Immune Response Flashcards

1
Q

What are the three ‘components’ of the innate immune response?

A
  1. Cellular response (by the innate immune system)
  2. Chemical response (by cytokines and complement)
  3. Acute inflammatory response (initiated by the above)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What cells are involved in the innate cellular immune response?

A

Phagocytes (dendritic cells, blood monocytes, tissue macrophages, neutrophils)

NK cells

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

How do phagocytes recognise pathogens?

A

Via PAMPs (pathogen-associated molecular patterns).

They bind PAMPs using PRRs (pathogen recognition receptors), e.g Toll-like receptors (TLRs).

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

What are the stages of phagocytes’ immune response?

A
  • identify PAMPs of pathogens via PRRs
  • internalise pathogen, kill and digest it
  • present protein antigens to the cells of the adaptive immune system via MHC (major histocompatibility complex)
  • binding of PAMPs to PRRs triggers activation of NFKB, a transcription factor which upregulates the release of proinflammatory cytokines and initiation of the inflammatory response.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are NK cells involved in the innate immune response?

A
  • respond immediately when exposed to a pathogen
  • target cells which do not express surface MHC I
  • target cells are killed by release of toxic granules, which trigger apoptosis
  • MHC I expression is suppressed in virus-infected and tumour cells; NK cells kill these
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the components of the innate chemical immune response?

A
  • complement system

- proinflammatory cytokines

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

Pathways of complement activation?

A
  • Classical pathway (activated by antigen-antigen complexes on pathogen surface).
  • Mannose-binding lectin pathway (lectin binding to mannose on pathogen surface triggers activation).
  • Alternative pathway (C3 reacts directly with pathogen surfaces).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What complement protein is generated in all three pathways?

A

C3 convertase.

It cleaves C3 into C3a and C3b.

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

Role of C3a, C4a and C5a?

A
  • Inflammatory mediators.

- Trigger maste cell degranulation, causing release of histamine (anaphylotoxins)

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

Role of C3b?

A

Opsonisation - coats pathogens, marking them for phagocytosis.

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

Role of C5b?

A

Memrane Attack Complex (MAC).

Osmotic lysis of bacterial cells.

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

Role of proinflammatory cytokines?

A

Released by immune cells in response to infection.

Mediate the acute inflammatory response.

IL-1,4,5,6,8,10,12,13; TNF-alpha, INF-gamma

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

Il-1 ?

A

activates lymphocytes and causes fever (systemic effect)

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

Il-6?

A
  • Causes fever
  • stimulates CRP production by the liver
  • activates lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Il-8?

A

causes chemotaxis of neutrophils

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

Il-12?

A

activates NK cells and TH1 cells

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

TNF-alpha?

A

increases vascular permeability, allowing immune cells to access tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Il-4, Il-5 and Il-13

A

promote IgE production

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

IFNγ

A

activates cell-mediated immunity in viral infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Il-10

A

anti-inflammatory effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the triggers of the acute inflammatory response?

A

innate immune cells’ activity
proinflammatory cytokines
complement

Occurs 4-96h after onset of infection.

22
Q

What are the main effects of the acute inflammatory response?

A

vasodilation
increased vascular permeability (swelling/oedema)
pain sensitisation (by bradykinins and prostaglandins)
neutrophil chemotaxis
microvascular coagulation (confines the infection)
Fever, CRP, ferritin(systemic)

23
Q

What are the main cells responsible for Antigen Presentation?

A

Dendritic cells

They carry digested antigens to lymph nodes, where they present them to naive T helper cells (TH0).

24
Q

How is inappropriate activation of the immune system by antigens prevented?

A
  • MHC restriction: antigens have to be presented in complex with MHC II to activate T helper cells.
  • second signal: B7 proteins from Dendritic cells must bind CD28 receptors on T helper cell surface.
25
Q

What cell types do activated T helper cell differentiate into?

A

TH1 cells (promote cytotoxic T cells and cell-mediated immunity)

TH2 cells (promote B cells and humoral immunity)

26
Q

What is humoral immunity?

A

Specific adaptive immune response activated by TH2 cells, which leads to the production of B cells and antibodies.

27
Q

What infections does the humoral immunity fight?

A
extracellular infections (bacteria, fungi, protozoans)
parasitic worms
28
Q

Structure of antibodies?

A
  • two heavy chains (determine the Ig type)
  • two light chains (kappa or lambda)
  • connected by disulfide bonds
  • constant and variable regions in all 4 chains
29
Q

Which part of the antibody confers its specificity?

