L09 Flashcards

1
Q

Different effector mechanisms depend on

A

Type of pathogen, localisation and stage of infection

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2
Q

What type of MHC class would be required for an extracellular infection?

A

MHC II

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3
Q

What type of MHC class would be required for an intracellular infection?

A

MHC I

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4
Q

What are the innate defenses against viruses

A

Interferons and NK cells

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5
Q

What type of interferons are present in responding to a virus

A

IFN - alpha and beta

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6
Q

How do IFN-alpha and IFN-beta help respond to the virus?

A

Prevents nucleic acid production/replication

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7
Q

What do chemokines recruit?

A

Lymphocytes

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7
Q

How does IFN-alpha and IFN-beta prevent viral nucleic acid production/replication

A

Induce resistance to viral replication in all cells by inducing Mx proteins, 2’-5’ linked adenosine oligomers, and the kinase PKR.

Increase MHC class I expression and AG presentation in all cells

Activate dendritic cells and MQ

Activate NK cells to kill virus-infected cells

Induce chemokines to recruit lymphocytes

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8
Q

What type of interferons are there?

A

1

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9
Q

How does IFN result in viral mRNA degradation?

A

2,5’ - oligoadenylate synthetase = adenine trinucleotide synthesis = activates endonuclease = degrades viral mRNA

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10
Q

How does IFN inhibit protein synthesis

A

Protein kinase = phosphorlyation and inactivation of eIF-2 = inhibits protein synthesis

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11
Q

What cells make IFN alpha and beta?

A

Infected cell

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12
Q

When is IFN alpha and beta synthesised?

A

Early response to infection

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13
Q

What cells secrete type II IFN (IFN - gamma)

A

NK and activated T cells

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14
Q

What does IFN gamma do?

A

Inhibits TH2 response (Ab), promotes TH1 (NK), recruits Mq

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15
Q

What are the therapeutic use of interferons?

A

rIFN-alpha - hepatitis B and C, some cancers.

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16
Q

What are the disadvantages of using IFN for therapeutic treatments?

A

Side effects can be severe

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17
Q

Why can there be severe side effects for therapeutic treatments using IFN?

A

Cytokine storm -> excessive immune response can damage healthy cells and organs

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18
Q

Are NK cells large granular lymphocytes?

A

Yes

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19
Q

What are the components of the extracellular mechanism used by NK cells to kill infected cells?

A

Perforins and granzyme

19
Q

How do NK cells recognise stressed cells in the absence of Ig and MHC?

A

Recognise structures on viral infected cells

20
Q

What are the 2 types of NK cell receptors?

A

Activating receptors and inhibitory receptors

21
Q

What do activating receptors do?

A

recognise carbohydrate ligands = trigger killing of the cell

22
Q

What do inhibitory receptors do?

A

recognise MHC class I

23
What are the only type of receptors on T cells that can perform binding?
TCR
24
If a virus can reduce MHC expression - what would this result in?
Result in killing of the infected cell
25
How would reduced MHC result in apoptosis of the infected cell?
There would be no interaction between MHC and inhibitory receptor resulting in the activation of NK = apoptosis
26
What are the components of cell mediated specific immunity?IF
Cytotoxic T cells (CD8) and cytokines with anti-viral activity
27
Give an example of a cytokine involved in anti-viral activity and what it does?
IFN gamma - activates Mq
28
What are the two mechanisms through which cytotoxic T cells induce apoptosis
1. secretion of cytotoxic granules perforin & granzymes 2. Fas ligand on T cell interacts with Fas on target = apoptosis
29
How does perforin make pores in the membrane?
Through polymerisation
30
What cytokines are secreted by CD8?I
IFN gamma
31
What does IFN gamma result in?
Inhibits viral replication Upregulates MHC class I and II expression and antigen presentation Increases macrophage phagocytosis of dead cells Promotes NK cell killing activity
32
What is the role of Ab in viral infection responses
Antibodies Neutralise free virus (prevent entry into and spread between cells) Can prevent spread within the body (e.g. poliovirus) or protect mucosal surfaces against reinfection (e.g. ‘flu’) Opsonise to increase phagocytosis Activate complement leading to lysis (enveloped viruses)
33
What is the role of Ab in cell mediated immunity in influenza?
Antibody and cell mediated immunity in influenza Infection induces antibody and cytotoxic T cell (CTL) response Antibody recognises viral haemagglutinin and neuraminidase High levels of CTL activity correlates with reduced viral shedding Epidemics arise due to new strains not recognised by antibody (vaccine strains…….)
34
How does HIV impact immunity
Attacks specific immune system Targets CD4 T cell, macrophages and dendritic cells Progressive development of AIDS leads to opportunistic infections
35
List examples of opportunistic infections that arise from HIV
Oral candidiasis Kaposi's sarcoma Pneuomcystis pneumonia
36
Why can't we develop vaccines against HIV?
Antibodies do not seem to impact HIV
37
Can infections be controlled by cytotoxic T cell responses?
Potentially Patients with higher levels of CTL activity show slower disease progression Virus mutations that escape CTL recognition may lead to progression to AIDS
38
Describe SARS-COV-2 RNA?
22-32 kilobase ss +ve RNA
39
What sort of Ig response can helminths induce?
IgE
40
What is the role of IgE
Mast cell mediated inflammation Eosinophil ADCC (antibody-dependent cell-mediated cytotoxicity)
41
Why are cytokines important in a response against parasites?
MQ activation as some protozoa can survive in MQ hidden from Ig
42
Can differences in T cell responses result in different disease progression?
Yes
43
What elements of the T cell response is active in C57BL/6 mouse that allows it to survive Leishmania?
TH1
44
What elements of the T cell response is present in BALB/c mouse that allows it to succumb to Leishmania?
TH2 response
45
What are the different effector mechanisms that are active at different stages during malaria?
Sporozoite and merozoite may be susceptible to antibody Antibody may also kill infected red blood cells Cytotoxic T cells active against infected liver cells (RTS,S vaccine since 2019)
46
What is ADCC
Antibody dependent cell cytoxicity
47