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IMS Immunology > Lecture 42 Innate immune responses > Flashcards

Lecture 42 Innate immune responses Flashcards

1
Q

what two mediums does innate response involve

A

humoral (fliud phase) and cellular responses

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2
Q

humoral phase

A

complement activation = blood plasma

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3
Q

cellular responses in innate response = mechanisms

A

phagocytosis and induction of apoptosis

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4
Q

cells involves in innate response

A

phagocytes = macrophages, neutrophils, dendritic cells

apoptosis inducers = NK cells

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5
Q

functions of complement system

A
  • produce MAC
  • produce
    anaphylatoxins
  • opsonisation
  • attract neutrophils to
    infection site
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6
Q

MAC

A

Membrane Attack Complex = stabs invading pathogens by perforating cell membrane

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7
Q

Anaphylatoxins

A

byproducts from activated complement factors - play role in allergic reactions

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8
Q

C5a complement factor

A

attract neutrophils to site of inflammation

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9
Q

C3b complement factor

A

binding of C3b to pathogen = opsonisation

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10
Q

three complement activation pathways

A
  1. classical
  2. lectin or mannose-binding pathway
  3. alternative pathway
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11
Q

what factors are activated in all complement pathways

A

C3 and C5

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12
Q

what is classical pathway activated by

A

antigen-antibody complexes

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13
Q

what does classical pathway require activation of to give antigen-antibody complexes

A

activation of adaptive immune system

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14
Q

complement activation involves

A

limited proteolysis

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15
Q

limited proteolysis

A

where an enzyme cleaves only one (or a few) proteins in a specific place

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16
Q

products of limited proteolysis

A

activated complement factor and a byproduct

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17
Q

what are potential roles of byproducts of limited proteolysis

A

role in anaphalaxis or chemical attractant for neutrophils to the infection site

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18
Q

classical pathway is based on amplifications which means

A

small starting signal is needed for a significant response, signal is amplified

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19
Q

what are many of the complement factors in classical pathway

A

serine proteases

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20
Q

what does classical pathway produce

A

anaphylatoxons, opsonins and MAC

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21
Q

classical pathway step 1- C2…

A

cleaves C2 into C2a and C2b

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22
Q

classical pathway step 2- C4…

A

cleaves C4 into C4a and C4b

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23
Q

classical pathway step 3-

A

C2a and C4b join to form complex which cleaves C3 into C3a and C3b

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24
Q

classical pathway step 4-

A

C3b joins the C2a and C4b complex which cleaves C5 into C5a and C5b

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25
Q

classical pathway step 5-

A

C5b forms complex with C6, C7, C8 and C9

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26
Q

what does the final complex of C5b/C6/C7/C8/C9 form

A

the MAC = the Membrane Attack Complex

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27
Q

what does MAC do

A

perforates the cell membrane

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28
Q

Byproducts of classical pathway = anaphylatoxins

A

C3a, C4a and C5a

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29
Q

role of C3b

A

opsonisation

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30
Q

what is classical complement pathway activated by

A

when C1 binds to antigen/antibody complex

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31
Q

MBL

A

Mannose-Binding Lectin

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32
Q

Lectin or Mannose-binding pathway involves activated by

A

pathogens

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33
Q

why do pathogens activate the Mannose-binding pathway

A

particular sugar (mannose) is found on surface of many pathogens but not on host cells

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34
Q

what does MBL bind

A

MASP 1 and MASP 2

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35
Q

what does MASP stand for

A

MBL Associated Serine Protease

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36
Q

what do MASP 1 and MASP 2 activate

A

C2 and C4

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37
Q

common pathways of Lectin-binding and classical

A

C3-C9

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38
Q

viruses with mannose

A

HIV and Influenza A

39
Q

bacteria with mannose

A

salmonella and Steptococci

40
Q

Yeast with mannose

A

candida albicans

41
Q

parasite with mannose

A

Leishmania

42
Q

Alternative pathway is directly activated by

A

contact with pathogens

43
Q

step 1 of alternative pathway

A

auto-activation of C3 -> C3a and C3b = slow rate

44
Q

step 2 of alternative pathway

A

low levels of C3b bind to bacteria

45
Q

what two factors bind to bacteria surface after C3b binds

A

factor B and properdin

46
Q

factor B and properdin activate

A

more C3 and C5

47
Q

common pathway between alternative and classical

A

C6-C9

48
Q

three initiators of complement pathways

A
  1. antigen/antibody complex
  2. bacterial sugars
  3. auto-activation from pathogen contact
49
Q

