An overview of immunology, innate defences, and inflammation Flashcards

1
Q

Which cell lineage is primarily responsible or the innate immune response?

1 - Myeloid
2 - Lymphoid

A

1 - Myeloid

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

Which cells are more abundant in chronic inflammation?

1 - Neutrophils
2 - Monocytes
3 - Lymphocytes

A

3 - Lymphocytes

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

What are cytokines?

A
  • proteins involved in signalling within the immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are chemokines?

A
  • a sub group of cytokines

- responsible for recruiting immune cells

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

Once a cytokine binds with a cell receptor, what does it normally initiate within the cell?

A
  • intracellular cascade, generally resulting in changes in gene expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When looking at the effects of cytokines on cells, which of the following are cytokines NOT involved in?

1 - Cell proliferation
2 - Cell differentiation
3 - Cell apoptosis
4 - Cell activation
5 - Cell migration (chemokines specific)
A

3 - Cell apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 3 methods in which cytokines can signal other cells?

1 - hormonal, endocrine and autocrine
2 - endocrine, hormonal and paracrine
3 - paracrine autocrine and hormonal
4 - paracrine, endocrine and autocrine

A

4 - paracrine, endocrine and autocrine

  • paracrine =signalling cells close by
  • endocrine = travels systemically in the blood
  • autocrine = signal itself
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

There are 4 main functions of cytokines. One of these is pleiotropy, which is what?

1 - cytokines ability to affect only WBCs
2 - cytokines ability to affect only lymphocytes
3 - cytokines ability to affect only B cells
4 - cytokines ability to affect multiple cells in different ways

A

4 - cytokines ability to affect multiple cells in different ways

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

There are 4 main functions of cytokines. One of these is redundancy, which is what?

1 - cell can be stimulated by lots of cytokines but all have the same effect
2 - cell can be stimulated by lots of cytokines but all have no effect
3 - cell can be stimulated by lots of cytokines and all have different effects
4 - cell can be stimulated by one cytokines only

A

1 - cell can be stimulated by lots of cytokines but all have the same effect

  • the need for more than one cytokine with the same effect appears redundant
  • for example, a T helper cell can secrete IL-2, IL-5 and IL-4 which binds to B cell
  • all 3 cytokines signal the B cell to proliferate, so redundancy in some cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

There are 4 main functions of cytokines. One of these is synergy, which is what?

1 - 2 or more cytokines causes effect on cells to be nullified
2 - 2 or more cytokines needed to work in synergy to elicit effects on a cell
3 - 2 or more cytokines are required to stimulate some cells
4 - cell can be stimulated by one cytokines only

A

2 - 2 or more cytokines needed to work in synergy to elicit effects on a cell

  • for example, a T helper cell can secrete IL-5 and IL-4 which binds to B cell
  • alone they cause B cell to proliferate, BUT together they signal antibody class switching
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

There are 4 main functions of cytokines. One of these is antagonism, which is what?

1 - 2 or more cytokines causes effect on cells to be nullified
2 - 2 or more cytokines needed to work in synergy to elicit effects on a cell
3 - 2 or more cytokines are required to stimulate some cells
4 - cytokines can antagonise one another

A

4 - cytokines can inhibit the function of other cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Granulocyte macrophage colony-stimulating factor (GM-CSF) is a cytokine. What is its function?

1 - B cell growth factor
2 - T cell growth factor
3 - a white blood cell growth factor
4 - a lymphocyte cell growth factor

A

3 - a white blood cell growth factor

  • signals common myeloid progenitor cells
  • goes onto to stimulate all WBC with granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Stem cell factor (SCF) is a cytokine. What is its function?

1 - B cell growth factor
2 - T cell growth factor
3 - a white blood cell growth factor
4 - hematopoietic stem cell growth factor

A

4 - hematopoietic stem cell growth factor

- important in renewal and survival of white blood cells

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

Granulocyte-Colony Stimulating Factor (G-CSF) is a cytokine. What is its function (2 from the list below)?

