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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)
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2
Q

What cells are involved in the innate cellular immune response?

A

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

NK cells

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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).

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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.
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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
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6
Q

What are the components of the innate chemical immune response?

A
  • complement system

- proinflammatory cytokines

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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).
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8
Q

What complement protein is generated in all three pathways?

A

C3 convertase.

It cleaves C3 into C3a and C3b.

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9
Q

Role of C3a, C4a and C5a?

A
  • Inflammatory mediators.

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

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10
Q

Role of C3b?

A

Opsonisation - coats pathogens, marking them for phagocytosis.

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11
Q

Role of C5b?

A

Memrane Attack Complex (MAC).

Osmotic lysis of bacterial cells.

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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

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13
Q

Il-1 ?

A

activates lymphocytes and causes fever (systemic effect)

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14
Q

Il-6?

A
  • Causes fever
  • stimulates CRP production by the liver
  • activates lymphocytes
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15
Q

Il-8?

A

causes chemotaxis of neutrophils

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16
Q

Il-12?

A

activates NK cells and TH1 cells

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17
Q

TNF-alpha?

A

increases vascular permeability, allowing immune cells to access tissues

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18
Q

Il-4, Il-5 and Il-13

A

promote IgE production

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19
Q

IFNγ

A

activates cell-mediated immunity in viral infections

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20
Q

Il-10

A

anti-inflammatory effect

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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
What cell types do activated T helper cell differentiate into?
TH1 cells (promote cytotoxic T cells and cell-mediated immunity) TH2 cells (promote B cells and humoral immunity)
26
What is humoral immunity?
Specific adaptive immune response activated by TH2 cells, which leads to the production of B cells and antibodies.
27
What infections does the humoral immunity fight?
``` extracellular infections (bacteria, fungi, protozoans) parasitic worms ```
28
Structure of antibodies?
- 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
Which part of the antibody confers its specificity?
The variable regions
30
IgM?
- pentameric structure | - expressed on B cell surfaces
31
IgG?
- monomeric - found in circulating blood and tissues - crosses the placent to provide passive immunity to the foetus
32
IgA?
- forms dimers - found in mucosa (GI respiratory) and urinary tracts - secreted in saliva, tears and milk
33
IgE?
- forms monomer - mediates allergic reactions - provides immunity against parasitic worms
34
IgD?
- monomeric | - interacts with basophils and mast cells
35
What mechanisms enable B cells to create the vastly diverse array of specific antibodies?
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
How do antibodies fight extracellular infections?
- 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
What are the 3 stages of humoral immunity?
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
How do T helper cells activate B cells?
- 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
What is Isotype class switching?
- IgM antibodies are produced first | - then different Ig classes,as required
40
What is Cell-mediated immunity?
A specific adaptive immune response activated by TH1 cells, which leads to activation of antigen-presenting cells and a cytotoxic T cell response.
41
What infections does Cell-mediated Immunity fight?
- intracellular infections (viral, bacterial) | - protozoans (Plasmodium)
42
Why is T Cell Receptor diversity important?
It needs to cover all possible infection-derived antigens, just like B cells.
43
How is diversity of T cell receptors achieved?
- VDJ recombination - junctional diversity - addition of N regions
44
Where do T cells maturate?
in the thymus gland
45
To what selective processes are immature T cells subjected to in the thymus gland?
- 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
How are antigen-presenting cells (APCs) activated?
- 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
What is the cytotoxic T cell response?
The killing of infected cells, recognised by antigens displayed on MHC I on their surfaces.
48
How are cytotoxic T cells activated for an antigen-specific response?
- 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
What killing mechanisms do cytotoxic T cells use?
- 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
What signals are needed to activate the cytotoxic T cell response during re-infection?
-MHC + antigen only Thus can be activated by any antigen-presenting cell.
51
Adaptive immune response against extracellular infections?
Humoral immune response. -TH2-mediated activation of B cells, clonal expansion and Ig production
52
Adaptive immune response against intracellular infections?
Cell-mediated immune response. -TH1-mediated activation of the antigen-presenting cells and cytotoxic T cells.

Immunology (4 decks)

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