisms?

A
  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
Q

What are the different subgroups of vaccines?

A
  1. inactivated
  2. attenuated
  3. subunit
  4. toxoid
  5. conjugate
50
Q

What is a conjugate vaccine?

A

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
Q

What is an adjuvant?

A

a substance administered with an antigen to promote the immune response

52
Q

What are the characteristics of passive immunity?

A
  • short lived
  • Hypogammaglobulinaemia in infants as maternal IgG declines
  • IVIgG every 2-4 weeks
53
Q

What is an adjuvant?

A

a substance administered with an antigen to promote the immune response

54
Q

How can adjuvants act?

A
  • 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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