1 - bone marrow stimulator for granulocytes
2 - white blood cell growth factor
3 - stem cell stimulator
4 - hematopoietic stem cell growth factor

A

1 - bone marrow stimulator for granulocytes

3 - stem cell stimulator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Macrophage colony-stimulating factor (M-CSF) is a secreted cytokine. What is its function?

1 - bone marrow stimulator for granulocytes
2 - hematopoietic stem cells to differentiate into macrophages
3 - stem cell stimulator
4 - hematopoietic stem cell growth factor

A

2 - hematopoietic stem cells to differentiate into macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

A raised WBC on a blood sample is indicative of what?

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

Interferons are a group of cytokines that are released when what has happened to the body?

1 - infected with a virus (anti-virals)
2 - damage to tissues
3 - infected with bacteria
4 - infection with a parasite

A

1 - infected with a virus (anti-virals)

  • signal other cells to raise their anti-viral defences
  • IFN-α, IFN-β, IFN-γ are ones we need to know
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Class I and II cytokines signal cells by binding to what type of receptor?

1 - ligand gated ion channel
2 - GPCRs
3 - enzyme-linked receptors (tyrosine kinase-coupled)
4 - intracellular steroid

A

3 - enzyme-linked receptors (tyrosine kinase-coupled)

- requires 2 receptors as undergoes dimerisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the structure of receptor tyrosine kinase, which is what cytokines bind with?

A
  • protein structure placed transmembranal
  • ligand binding site is extracellularly
  • 3 tyrosine (amino acids) intracellularly
  • kinase remove phosphates from one molecule and add to another (ATP has 3 phosphates, so it could remove one and add it to another molecule
20
Q

How do receptor tyrosine kinase receptors work for class I and II cytokines? Organise the order using the labels below:

  • cytokine binds with ligand binding site
  • JAK phosphorylate the transcription factor STAT which form dimers and move to the nucleus
  • kinase removes phosphate from ATP and all 6 tyrosines become phosphorylated
  • phosphorylation and activation of janus kinase (JAK)
  • tyrosine is activated as receptors have become a dimer
  • 2 polypeptide receptor tyrosine kinase receptors come together forming a dimer
A
  • cytokine binds with ligand binding site
  • 2 polypeptide receptor tyrosine kinase receptors come together forming a dimer
  • tyrosine is activated as receptors have become a dimer
  • kinase removes phosphate from ATP and all 6 tyrosines become phosphorylated
  • phosphorylation and activation of janus kinase (JAK)
  • JAK phosphorylate the transcription factor STAT (a transcription factor) which form dimers and move to the nucleus and begin gene transcription
21
Q

The binding of class I and II cytokines to receptor tyrosine kinase receptors on cells triggers the intracellularly JAK-STAT pathway. What is this pathway?

A
  • chain of interactions between proteins in a cell, and is involved in processes such as immunity, cell division, cell death, and tumour formation
22
Q

Which molecules generally initiate the innate immune response?

1 - damage associated molecular patterns (DAMPs)
2 - pattern recognition receptors (PRR)
3 - toll like receptors (TLR)
4 - pathogen associated molecular patterns (PAMPs) with PRRs

A

4 - pathogen associated molecular patterns (PAMPs) with PRRs

23
Q

Interferons are a group of cytokines that are released when the body is infected with a virus (anti-virals). These interferons can signal other cells to raise their anti-viral defences. IFN-α, IFN-β are type I and IFN-γ is a type II interferon. What receptors do interferons bind with on cells?

1 - GPCR
2 - toll like receptor
3 - interferon heterodimer
4 - interferon dimer

A

3 - interferon heterodimer

24
Q

Once bound to a receptor on a cell what pathway do interferons signal within the cell?

A
  • JAK-STAT pathway
  • STAT molecules then translocate into nucleus and influence transcription
  • involved in immunity, cell division, cell death and tumour formation
25
Q

Once interferons is bound to a interferon heterodimer receptor on a cell, dimerisation occurs and the JAK-STAT pathway, which is involved in immunity, cell division, cell death and tumour formation is initiated. This then triggers further phosphorylation within the cell. The STAT molecules then translocate into nucleus and influence transcription. One aspect of transcription affected is protein Kinase R (PKR) and IFIT (IFN-induced proteins with tetratricopeptide repeats). What do PKR and IFIT then go onto to do?

