Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Principles 2018 > Immunology Part 3 > Flashcards

Immunology Part 3 Flashcards

1
Q

What is the local effects of

  • NO
  • Prostaglandins/leukotrienes
  • histamines

?

A

Vasodilatation

Increased vascular permeability

Smooth muscle contraction

Pain

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

What are the local effects of pro-inflammatory cytokines?

A

Increased vascular permeability

Endothelial cell activation

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

What are the local effects of chemokines?

A

Leukocyte (neutrophil) recruitment and activation

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

Transendothelial migration:

What is found on the suface of neutrophils?

A

On surface of neutrophils

  • Carbohydrates
    • ligands for selectins
  • integrins (LFA-1)
    • receptor for ICAM-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the neutrophil encounter as it rolls alon gthe endothelium?

A

Selectins

ICAM-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

`What happens to the neutrophil as it rolls alon the endothelium?

A
  1. weak binding ‘rolling’ to selectins
  2. strong binding to ICAM-1
  3. Stable adhesion and aggregation to ICAM-1
  4. Transendothelial migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens to the neutrophil after transendothelial migration?

A

Chemotaxis to site of infection, attracted by chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the result of increased vascular permeability in acute inflammation?

A

Tight junctions lost- gaps form between endothelial cells

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

What is the result of vasodilatation and increased blood flow in acute inflammation?

A

Loss of intravascular fluid and increased plasma viscocity slows flow allowing neutrophils to flow in the plasmatic zone; this is margination

This occurs only in venules…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens to endothelial cells at sites of acute inflammation?

A

Endothelial cellls become activated leading to expression of adhesion molecules

ICAM-1 and selectins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the process by which neutrophils squeeze between endothelial cells?

A

Diapedesis

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

What are some compounds that are chemotactic to neutrophils?

A

Bacterial products

Complement components

Cytokines: known as chemokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the killing mechanisms of neutrophils?

A

Phagocytosis

Degranulation

NETs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do neutrophils undergo phagocytosis?

A

Use PRRs to bind and phagocytose pathogens

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

What are the two distinct mechanisms by which neutrophils kill internalised pathogens?

A
  1. anti-microbial proteins and enzymes
  2. reactive oxygen species ROS
17
Q

What is degranulation used for by neutrophils?

A

Killing of extracellular pathogens:

bacteria and fungi

May cause tissue damage and systemic inflammation

18
Q

What do NETs do?

A

Immobilise pathogens

  • prevent them from spreading
  • facilitates their phagocytosis
19
Q

What do neutrophils release to cause acute inflammtion?

A

TNFa

20
Q

What are the three pathways of complement activation?

A
  • classical pathway
  • mannose binding lectin pathway
  • alternative pathway
21
Q

What does the activation of complement cause?

A

Activation of downstream complement proteins

leading to….

  1. pathogen killing
  2. pathogen opsonisation
  3. leukocyte recruitment and inflammation
  4. removal of immune complexes
22
Q

Where does MBL pathway activate complement?

A

C3

23
Q

How is the alternative pathway activated?

A

Spontaneous breakdown of C3 into C3a and C3b

24
Q

What does the alternative pathway trigger?

A

Amplification loop whereby C3b triggers conversion of C3 to C3b

25
Q

What does C3b result in?

A

Conversion of C5 to C5a and C5b

26
Q

What does C5b do?

A

Bind to surface of pathogens

Assembles with C6, C7, C8 and C9 to form membrane attack complex

27
Q

What is the role of MAC?

A

Inserts into target cell walls- making a funnel shaped hole

Causing osmotic cell lysis of pathogen

28
Q

Define opsonisation?

A

coating of pathogens by humoral factors (opsonins) to facilitate phagocytosis

29
Q

What are examples of opsonins?

A
  • C3b
  • C-reactive protein (CRP)
  • IgG / IgM
30
Q

Where are receptors for opsonins located?

A

Surface of phagocytes

31
Q
A
32
Q

What are C3a and C5a known as?

A

Anaphylatoxins

33
Q

What is the tole of anaphylatoxins?

A

Promote inflammation BY;

  • acting directly on blood vessels
    • increasing permeability
  • activating mast cells
    • causing the release of pro-inflammatory mediators and chemokines
34
Q

Describe the regulation of complement?

A
  1. Only cleaved Complement proteins are active
  2. Active Complement proteins have very short half-life
  3. Some Complement proteins are only produced during an Acute Phase Response
  4. Some Complement proteins do not bind to human cells
  5. Complement inhibitors and regulatory proteins limit activation of the system
35
Q

What is a dendritic cell?

A

Professional antigen presenting cell

Principles 2018 (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions