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Infection and immunity > 3. Defence against infection > Flashcards

3. Defence against infection Flashcards

1
Q

What different things can be human pathogens?

A

bacteria
viruses
fungi
protozoa
parasites
worms

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2
Q

what cells does HIV1 infect?

A

T cells, macrophages, dendritic cells

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3
Q

what is the number 1 killer if you have AIDS?

A

Tuberculosis

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4
Q

what organism can cause toxic stock syndrome?

A

S. aureus

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5
Q

What happens to pathogens that are too big to be phagocytosed?

A

Large IgE presence and eosinophils release toxic granules

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6
Q

What can vary depending on the lifecycle of the pathogen?

A

site of infection - intracellular vs extracellular

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7
Q

Why are pathogens vulnerable when outside the cell?

A

attack from: innate cells, antibodies, and the complement

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8
Q

what receptors do innate immune cells express?

A

pattern recognition receptors

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9
Q

What receptors do adaptive lymphocytes express?

A

specific BCR and TCR
1 receptor for 1 antigen

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10
Q

how quickly does the innate immune system react?

A

rapidly within minuets

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11
Q

why is adaptive immunity slower to act?

A

clonal expansion of individual b and t cells takes time, over several days

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12
Q

does innate immunity change after repeated exposure?

A

no

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13
Q

How do t and b cells get their specific receptors?

A

genetic rearrangement

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14
Q

why is innate response important?

A

it limits the infection to local tissues

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15
Q

why is adaptive immunity important?

A

it clears the infection

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16
Q

what is the role of macrophages in the initial immune response?

A

recognise the bacteria as foreign and mount an immune response
cause wound healing to commence

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17
Q

what is the role of dendritic cells in the initial immune response?

A

takes up the bacteria and becomes an antigen-presenting cell then travels to the lymph node

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18
Q

what is the role of dendritic cells in the activation of t cells?

A

dendritic cells enter the lymph node and present the antigen to the specific T to activate them and cause clonal expansion

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19
Q

what is the role of activated t cells in the lymph node?

A

encounter the b cells to activate and trigger antibody production

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20
Q

Where to activated B and T cells go?

A

they leave the lymph node and circulate in the blood to the site of infection

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21
Q

what are the physical barriers?

A

skin, hair, nails
mucosal membranes
mechanical barriers like cilia moving mucus

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22
Q

what are the chemical barriers?

A

fatty acids on the skin
enzymes like lysozyme and pepsin
low pH
antibacterial peptides

23
Q

what are the microbiological barriers?

A

normal microbiota competing for nutrients and space
production of antibacterial substances like defensins

24
Q

Is the complement innate or adaptive?

A

innate

25
Q

what are the complement proteins produced as?

A

inactive precursors called zymogens

26
Q

what activates the complement zymogens?

A

each component cleaved and then activating the next

27
Q

what is C3 in the complement?

A

a key starting component for the cascade

28
Q

what is produced when C3 is spontaneously cleaved in serum?

A

C3a and C3b

29
Q

what is C3a?

A

soluble in serum

30
Q

What does C3b do?

A

forms a thioester bond to bacterial membrane

31
Q

What does C3b bind once it is attached to the bacterial membrane?

A

Factor B

32
Q

what happens to factor B once it is bound to C3b?

A

it is cleaved by factor D to produce Bb and Ba fragments
Bb remains attached to C3b making C3bBb

33
Q

what is C3bBb?

A

a C3 convertase which makes more C3a and C3b

34
Q

also made is (C3b)2Bb which is what?

A

a C5 convertase that makes C5a and C5b

35
Q

what are the 3 ways to activate the complement?

A

classical pathway, alternative pathway, mannose-binding lectin pathway

36
Q

where is mannose-binding lectin normally found?

A

in the plasma at low concentration

37
Q

what is a cytokine that macrophages produce that triggers the release of proteins from hepatocytes?

A

IL-6

38
Q

where is mannose-binding lectin released from?

A

hepatocytes

39
Q

where to mannose binding lectins bind?

A

mannose residues on bacterial surfaces

40
Q

what else can mannose-binding lectins bind?

A

Fucose
N-acetylglucosamine
both on bacteria

41
Q

what does binding to the mannose cause?

A

activation of serine protease MASP-1 and MASP-2

42
Q

what do MASP-1 and MASP-2 do?

A

cleave complement components C2 and C4

43
Q

what does C4b do ?

A

Covalently binds to the bacterial surface

44
Q

what is C4bC2a?

A

a C3 convertase

45
Q

what is C4bC2aC3b?

A

A C5 convertase

46
Q

what is C2a an exception to?

A

the rule that A fragments are soluble

47
Q

where do ficolins bind?

A

acetylated sugars on bacteria membrane

48
Q

what does ficolin binding cause?

A

activation of serine protease MASP-1 and MASP-2

49
Q

what do C3a and C5a do?

A

recruit macrophages and neutrophils to cause inflammation

50
Q

how does C3b trigger phagocytosis?

A

Binds to complement receptors on phagocytes

51
Q

what does C5b and other components form?

A

membrane attack complex

52
Q

how does the membrane attack complex form?

A

C8 penetrates the lipid bilayer and recruits up to 16 C9 fragments which form a pore to lyse the bacteria

53
Q

what do defects in C3 and its activation lead to?

A

pyogenic infections like staph and strep

54
Q

what to defects in membrane attack complex cause?

A

Susceptibility to Neisseria infections
Neisseria meningitidis
Neisseria gonorrhoea

Infection and immunity (22 decks)

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