1 - inhibit the translation of viral RNA
2 - degrades viral RNA
3 - inhibit viral RNA transcription
4 - inhibit assembly of new viral particles.

A

1 - inhibit the translation of viral RNA

26
Q

Once interferons is bound to an interferon heterodimer receptor on a cell, dimerisation occurs and the JAK-STAT pathway, which is involved in immunity, cell division, cell death and tumour formation is initiated. This then triggers further phosphorylation within the cell. The STAT molecules then translocate into nucleus and influence transcription. One aspect of transcription affected is RNAseL. What does RNAse L then go onto to do?

1 - inhibit the translation of viral RNA
2 - degrades viral RNA
3 - inhibit viral RNA transcription
4 - inhibit assembly of new viral particles.

A

2 - degrades viral RNA

27
Q

Once interferons is bound to a interferon heterodimer receptor on a cell, dimerisation occurs and the JAK-STAT pathway, which is involved in immunity, cell division, cell death and tumour formation is initiated. This then triggers further phosphorylation within the cell. The STAT molecules then translocate into nucleus and influence transcription. One aspect of transcription affected is Mx proteins. What do Mx proteins then go onto to do?

1 - inhibit the translation of viral RNA
2 - degrades viral RNA
3 - inhibit viral RNA transcription
4 - inhibit assembly of new viral particles.

A

3 - inhibit viral RNA transcription

4 - inhibit assembly of new viral particles.

28
Q

Which cytokine is important for activation and proliferation of T and B cells through an autocrine pathway?

1 - IL-6
2 - IL-1
3 - IL-2
4 - TNF-a

A

3 - IL-2

29
Q

Microorganisms contain pathogen associated molecular patterns (PAMPs). How do immune cells recognised the PAMPS?

1 - damage associated molecule patterns (DAMPs)
2 - pattern recognition receptors (PRRs)
3 - MHC-II
4 - MHC-I

A

2 - pattern recognition receptors (PRRs)

  • macrophages, neutrophils, eosinophils, basophils, and mast cells contain PRRs
  • PRRs can also be soluble (pentraxins, ficolins, collectins)
30
Q

Microorganisms contain pathogen associated molecular patterns (PAMPs). Pattern recognition receptors (PRRs) are able to bind with these and alert the immune response. There are 2 types of PRR, phagocytic and signal inducing PRRs. What are phagocytic PRRs?

A
  • bind to PAMPs and phagocytose foreign body or encourage phagocytic cells to phagocytose
  • do not automatically release cytokines though
  • like hearing a noise and investigating before phoning the police
31
Q

Microorganisms contain pathogen associated molecular patterns (PAMPs). Pattern recognition receptors (PRRs) are able to bind with these and alert the immune response. There are 2 types of PRR, phagocytic and signal inducing PRRs. What are signal PRRs?

A
  • PRRs that are able to call in additional support from the immune system
  • here both signal and phagocytic PRRs will be stimulated
32
Q

When a pathogen associated molecular pattern (PAMPs) binds with a PRR on an antigen presenting cell the antigen presenting cell will be able to stimulate both signalling and phagocytic cytokines. The specific PAMP encountered will determine the specific cytokine that is produces. Why is this important for adaptive immunity?

A
  • specific PAMPs need to be targeted individually

- for example if a virus PAMPs is detected by a PRR, interferons will be released to identify a viral infection

33
Q

When a pathogen associated molecular pattern (PAMPs) binds with a PRR on an antigen presenting cell the antigen presenting cell will be able to stimulate both signalling and phagocytic cytokines. The specific PAMP encountered will determine the specific cytokine that is produces. This is important for adaptive immunity because each specific PAMP need to be targeted individually. For example if a virus PAMPs is detected by a PRR, interferons will be released to identify a viral infection. Specifically, in addition to IL-2 that is able to activate and stimulate proliferation in T cells, what other cytokine is produced by the antigen presenting cell that is able to determine what type of T cell is produced (Th1 or Th2 for example)?