Anaphylatoxins

A

C3a, C4a and C5a

50
Q

what do anaphylatoxins induce

A
  • degranulation of endothelial cells, mast cells and phagocytes
  • smooth muscle contraction
  • increased vascular permeability
51
Q

mast cell degranulation

A

releases histamines

52
Q

phagocyte degranulation

A

releases cytokines

53
Q

anaphylatoxins increased vascular permeability

A

makes blood vessels walls leaky

54
Q

anaphylatoxins smooth muscle contraction

A

through vasodilation

55
Q

what does leaky blood vessels mean

A

easier for neutrophils and NK cells to infiltrate infected cells

56
Q

opsonisation by 3b

A

C3b binds to surface of bacteria where it is cleaved to iC3b, macrophage membrane has receptors for iC3b = phagocytosis

57
Q

professional phagocytes

A

macrophages, dendritic cells, neutrophils

58
Q

pathway for phagocytosis

A
  1. chemotaxis and adherence of microbe by phagocyte
  2. pathogen engulfed
  3. phagosome formed
  4. fusion of phagosome with lysosome = phagolysosome
  5. digestion of pathogen in phagolysosome
  6. formation of residual body containing indigestible material
  7. discharge of waste
59
Q

where are macrophages located

A

under skin, in lungs, around intestines

60
Q

three activation states of macrophage

A
  1. resting
  2. primed
  3. hyper-active
61
Q

resting macrophage

A
  • eliminates apoptotic cells

- expresses very little MHC class II on surface

62
Q

primed macrophage by what

A

cytokine interferon gamma (IFN-y) produced by NK and helper T cells

63
Q

what produces IFN-y

A
  • NK cells

- helper T cells

64
Q

what do primed macrophages do

A
  • express more MHC class II molecules on surface

- take up larger objects by phagocytosis

65
Q

how are hyper-active macrophages activated

A
  • IFN-y

- LPS by Gram +ve bacteria

66
Q

LPS produced by gram +ve bacteria

A

lipopolysaccaride

67
Q

what do hyperactive macrophages do

A
  • stop proliferating
  • increase in size
  • increase rate of phagocytosis
  • produce cytokines
68
Q

what cytokines do hyperactive macrophages produce

A
  • tumour necrosis factor = TNF

- interleukin-1 = IL-1

69
Q

life of a neutrophil

A

5 days = short lived

70
Q

what mechanism is used by neutrophils

A

“double key” mechanism

71
Q

CAMs

A

cell adhesion molecule

72
Q

selectins

A

single-chain transmembrane glycoproteins = part of family of CAMs

73
Q

double key mechanism

A
  1. Selectin-ligand (neutrophil) : Selectin (endothelium)

2. Integrin (neutrophil) : ICAM (endothelium)

74
Q

endothelial and neutrophil selectin expressed in response to…

A

IL-1, TNF, LPS and C5a at site of inflammation

75
Q

normal conditions = neutrophil expresses…

A

Selectin Ligand = SLIG

76
Q

normal conditions = endothelial cell expresses…

A

Intracellular Adhesion Molecule = ICAM

77
Q

abnormal conditions = infected tissue = endothelial cell now expresses

A

SLIG

78
Q

infected tissue ligand interaction = selectin

A

selectin - ligand (neutrophil) interacts with selectin (on endothelial cells) and this causes neutrophil cells to bind and “roll” along endothelium surface

79
Q

what stimulates expression of selectin on endothelium

A

cytokines = IL-1 and TNF produced by activated macrophages

80
Q

strength of SLIG - selectin interaction

A

weak : not strong enough to secure the neutrophils to the infection site

81
Q

INT

A

integrin

82
Q

SLIG

A

selectin - ligand

83
Q

stimulation of INT expression on neutrophil

A

at inflammation site = C5a and LSP, activate expression of integrin on neutrophil surface

84
Q

strength of INT - ICAM interaction

A

strong : neutrophil – endothelium interaction is so strong, that the cells stop rolling and stick to the vascular wall close to the site of infection

85
Q

how neutrophils recognise bacteria

A

mammalian cells = methionine
bacteria cells = formyl-methionine (f-Met)
difference in N-terminal amino acid

86
Q

key facts on neutrophils

A
  • once activated = become extremely phagocytotic

- produce cytokines (TNF) to activate other immune cells

87
Q

what is pus

A

mainly dead neutrophils

88
Q

The Natural Killer cell

A

the assisted suicide cell

89
Q

difference in lineage between NK cells compared to macrophage and neutrophils

A

NK cells = lymphoid

macrophage/neutrophils = myeloid

90
Q

where are NK cells produced

A

bone marrow

91
Q

where are NK cells mostly found

A

blood, liver and spleen

92
Q

what cytokines do NK cells produce

A

IFN-y and IL-2 and destroy infected cells

93
Q

NK cells ligand

A

Fas ligand to bind to target cells

94
Q

NK cells suicide enzyme

A

perforin protein to inject granzyme B into cell = kills cell

IMS Immunology (4 decks)

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