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Immunology > Cytokines- the good and bad of the immune system > Flashcards

Cytokines- the good and bad of the immune system Flashcards

1
Q

List the two main ways the immune system can communicate with each other? Give examples for each

A
  1. Cell- cell contact (apc presenting to T cells)

2. Soluable cytokines signal between cells bind to cytokine receptors on target cell

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2
Q

What are cytokines? What do they act on?

A

They are small proteins or glycoproteins

They act on cytokine receptors

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3
Q

Which physiological mechanisms, immune or not do cytokines influence?

A

innate immunity, adaptive immunity & haematopoiesis

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4
Q

What are Pleiotropy cytokines?

A

a cytokine which can multiple effects

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5
Q

What are Redundancy cytokines?

A

different cytokines can do the same job

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6
Q

What are Synergy cytokines?

A

cytokines act together to cause an effect

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7
Q

What are Antagonism cytokines

A

cytokines can also have opposing effects

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8
Q

How do cytokines effect other cells? (near or far) 3 ways.

Hint similar to hormones

A

Autocrine- same cell is target
Paracrine- nearby cell is target
Endocrine- distant cell is target (enters circulation the travels to target cell)

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9
Q

Meaning of endocrine, autocrine and paracrine?

A

Autocrine- same cell is target
Paracrine- nearby cell is target
Endocrine- distant cell is target

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10
Q

What are chemokines? What effect do they have on cells?

A 
Small polypeptides (90-130aa)
Sub-family of cytokines. Involved in cell movement
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11
Q

How do chemokines effect cell movement?

A

Chemokin producing cell secretes chemokin. The concentration of this chemokin decreases the further away it is from the cell. The target cell recognises this concentration gradient and moves along it to get closer to the chemokin producing cell

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12
Q

What type of receptor do chemokines act on?

Or what type of receptor is a chemokin receptor?

A

G protein coupled receptors

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13
Q

How many times do G protein coupled chemokin receptors span a cells membrane?

A

7 Times

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14
Q

Is it 1 chemokin receptor for 1 chemokin molecule?

A

No! I chemokin receptor can bind to many chemokines

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15
Q

Name a cell which expresses different chemokin receptors

A

Leukocytes

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16
Q

What immune activities do chemokines help control? (3)

A

Adhesion
Chemotaxis
Activation

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17
Q

Which cytokines are inflammatory?

A

IL-1, TNFa, IL-6

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18
Q

Which cytokines are anti-inflammatory?

A

IL-10, TGFb

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19
Q

How to cytokines influence inflammation?

A

They cause the rapid recruitment of immune cells to the infected tissue

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20
Q

How do macrophages cause an inflammatory immune response?

A

They secrete cytokines (TNFalpha) and chemokines (CXCL8) to attract leukocytes to the area of infection

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21
Q

Which category of cells migrate to the site of infection when chemokines and cytokines are released- given examples?

A 
Leukocytes 
First
Neutrophils
Monocytes 
Second
T and B cells
22
Q

Describe the stages of cytokine mediated immune cell recruitment.

A
  1. Tethering- Cytokines make endothelial lining of the blood vesseles sticky. This causes ;eukocytes to ‘tether’ stick on
  2. Rolling and activation- The leukocyte becomes activated and rolls along the endothelim of blood vessel
  3. Arrest- Chemokines activate adhesion molecules on leukocyte causing it to stop (arrest)
  4. Migration- Leukocyte enters the endothelial cell (between or across)
  5. Positioning- Once inside the cell signals position leukocytes within the tissue to exerte immune response
23
Q

Name the stages o cytokine mediated immune cell recruitment.

A
  1. Tethering
  2. Rolling/activation
  3. Arrest
  4. Migration
  5. Positioning
24
Q

Which cytokine increases the stickyness of endothelim and how?

A

TNFa-

Increasing the expression of adhesion molecules (P-selectin) released from Weibel-Palade bodies (WP)

25
Q

What are Weibel-Palade bodies?

