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Immunology > Lecture 11 - Innate immunity > Flashcards

Lecture 11 - Innate immunity Flashcards

1
Q

What is the timing of an innate immune response?

A

0-4 hours - Innate immunity, recognition by preformed nonspecific receptors and removal
4-96 hours - Early induced response, recognition of microbial associated molecular patterns leads to inflammation and recruitment and activation of effector cells, removal

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2
Q

What are some barriers to infection?

A

1) Eyes - washing with tears, enzyme lysozyme
2) Skin - sweat, sebum = microbes cannot adhear
- antimicrobial secretions (defensins)
- low pH
- commensal microbes
- dead, dry skin cells
3) Respiratory tract - mucus
- cilliated epithelium
- pulmonary surfectants A&D
4) Genitourinary tract - washing and acidity of urine
- lysozyme
- vaginal lactic acid
5) Digestive tract
- stomach acidity
- mechanical flushing
- gut flora
- lysozyme
- bacteriocins
- intestine alkaline
- antibacterial peptides (defensins)

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3
Q

What are the first line of immune system defence?

A

macrophages

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4
Q

What are macrophages derived from?

A

Monocytes that circulate in the blood and migrate into tissues

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5
Q

What is the difference between macrophages and dentritic cells?

A

Macrophages not as efficient as dendritic cells

-dendritic cells have longer pseudopodia

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6
Q

What are the features of Neutrophils?

A

30-70% WBC higher in infection

  • short lived
  • quick acting
  • bad host cell for pathogens
  • role in recognising and ingesting and destroy microbes
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7
Q

What is the operation of dendritic cells and macrophages?

A

1) Dendritic cells and macrophages first cells come into contact with microbes in tissue
2) recruit neutrophils to tissue
3) second wave of macrophages to clean up and heal wound

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8
Q

What is the process of phagocytosis?

A

1) attachement/adhesion and engulfment
2) phagosome formation
3) recruitment of lyso somes
4) phagosome and lysosome fusion = phagolysosome
5) killing and digestion

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9
Q

What killing mechanisms do macrophages have to kill pathogens?

A

1) ROI
2) Toxic nitrogen oxides
3) Antimicrobial peptides
4) enzymes
5) Acidification

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10
Q

How do ROI kill pathogens?

A

-oxidative/respiratory burst in activated macrophage
-30-60s after receptor stimulation
Pathway
1)O2 made into superoxide anion O2- by membrane bound NADPH oxidase
2) can be converted by hydrolysis in OH- hydroxide
OR 2b) can be converted by superoxide dimutase into H2O2
3b) with the addition of Cl- into OCl- by myeloperoxidase
4b) then into 1O2

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11
Q

How do Toxic nitogen oxides kill microbes?

A

-microbes killed 10-30 mins after ingestion
-relies on inducible nitric oxide synthase (iNOS)
Pathway
1) L-arginine from membrane combined with O2 by iNOS leads to Nitric Oxide (toxic)
2a) addition of O2- leads to HNO2
2b) addition of superoxide anion O2 leads to NO2- then to NO3-
Anions from ROI help to make even more toxic components

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12
Q

How do antimicrobial peptides killl microbes?

A

e. g. defensins, cryptidins
- cause ion-permeable channels in bacterial cell membrane
- present in neutrophil granules

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13
Q

How do enzymes kill microbes?

A

from neutrophil granules

  • lysozymes
  • proteases
  • phospholipases
  • elastases
  • collagenase
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14
Q

How does acidification kill microbes?

A

pH 3.5 - 4 in endosomes

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15
Q

What are the differences between innate and adaptive response cells?

A

Innate
-specificty inherited in genome
- expressed by all cells of particular type
-triggers an immediate immune response
-recognises broad classes of pathogen
-interacts with range of molecular structure of given type
Adaptive
-specificty encoded in multiple gene segments
-requires gene rearrangement
-clonal distribution
-able to discriminate between closely related molecular structures

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16
Q

What is a lipopolysaccharide as an example of a bacterial molecule that triggers an innate immune response on macrophaghes

A
  • found on nearly all gram negative bacteria
  • endotoxin
  • not protein, largely carb molecular motif, invariant
  • essential for microbe survival
  • not in eukaryotes
17
Q

How is respiratory burst initated in a macrophage?

A

1) microbe opsonised with antibody bound to Fc receptor

2) transmembrane signals within macrophage iniaate a respiratory burst leading to ROIs

18
Q

What happens when microbe is opsonised with C’?

A

1) microbe opsonised with C’
2) c3bi binds to CR3 and mannose receptor
3) leads to phagocytosis of microbe into phagosome

19
Q

What is the operation of mannose receptor?

A

1) mannose receptor (along with glucan receptor and scavenger receptor) on surface of macrophae
2) bacteria bind to macrophage receptorand initate activation and release of cytokines and small lipid mediators of infection
3) macrobphages engulf and digest bacteria

20
Q

What are TLRs

A

Toll-like receptors

  • transmembrane
  • bind to very broad ligands
  • also in endosome for recognising bacterial component and viral components
21
Q

How do TLR e.g. TLR4 turn on cytokine production?

A

1) Lipopolysaccharide binds to CD14 on surface of phagocytes
2) CD14 interacts with TLR4:MD-2 resulting in activation of NFalphaB in the nucleus
3) leads to activation of NFkB
4) leads to cytokine production (IL-12, TNFalpha, IL-6, IL-IB, IFNalpha, IFNbeta)

22
Q

What cytokines/chemokines are released by macrophages?

A 
IL-1beta
IL-6
TNFalpha
CXCL8 (IL-8)
IL-12
mediators of infection
23
Q

What are the three major changes in local blood vessels caused by inflammation?

A

1) increased vascular diameter
- increased blood entering site and reduced speed of flow in capillaries, more cells being brought into s.o.i
2) increased adhesion molecules
- promotes binding of circulating lymphocytes
3) increase in vascular permeability
- exit of fluids and proteins into tissue leads to oedema and extraversion

24
Q

What cytokines are involved in mediating inflammation?

A

IL-1B, TNF-alpha, IL-6, CXL8, IL-12

25
Q

What are the local effects of IL-1B?

A

-activavtes vascular endothelium
-activates lymphocytes
-local tissue destruction
-increases access of effector cells
LEADING TO fever and production on IL-6

26
Q

What are the local effects of TNF-alpha?

A

-activated vascular endothelium
-increases vascular permeability
-leads to increased entry of IgG, complement and cells to tissues and increased fluid drainage to lymph nodes
LEADS TO
Fever
mobilisation of metabolites
shock

27
Q

What are the local effects of IL-6?

A

-lyphocyte activation
-increased antibody production
LEADS TO
fever
induced acute-phase protein production

28
Q

What are the local effects of CXCL8?

A

Chemotactic factor recruits neutrophils basophils and T cells to site of infection

29
Q

What are the effects of IL-12?

A
  • activated NK cells

- induces the differentiaion on CD4 cells into Th1 cells

30
Q

What are properties of innate natural killer cells?

A
  • kill viral infections
  • derived from lymphoid progenitor, 5-20% blood lymphocytes
  • don’t express TCR CD3
  • not MHCI restricted
  • innate immune cell
  • not generated in innume response
  • act in similar way to CTL, release perforin and granzymes kill virally infected cells

Immunology (13 decks)

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