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MII2 > 7. Immunity (extracellular + intracellular pathogens) > Flashcards

7. Immunity (extracellular + intracellular pathogens) Flashcards

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1
Q

What is the main function of innate immune system?

A
  • To detect that there are Ag present
  • To hold off pathogen infection to buy time for adaptive immune system
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2
Q

Explain the sequence of events in initial inflammatory response

A

Innate sensing:
1. Barrier break - microbe enters the host
2. Pathogen PAMPs + tissue DAMPs detected by PRRs by sentinel cells - activated
3. Sentinel cells secrete inflammatory mediators - cytokines
4. Increased vascular permeability - secreted molecules into blood
5. Complement system, Ab, macrophages, neutrophils, NK cells, anti-microbial peptides sent to infection site to kill
6. Secreted inflammatory mediators : adhesion + chemokines cause leukocyte (B / T cell) migration into tissue
7. Phagocytosis of microbes in infection site

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3
Q

What is the role of DCs in innate sensing?

A
  1. DCs sample the env
  2. If detect Ag - activated
  3. Activated DCs mature and travel to NL
  4. In LN DCs present antigens to T naive cells
  5. T cell activation

DC three modes:
- sampler
- traveller with cargo
- presenter

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4
Q

What are the types of T cells and what are their functions?

A
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5
Q

Which T cell types recognise extracellular Ags?

A
  • Helper T cells (Th cells) - CD4+
  • Regulatory T cells (Treg cells) - CD4+
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6
Q

Explain the whole sequence of events of T cells

A
  1. APCs present Ags to naive T cells -> T cells activated - mature
  2. Secrete cytokines, express receptors - TCR
  3. Proliferate - ‘clonal expansion’ of T cells
  4. T cell differentiation into one of the specific subtypes
  5. Differentiated T cell subtypes exhibit effector functions against specific Ag
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7
Q

What are the different Th cell subtypes? Which immune cells do they activate?

A
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8
Q

How is T cell subset differentiation started?

A

3 Signals needed:
- Signal 1: APC presents Ag by MHC - TCR (receptor) binds -> T cell activated - clonal expansion (but doesn’t know the type of infection)

  • Signal 2: APC upregulates B7 - binds with CD28 on Th cell -> signals that the Ag comes from microbe
  • Signal 3: APC secretes specific cytokines - tells T cell infection type -> knows into which subset to differentiate
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9
Q

What are the destinations of differentiated T cell subsets?

A
  • Th cells migrate to sites of infection through bloodstream
  • Tfh cells remain in LN, activate B cells produce Ab
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10
Q

What is the differentiation sequence of B cells?

A
  1. Naive B cells don’t produce Ab until activated
  2. Activated by Tfh cells - plasma cells - Ab factories
  3. Secrete BCRs - Ab as effector molecules
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11
Q

What are the functions of Abs?

A

Antibodies - effectors molecules - effector mechanisms

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12
Q

What are the types of antibodies and what are their properties?

A

MEGA

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13
Q

What are sentinel cells?

A

Sentinel cells - cells in body’s first line of defense - embeded in tissues - some of them also referred as APCs (but not all are APCs)

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14
Q

What are extracellular microbes?

A

Extracellular microbe pathogens - do not invade cells - replicate in extracellular environment - enriched with body fluids

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15
Q

What is the complement system? What are its functions?

A
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16
Q

Whar are the different pathways of the complement system?

A
  1. Alternative pathway
  2. Classical pathway
  3. Lectin pathway
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17
Q

What are the three main effector functions of the complement system?

A
  1. Opsonisation to enhance phagocytosis
  2. Stimulating inflammation by recruiting and activating immune cells
  3. Lysing microbes and cells
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18
Q

What is complement mediated opsonisation?

A

Opsonisation - immune process - uses opsonins to tag foreign pathogens for elimination by phagocytes

C3b bound to microbe - phagocyte receptor for C3b recognises - phagocytosis and killing

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19
Q

What is complement mediated inflammation?

A

Complement system mediates inflammation-like process: in complement activation mast cells release C3a, C4a, C5a - act similarly to cytokines - act locally to recruit cells to infection site + can activate cells

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20
Q

What is complement mediated cytolysis?

