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MCD Immunology > 9 Host Defence Overview > Flashcards

9 Host Defence Overview Flashcards

1
Q

Q: What is the role of the immune system? (2)

A

A: defend against viruses, bacteria, fungi and parasites

has to detect and react to dangerous ones (differentiate from the foreign but safe)

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2
Q

Q: Name 2 ideal modes of transmission. Compare.

A

A: respiratory infections that spread via sneezes- droplet etc

upper GI tract- when vomiting
-> less effective as it’s easier to avoid

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3
Q

Q: When do you experience most colds in you life?

A

A: 1st year of life

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4
Q

Q: Describe how evolution of flu viruses works against us.

A

A: if we are infected by one strain and our immune system is competent we gave immunity to it

but if virus keeps evolving so that our antibodies/humeral response don’t match -> we can keep getting infected

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5
Q

Q: What are the mechanical defences? (3)

A

A: -epithelial tight junctions (integrity)

  • skin waterproofed by fatty secretions
  • social conditioning eg washing hand
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6
Q

Q: What are the chemical defences? (5)

A

A: -fatty acids (on skin) have antimicrobial properties

  • enzyme lysozyme in saliva, sweat and tears
  • enzyme pepsin in gut
  • low pH in stomach and sweat
  • antimicrobial peptides in paneth cells in intetine
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7
Q

Q: What are the microbiological defences? (2)

A

A: -normal flora compete for nutrients/attachment sites

-production of antimicrobial substances

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8
Q

Q: What is the first and the last barrier concept?

A

A: skin surface is made of dead or dying cells

even if they get infected they will slough off or die so disease does not spread

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9
Q

Q: What are the surface defences against infection? (7)

A 
A: -Coughing 
-Sneezing 
-Mucus 
-Cilia 
=> mucocillary escalator which takes things to back of throat to be swallowed to enter low pH of stomach
-Rapid cell turnover 
-Wall of dead cells
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10
Q

Q: Describe one way smoking promotes infection.

A

A: weakens action of cilia/confuses them

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11
Q

Q: What do type I mucosa cells line? (4) Structure? (2)

A

A: gut, ciliated respiratory, upper vagina, posterior nose

=>includes cilia, single layer

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12
Q

Q: What do type II mucosa cells line? (5) Structure? (2)

A

A: cornea, mouth, oesophagus, lower vagina, anterior nose

=> flat, multi layered

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13
Q

Q: Describe the sequential action of the immune system. (3) How do they vary? (3)

A

A: events occur in specific order

pre-infection/ ‘first line’

early infection/ ‘second line’

late infection/ ‘specific/acquired’

  • specificity increases
  • breadth decreases
  • learning increases
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14
Q

Q: What is involved in preinfection? (3)

A

A: -avoidance

  • mucus
  • physical barriers
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15
Q

Q: What is involved in early infection? (6)

A

A: -phagocytes

  • opsonins
  • some lymphocytes
  • interferons
  • acute phase proteins
  • toll-like receptors
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16
Q

Q: What is involved in late infection? (2)

A

A: -T cells

-antibody

17
Q

Q: What’s involved in innate sensing? (3)

A

A: detecting PAMPs and DAMPs and differentiating between what’s dangerous and what’s not

18
Q

Q: What are PAMPs?

A

A: Pathogen-associated molecular patterns are molecules associated with groups of pathogens, that are recognised by cells of the innate immune system

19
Q

Q: What are DAMPs?

A

A: danger-associated molecular patterns, danger signals, and alarmin, are host biomolecules that can initiate and perpetuate a noninfectious inflammatory

host biomolecules that can initiate and perpetuate a noninfectious inflammatory response.response

20
Q

Q: What happens when PAMPs and DAMPs are recognised? Difference?

A

A: the cells produce interferons and a wave of information spreads out

danger-associated molecular patterns initiate and perpetuate a NONinfectious inflammatory response

pathogen-associated molecular patterns (PAMPs) initiate and perpetuate the INFECTIOUS pathogen-induced inflammatory response.

21
Q

Q: What are the types of interferons? (3) When are they activated? What do they do? (5,2)

A 
A: Type I/III: alpha/beta/lamda
=> important in early stage of infection
-activation of neighbouring cells
-Activates NK cells 
-Upregulates MHC and Mx proteins 
-Activates RNase L and Protein Kinase R (PKR) 
-Induces anti-viral state

Type II: IFNgamma (interferon gamma)

  • Proinflammatory
  • Th1 cytokine
22
Q

Q: What releases type I/III interferons? II?

A

A: all nucleated cells in response to infection

T cells

23
Q

Q: Summarise the role of phagocytes. What happens within?

A

A: engulf invaders-> antigen is destroyed in intracellular vesicles

24
Q

Q: What’s the importance of IgA?

A

A: defence on mucosal surface

25
Q

Q: What is the basic structure of antibodies? (2)

A

A: Fab: antigen binding part = variable

Fc= binds to host sensors

26
Q

Q: What are the possible actions of antibodies? (3)

A

A: -direct neutralisation (prevents binding and entering cells)

  • opsonised and engulfed
  • agglutination
27
Q

Q: What does each T cell express? What does this see?

A

A: one TcR

-each TcR sees a specific combination of MHC and peptide at high affinity

28
Q

Q: What are the 2 types of T cells? Role? (1,3)

A

A: cytotixic (CTL)- kill target cells

helper T- activate macrophages to kill, B cells to secrete antibodies and CTL to kill

29
Q

Q: Name 6 defences against viruses. Most important? Name 6 defences against bacteria.

A

A: 1. Surface defences

  1. Inflammatory mediators and acute phase proteins
    - Antibody, complement, ADCC (antibody dependent cell-mediated cytotoxicity)
    - NK cells
    - T cells (mostly resolving infection)
    - Interferons - VERY IMPORTANT AGAINST VIRUSES
  2. Surface defences (mechanical and chemical)
  3. Release of inflammatory mediators and acute phase proteins (and opsonins)
    - Antibody opsonisation
    - Complement (alternative pathway) causing lysis/opsonisation
    - Phagocytosis
    - Fever
30
Q

Q: What is a cytokine storm? Can lead to? (5)

A

A: a dis-regulated exaggeration production of pro-inflammatory cytokines

leads to excessive accumulation of inflammatory cells, pulmonary oedema and eventually lung damage and airway occlusion potentially resulting in death

31
Q

Q: What are the characteristics of an eradicable infectious disease? (5)

A

A: -simple (and cheap) to diagnose

  • genetically stable pathogen
  • accessible host species
  • eliminates persistent infection OR persistently infected host can’t transmit
  • safe and effective vaccine

MCD Immunology (10 decks)

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