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MIIM20002 - Microbes, Infections, Responses > Lecture 11 - Manipulating the Immune Response > Flashcards

Lecture 11 - Manipulating the Immune Response Flashcards

0
Q

What are the components of the innate response that may be manipulated?

A
  • PRRs
  • Cytokines
  • Cell trafficking
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1
Q

How can PRRs be exploited to manipulate the immune response?

A
  • PAMP agonist to activate PRRs
  • -> increase immune response
  • PAMP antagonist
  • -> dampens immune response
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2
Q

How may cytokines be used to manipulate the immune response?

A

Using innate cytokines

–> boost the immune response

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3
Q

TLR-5 recognises …?

A

Flagellin

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4
Q

TLR-4 recognises …?

A

LPS

Endotoxin

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5
Q

TLR-9 recognises …?

A

CpGDNA

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6
Q

What is RLH?

What does it recognise?

A

Rig like helicase

Viral RNA

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7
Q

When a macrophage binds and engulfs a pathogen, what are the general groups of cytokines that it releases?

A

Inflammatory cytokines
Antiviral cytokines
Stimulatory cytokines

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8
Q

What are the Inflammatory cytokines?

A

IL-1
TNF-a
IL-6

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9
Q

What are the antiviral cytokines?

A

IFN-alpha

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10
Q

What are the stimulatory cytokines?

A

GM-CSF

IL-12

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11
Q

What is Imiquod?

What does it bring about?

What is it used to treat?

A

It is a TLR-7 agonist

It binds to the PRR and brings about a local antiviral response

It is used to treat some viral infections, eg. HPV

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12
Q

What does TLR-7 recognise?

A

ssRNA

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13
Q

What may sometimes be added to vaccine antigens to generate a more specific immune response?
- how does it do this?
Give an example

A

Adjuvants
- PRR agonists
For example, CpGDNA / TLR-9

Induces more, and more appropriate, cytokines

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14
Q

In which cases would a PRR antagonist be used?

A
  • Septic shock
    (TLR-4)
  • Allergies
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15
Q

Describe what happens in Septic Shock, and how this may be blocked

A

Too much bacteria present (LPS)
Excessive macrophage activation
Macrophages release too many inflammatory and stimulatory cytokines
Widespread vasodilation
Coagulation cascade activated –> fibrinous clots form

By blocking TLR-4, LPS can’t activate all the macrophages

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16
Q

How may cytokines be used to boost antiviral responses?

A

Administration of
IFN-a
IFN-B

17
Q

How can antibodies be used to shape the cytokine response?

In which cases would we use this?

A

Abs against IL-1, IL-1R

  • type 2 diabetes
  • gout
  • autoimmune diseases

Abs for TNF-a, TNFR
- rheumatoid arthritis

18
Q

How can cell trafficking be blocked?

What would be the response ?

A

Blocking:

  • CXCL8R
  • LFA-1
  • ICAM-1

This would stop neutrophils from being recruited as they are marginised in the capillary
–> dampening of inflammatory response

19
Q

Compare what is administered to deliver a passive and active immune response, as well as in Immunotherapy

A

Passive:
- preformed antibodies

Active:
- antigen

Immunotherapy:
- adaptive immune response cytokines

20
Q

What are the pros of a passive immune response?

A

Fast

21
Q

What are the cons of a passive immune response?

A
  • not long lived
  • only a B cell (Ab) response
  • only for serum, not mucosa
  • only can be used a few times –> rejected after a few uses
22
Q

What are the sources of Ab for passive immunity?

A
  • animals
  • blood bank serum
  • recombinant antibodies
23
Q

What are the pros of active immunity?

A
  • long lasting
  • humoral and cellular response activated
  • can be target to tissue
24
Q

What are the cons of active immunity?

A
  • slow

- variable response in the young and old

25
Q

Which diseases have been eradicated in the western world due to vaccines?

A

Polio

Smallpox

26
Q

Which diseases do we still not have vaccines for?

A

HIV

TB

27
Q

Why do we need to understand Pathogenesis to be able to make effective vaccines?

A

Need to know about:

  • adhesins
  • evasion mechanisms (capsules)
  • toxins

So that we can block these things

28
Q

Why do we need to know the localisation of an infection

A

Some infections are localised (gastro, respiratory tract infection), whilst others become systemic (rubella, tetanus).

This dictates where we need to target the response to

29
Q

What are the four different types of vaccines?

A
  1. Live attenuated
  2. Subunits
  3. Killed
  4. Virus like particules
30
Q

What are the pros of live attenuated vaccines?

A

Longer lasting response
Can be taken orally
Multiple antigens present
Replicates –> don’t need boosters

31
Q

What are the cons of live attenuated vaccine?

A

Cold chain required

Can revert to virulence

32
Q

What are the pros of killed vaccine?

A

Never reverts to virulence

No cold chain required

33
Q

What are the cons of killed pathogen vaccines?

A

Short lived
Must be injected
Restricted antigens present
Boosters required

34
Q

In terms of B cells, what do we want the vaccine to provide?

A
  • isotype switching
  • high affinity Ab
  • memory B cells
35
Q

Why is activating B cells alone insufficient to produce a good immune response?

A

There is no T cell response

No Th cells to induce isotype switching

  • only get IgM
  • not memory
  • low affinity Ab
36
Q

How are T cells activated?

CD4+, specifically

A 
Signal 1: presentation of antigen by APC on MHC II
Signal 2: co stimulation
- CD80 and CD86
- CD28
Signal 3: cytokines
- expression of CD40 L 
- skew response to Th1 and Th2
37
Q

What happens after Th cells are activated?

A

After they are activated by APC, they move to the B cell area of the lymphoid tissue

  1. B cell presents the antigen on its MHC II for the TCR to bind
  2. Costimulation: CD40L and CD40

–> isotype switching, higher affinity Ab, memory B cells

38
Q

Which T cells do we need to induce and why?

A

CD4+:

  • antibody isotype switching
  • help and memory for CD8+ and B cells

CD8+:
- killing infected cells
(Virus, intracellular pathogen)

39
Q

How do we activate a APC so that CD4+ can be activated

A

Antigen presentation:
- MHC II –> antigen only needs to be in an endosome
(Easy)

Costimulatory molecule expression:
- Adjuvants mimic PAMPs induce the expression of CD80 and CD86

40
Q

How do we activate APCs with a vaccine so they can activate CD8+ cells?

A

Antigen presentation:
Much more difficult, as the antigen must be in the cytosol if it is going to be presented on MHC I

Live vaccines:
- live viruses will get antigen into cytosol –> not a problem

Killed vaccines:

  • ISCOMs
  • Virus like particles

MIIM20002 - Microbes, Infections, Responses (32 decks)

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