A

Complement activated - releases C5a - for inflammation and C5b - for membrane attack complex (MAC) assembly - assembles MAC in microbe plasma membrane - channel - water passes in, ions rush out - ion imbalance - bursts => killed pathogen

Can also kill host / foreign cells (ex transplant)

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21
Q

What is the main process for killing pathogens?

A

Phagocytosis

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22
Q

What are the main types of phagocytes?

A
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23
Q

What are the steps in phagocytosis?

A
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24
Q

What are the pathogen killing mechanisms in phagosomes?

Study These Flashcards
A
  • Acidic env
  • Respiratory burst, converting O2 into ROS
  • Making hypochlorite (HOCl)
  • Proteolytic enzymes
  • NO combines with superoxide - peroxynitrite
  • Starving pathogens within macrophages - withold iron
  • Secreting defensins - microbicidal proteins
25
How do Ab make phagocytosis more effcient?
26
What are NETs?
27
How do T cells enhance macrophage and neutrophil killing?
By releasing cytokines
28
What are the types of neutralisation performed by Ab?
29
What are granulocytes?
**Granulocytes** - **innate** immune cell that **prestore effector molecules in granules** (small particles) with enzymes that are released during infections / allergic reactions / asthma - Mast cells - Neutrophils - Basophils - Eosinophils
30
What is antibody dependent cell mediated cytotoxicity (ADCC)?
**Antibody dependent cell mediated cytotoxicity** (ADCC) - mechanism of cell-mediated immune defense whereby an **effector cell** of the immune system **actively lyses a target cell**, whose **membrane-surface Ag have been bound by specific Ab**
31
Explain ADCC example: fighting helminths
32
Explain ADCC example: mast cell degranulation in fighting helminths
Mast cells secrete cytokines to attract more immune cells - inflammation
33
How to Th2 cels enhance immunity to helminths?
34
How do extracellular pathogens contribute to immune memory?
Extracellular - on the surface: - more APCs can be activated by extracellular Ag - easier to activate B / T cells - easier for memory cells to secreet effector molecules
35
Why is it beneficial for pathogens to be intracellular?
1. **Hide** from immune effector mechanisms 2. Host cells provide **resources** 3. Host cells can help **migrate**
36
Which cells do intracellular pathogens invade?
- **Phagocytes**: survive within phagolysosomes - Non-phagocyte cells, ex: **somatic** - IECs
37
Why do intracellular pathogens choose to invade immune cells?
- **High numbers**, especially during infections - Immune cells migrate around the host - **perfect transporters** - **Immune evasion** - easier to manipulate if inside immune cell - Macrophages are trying to kill pathogens anyway - if evade killing mechanism - make infection easier
38
What are the killing mechanisms used to kill intracellular pathogens?
Diff. intracell. pathogens - diff. effector mechanisms (match with extracellular killing mechanisms): - phagocytosis - Type 1 IFNs - NK cells
39
How does the immunity detect intracellular microbes?
Use **intracellular PRRs** - as extracellular - just **PRRs inside the cells** rather than outside - different PRRs: - **endosomes**: TLRs - **cytosol**: NOD-like receptors recognise bacteria, RIG-like receptors recognise viral RNA
40
What is the war between intracellular microbes and macrophages?
**Macrophages try to kill microbes** - intracellular **microbes try to invade macrophages** as host cells Depends on speed + strength of macrophage response (same mechanism as for extracellular) vs immune evasion of microbe
41
How do intracellular pathogens avoid phagocytosis?
1. **Prevent lysosome fusion with phagosome** -> microbe ends up in rER-like vesicle - can proliferate until lyses the vesicle -> lyses the cell to spread => ex: Legionella pheumophila, Salmonella 2. **Break phagosome** - use **listeriolysin O** (LLO) - use host actin to move around -> lives + replicates in cytosol intracellularly => ex: Listeria monocytogenes, Shigella
42
What other cells work in combination with macrophages to fight intracellular microbes?
Macrophages rarely work on their own - are fully activated by IFN-γ from: - **NK cells** - **T cells** (Th1 / CTL)
43
What is the importance of T cell help in macrophage activation for intracellular microbe killing?