1 - IL-10
2 - IL-12
3 - IL-6
4 - IL-1

A

2 - IL-12

- called polarising cytokines

34
Q

Chemokines are important for recruiting immune cells to the site of infection or tissue damage. Neutrophils are the dominant cell type in an acute infection. What chemokine (a subclass of cytokines) is important for signalling neutrophils to the site of damage or infection?

  • IL8 (CXCL8)
  • IL-9 (CXCL9)
  • IL-2 (CXCL2)
  • IL-12 (CXCL12)
A
  • IL8 (CXCL8)
35
Q

In addition to attracting immune cells to a specific area of infection or tissue damage, what else can chemokines assist with, specifically in the acute phase of inflammation?

1 - leukocyte recruitment (tethering, rolling, triggering and adhesion)
2 - recruit mature B and T cells to the area
3 - release other cytokines to assist with immune response
4 - initiate repair of damaged tissue

A

1 - leukocyte recruitment (tethering, rolling, triggering and adhesion)

36
Q

What does chemoattractant mean?

1 - initiates the movement of cells based on chemotaxis
2 - inhibits the movement of cells based on chemotaxis
3 - signals the movement of cells based on inflammatory markers
4 - initiates the movement of cells based on anti-inflammatory markers

A

1 - initiates the movement of cells based on chemotaxis
- chemotaxis is attraction of a cell based on concentration gradient (essentially cells move up the concentration gradient until they reach the source)

37
Q

What type of receptors are chemokines able to bind with?

1 - ligand gated ion channel
2 - GPCRs
3 - enzyme-linked receptors (tyrosine kinase-coupled)
4 - intracellular steroid

A

2 - GPCRs

38
Q

Which 3 cytokines are commonly associated with chronic inflammation that can lead to systemic effects, tissue effects and/or metabolic changes?

1 - IL-6, IL-2 and TNF-a
2 - IL-1, IL-2 and TNF-a
3 - IL-1, IL-6 and TNF-a
4 - IL-1, IL-2 and IL-12

A

3 - IL-1, IL-6 and TNF-a

39
Q

What is cytokine release syndrome?

1 - large rise in inflammatory cytokines
2 - lack of cytokine release
3 - chronic slow release of cytokines
4 - lack of immune cells to produce cytokines

A

1 - large rise in inflammatory cytokines

  • causes fever and multiple organ dysfunction
  • can be mild to moderate, but not as severe as cytokine storm
40
Q

What is a cytokine storm?

1 - large rise in inflammatory cytokines
2 - lack of cytokine release
3 - chronic slow release of cytokines
4 - lack of immune cells to produce cytokines

A

1 - large rise in inflammatory cytokines

  • can cause organ failure and even death
  • more severe than cytokine release syndrome
41
Q

Cytokine release syndrome and cytokine storm are both characterised by a rapid rise in cytokine levels. What are the 2 main triggers for these?

1 - immunotherapeutic agents and infection
2 - immunotherapeutic agents and tissue damage
3 - infection and non immunotherapy medication
4 - infection and tissue damage

A

1 - immunotherapeutic agents and infection (sepsis)

42
Q

Recombinant cytokines are pharmaceutical analogs (proteins that have the same effect as endogenous cytokines) of endogenously produced cytokines and colony-stimulating factors. How can recombinant cytokines be used therapeutically?

A
  • in patients who’s immune system is not responding effectively
  • recombinant cytokines can increase the activity of the immune system or the production of particular populations of blood cells
43
Q

What are anti-cytokine antibodies and how can they be used therapeutically?

A
  • antibodies that bind to cytokines
  • anti-RANK-L adalimumab inhibits RANK-L in osteoporosis
  • cytokines can then not bind to receptors on cells and initiate immune response
  • useful in chronic infection, cancer and cytokine release syndrome and storm
44
Q

What are soluble receptors in terms of cytokine therapeutic effects?

A
  • receptors that are soluble in blood that can bind cytokines, stabilise cytokines, increase efficacy of cytokines and reduce degradation of cytokines
45
Q

What are receptor antagonists in terms of cytokine therapeutics?

A
  • therapies that bind to cytokine receptors
  • cytokines are then unable to bind to the cell and elicit a response
  • IL-6S tocilizumab inhibits IL-6 and this osteoclasts in bone, treatment for osteoporosis