A

Storage granules of endothelial cells. They store and release adhesion molecules- P-selectin

26
Q

Which chemokine activates adhesion molecules in leukocytes? How does it do this?

A

Chemokin- CXCL8
How- Interacts with leukocyte via G coupled protein receptors.
Causes the activation of adhesion molecules called intergrins on leukocyte surface
Cell binds strongly to receptors on surface of endothelium- arrests

27
Q

Which cytokine acts on T cells? How does it do so?

A

IL-2
Drives clonal expansion
Activated T cells not only produce IL2 but also express high affinity receptors to respond to it

28
Q

Describe an autocrine cytokine effect?

A

Activated T cells produce IL-2 and also respond to it by expressing high- affinity IL-2 receptors

29
Q

What happens to people who have non-functional IFNg?

A

They are are highly susceptible to mycobacterial infections

30
Q

Effect if cytokines on B cells

A 
Influences plasma cell production
Influences class switching
31
Q

Effect of IL-4 on B cells?

A

Causes class switching to IgE

32
Q

Consequence of mutations in IL-10 receptor? And why?

A

Develop sever gut inflammation early in life and need bone transplant.
why? IL-10 is anti-inflammatory. Without it inflammation is not controlled

33
Q

What causes septic shock?

A

Hyperactivation and over production of cytokines TNFa,

IL-1, IL-6

34
Q

What are the symptoms of septic shock? Name 5

A 
Decrease in blood pressure
Fever
Diarrhea
Clotting
Death
35
Q

What is toxic shock syndrome?

A

When superantigens activate many T cells and rive overproduction of cytokines

36
Q

What is the cytokine storm?

A

A positive feed back system which occurs during uncontrolled cytokine production.
Cytokine stimulates immune cell- immune cell produces cytokine-.Cytokine stymulates immune cell- immune cell produces more cytokine

37
Q

What can stimulte a cytokine storm? Give examples

A

Viral infection
Ebola
Bird flu

38
Q

Which drug can cause a cytokine storm?

A

TGN1412

39
Q

What is TGN1412, what does it bind to?

A

It is a monoclonal super antagonist antibidy which binds to CD28 on T cells

40
Q

What was the intended effect of TGN1412?

A

Selective activation of Regulatory T cells

Anti-inflammatory

41
Q

What was the actual effect of TGN1412

A

Effector T cells activated
Massive cytokine release (‘cytokine storm’)
Systemic inflammation
Organ failure

42
Q

Diseases caused by chronic over production of cytokines

A 
Asthma
Crohns
Psoriasis
RHEUMATOID ARTHRITIS
MULTIPLE SCLEROSIS
Type 1 diabetes ]
ulcertaive colittis
43
Q

What drives allergies and asthma?

A

Over production of IL-4

44
Q

What is caused by the over production of Th1 cytokines?

A

Chronic inflammation- e.g. crohns diseases

45
Q

What is the proof that crohns disease is enviromental?

A

Children of immigrants from areas with low crohns disease have a high incidence of crohns disease when they move to areas with a high incidence

46
Q

What is the hygiene hypothesis?

A

exposure to microbes early in can protect against immunological diseases
Modern hygiene may reduce these protective exposures

47
Q

What can microbial exposure early in life protect against?

A

Asthma and atopic disease

48
Q

What are the antiviral actions of IFN alpha and beta

A

PRR engagment by viruses stimulates IFN production.
IFN increases MHC expression and activates NK cells.
It also induces a resistant state in adjacent cells

49
Q

Ways to block the action of cytokines

A

monoclonal antibodies bind to the cytokines (anti TNFalpha- infliximab_

Soluable receptors mop up the cytokines (TNF alpha- enteracept)

50
Q

What can Anti-TNFa (Infliximab) therapy treat?

A

Crohns disease

Immunology (6 decks)

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