A

The variable regions

30
Q

IgM?

A
  • pentameric structure

- expressed on B cell surfaces

31
Q

IgG?

A
  • monomeric
  • found in circulating blood and tissues
  • crosses the placent to provide passive immunity to the foetus
32
Q

IgA?

A
  • forms dimers
  • found in mucosa (GI respiratory) and urinary tracts
  • secreted in saliva, tears and milk
33
Q

IgE?

A
  • forms monomer
  • mediates allergic reactions
  • provides immunity against parasitic worms
34
Q

IgD?

A
  • monomeric

- interacts with basophils and mast cells

35
Q

What mechanisms enable B cells to create the vastly diverse array of specific antibodies?

A

B cells manipulate their own genome:

  • VDJ recombination (shuffling of gene segments encoding the varable regions)
  • imprecise joining of VDJ segments
  • isotype class swithching (generates different antibody types)
  • somatic hypermutation (generates variants of antibodies with the same specificity and varying affinity - high affinity antibodies are selected)
36
Q

How do antibodies fight extracellular infections?

A
  • they neutralise toxins by direct binding
  • bind to antibodies on pathogen surface (opsonisation and agglutination)
  • antibody-antigen complexes activate teh classical complement pathway
  • directly activate dendritic cells, NK cells and cytotoxic T cells
37
Q

What are the 3 stages of humoral immunity?

A
  1. activation of B cells by T helper cells
  2. maturation of activated B cells into plasma cells (these produce antibodies)
  3. dormant memory B cell formation
38
Q

How do T helper cells activate B cells?

A
  • activated naive Th0 cells differentiate into TH2 cells
  • TH2 cells idenitfy the correct antigen bound to the MHC II on the B cell’s surface.
  • the CD40 ligand is provided as the second signal to the B cell
  • TH2 cells also release cytokines (IL-2, IL-4, IL-5). These promote B cell development.
39
Q

What is Isotype class switching?

A
  • IgM antibodies are produced first

- then different Ig classes,as required

40
Q

What is Cell-mediated immunity?

A

A specific adaptive immune response activated by TH1 cells, which leads to activation of antigen-presenting cells and a cytotoxic T cell response.

41
Q

What infections does Cell-mediated Immunity fight?

A
  • intracellular infections (viral, bacterial)

- protozoans (Plasmodium)

42
Q

Why is T Cell Receptor diversity important?

A

It needs to cover all possible infection-derived antigens, just like B cells.

43
Q

How is diversity of T cell receptors achieved?

A
  • VDJ recombination
  • junctional diversity
  • addition of N regions
44
Q

Where do T cells maturate?

A

in the thymus gland

45
Q

To what selective processes are immature T cells subjected to in the thymus gland?

A
  • immunological tolerance (removal of T cells with receptors recognising self cell antigens)
  • must express CD3 and CD4 or CD8
  • must bind to self MHC complexes
46
Q

How are antigen-presenting cells (APCs) activated?

A
  • TH1 cell recognises the antigen presented on MHC II
  • it activates the APC with a CD40 ligand and IFNγ
  • activated APCs produce NO and superoxide radicals, enhancing their pathogen-killing abilities
47
Q

What is the cytotoxic T cell response?

A

The killing of infected cells, recognised by antigens displayed on MHC I on their surfaces.

48
Q

How are cytotoxic T cells activated for an antigen-specific response?

A
  • activated APCs present their MHC I-bound antigen to the specific cytotoxic T cell receptor
  • second signals must be present
  • IL-2 enhances this process
49
Q

What killing mechanisms do cytotoxic T cells use?

A
  • perforin released into an immunological synapse makes a hole in the bacterial cell wall. Apoptotic agents are released through that hole.
  • apoptosis can also be triggered by Fas ligand interactions
  • IFNγ from cytotoxic T cells can block viral replication without killing the infected cell
50
Q

What signals are needed to activate the cytotoxic T cell response during re-infection?

A

-MHC + antigen only

Thus can be activated by any antigen-presenting cell.

51
Q

Adaptive immune response against extracellular infections?

A

Humoral immune response.

-TH2-mediated activation of B cells, clonal expansion and Ig production

52
Q

Adaptive immune response against intracellular infections?

A

Cell-mediated immune response.

-TH1-mediated activation of the antigen-presenting cells and cytotoxic T cells.