Naive T cells have to differentiate - **differentiate into Th1 to produce IFN-γ** to activate macrophages - if **incorrect differentiation** - not suitable signalling - could **inhibit macrophage activation** for successful killing
44
How are Tuberculosis bacteria adapted to evade phagocytosis?
TB - good at evading phagocytosis - **causes granuloma formation** - **immune cell agreggates** - **replicate inside them** -> continual production of IFN-γ -> continual macrophage activation -> **lung tissue damage** -> chronic infection
45
What is the anti-viral state?
**Anti-viral state** - result of signaling pathway - **type 1 interferon production** (antiviral genes) - IFN-α / IFN-β induce ant-viral state: cell signals surrounding cells to **enter anti-viral state** - protect themselves from viral infection Infection not fought directly - spread prevented to surrounding cells
46
What are the functions of type 1 interferons in viral-state?
Type 1 interferons (IFN-α / IFN-β): - **inhibit viral gene expression** - **induce apoptosis** of infected cell - promote **T cell and NK activation**
47
What are the functions of NK cells in fighting intracellular pathogens?
NK cells kill intracellularly infected cells - **need interferon (IFN-γ)** from Th1 + CTL for **full activation**: - **faster than CTL** but **less precise** - important **if pathogen adapted to evade CTLs** - act as **source of IFN-γ** for macrophage activation
48
How do NK cells and CTL kill pathogens?
NK cells + CTL kill infected host cells - **induce apoptosis** - apoptotic cells cleared by phagocytosis - **non-inflammatory**
49
Explain NK cell activation
NK cells need to be activated: NK cells **express activating + inhibitory receptors**: - **bind activating ligand** on infected / injured cells - **bind inhibiting ligand** on healthy cells - presented on **MHC I** - engaged - **bind inhibiting ligand** on tumour cells **without MHC I** - non-engaged - downregulated MHC class 1 -> **'missing'self'** **NK activation depends on balance of activating / inhibitory signals** received from the cell => more inhibitory - not kill / more activating and/or 'missing self' -> kill For killing use same mechanism as CTL (perforin/granzyme or FASL)
50
How can Ab enhance NK killing?
**Ab can enhance NK killing by ADCC** - when microbe **Ag remains on cell surface** (ex: microbe leaves Ag behind while invading cell) - not when Ag presented via MHC I / II
51
How can adaptive immunity clear intracellular infections?
- Directly - Indirectly
52
How do Th1 and CTL cooperate to kill intracellular pathogens?
53
How do Th1 cells induce CTL differentiation?
**Th1 cells enhance CD8 activation** -> CTL differentiation: - Th1 cells produce **cytokines - IFN-gamma** - stimulates **CTL differentiation** - Th1 cells **enhance APC ability to stimulate CTL differentiation** by cytokines release
54
How do CTL cells recognise intracellularly infected host cells?
CTL recognise **intracellular Ag presented by MHC I** - more specific, accurate, efficient than NK **MHC I are expressed by all nucleate cells** - any cell can present intracellular Ag - be identified as infected by CTL
55
How do CTL cells kill infected cells?
CTL cells **form synapse with infected cell** - all interactions occur through the synapse - p**recise control which cell is killed** - **induce apoptosis** - must be precise because killing mechanisms could damage healthy cells
56
What are the two killing mechanisms employed by NK cells and CTLs?
- Perforin / granzyme mediated killing - Fas/FasL mediated killing
57
How are naive CTL cells activated?
Naive CTL cells have to be **activated by professional APCs** -** if DC not infected intracellularly** - **cross-presentation**: allows specialised **DCs to take up Ag from infected cells**-> **present on MHC I** instead of MHC II => CTL can be activated without DC infection
58
What is the mechanism of viral evasion of NK cells and CTLs?
Viruses evade NK cells and CTLs by **disrupting Ag presentation by MHC I** -> reason why NK cells detect MHC I downregulation
59
How can Ab contribute to intracellular pathogen neutralisation?
**Ab can target** intracellular pathogens in **their extracellular stages** (ex moving between cells) - ex: SARS-CoV-2 vaccine targets viral spike protein which is used to invade host cells - Ab binding prevents invasion

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