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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
classical pathway step 5-
C5b forms complex with C6, C7, C8 and C9
26
what does the final complex of C5b/C6/C7/C8/C9 form
the MAC = the Membrane Attack Complex
27
what does MAC do
perforates the cell membrane
28
Byproducts of classical pathway = anaphylatoxins
C3a, C4a and C5a
29
role of C3b
opsonisation
30
what is classical complement pathway activated by
when C1 binds to antigen/antibody complex
31
MBL
Mannose-Binding Lectin
32
Lectin or Mannose-binding pathway involves activated by
pathogens
33
why do pathogens activate the Mannose-binding pathway
particular sugar (mannose) is found on surface of many pathogens but not on host cells
34
what does MBL bind
MASP 1 and MASP 2
35
what does MASP stand for
MBL Associated Serine Protease
36
what do MASP 1 and MASP 2 activate
C2 and C4
37
common pathways of Lectin-binding and classical
C3-C9
38
viruses with mannose
HIV and Influenza A
39
bacteria with mannose
salmonella and Steptococci
40
Yeast with mannose
candida albicans
41
parasite with mannose
Leishmania
42
Alternative pathway is directly activated by
contact with pathogens
43
step 1 of alternative pathway
auto-activation of C3 -> C3a and C3b = slow rate
44
step 2 of alternative pathway
low levels of C3b bind to bacteria
45
what two factors bind to bacteria surface after C3b binds
factor B and properdin
46
factor B and properdin activate
more C3 and C5
47
common pathway between alternative and classical
C6-C9
48
three initiators of complement pathways
1. antigen/antibody complex 2. bacterial sugars 3. auto-activation from pathogen contact
49
Anaphylatoxins
C3a, C4a and C5a
50
what do anaphylatoxins induce
- degranulation of endothelial cells, mast cells and phagocytes - smooth muscle contraction - increased vascular permeability
51
mast cell degranulation
releases histamines
52
phagocyte degranulation
releases cytokines
53
anaphylatoxins increased vascular permeability
makes blood vessels walls leaky
54
anaphylatoxins smooth muscle contraction
through vasodilation
55
what does leaky blood vessels mean
easier for neutrophils and NK cells to infiltrate infected cells
56
opsonisation by 3b
C3b binds to surface of bacteria where it is cleaved to iC3b, macrophage membrane has receptors for iC3b = phagocytosis
57
professional phagocytes
macrophages, dendritic cells, neutrophils
58
pathway for phagocytosis
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
where are macrophages located
under skin, in lungs, around intestines
60
three activation states of macrophage
1. resting 2. primed 3. hyper-active
61
resting macrophage
- eliminates apoptotic cells | - expresses very little MHC class II on surface
62
primed macrophage by what
cytokine interferon gamma (IFN-y) produced by NK and helper T cells
63
what produces IFN-y
- NK cells | - helper T cells
64
what do primed macrophages do
- express more MHC class II molecules on surface | - take up larger objects by phagocytosis
65
how are hyper-active macrophages activated
- IFN-y | - LPS by Gram +ve bacteria
66
LPS produced by gram +ve bacteria
lipopolysaccaride
67
what do hyperactive macrophages do
- stop proliferating - increase in size - increase rate of phagocytosis - produce cytokines
68
what cytokines do hyperactive macrophages produce
- tumour necrosis factor = TNF | - interleukin-1 = IL-1
69
life of a neutrophil
5 days = short lived
70
what mechanism is used by neutrophils
"double key" mechanism
71
CAMs
cell adhesion molecule
72
selectins
single-chain transmembrane glycoproteins = part of family of CAMs
73
double key mechanism
1. Selectin-ligand (neutrophil) : Selectin (endothelium) | 2. Integrin (neutrophil) : ICAM (endothelium)
74
endothelial and neutrophil selectin expressed in response to...
IL-1, TNF, LPS and C5a at site of inflammation
75
normal conditions = neutrophil expresses...
Selectin Ligand = SLIG
76
normal conditions = endothelial cell expresses...
Intracellular Adhesion Molecule = ICAM
77
abnormal conditions = infected tissue = endothelial cell now expresses
SLIG
78
infected tissue ligand interaction = selectin
selectin - ligand (neutrophil) interacts with selectin (on endothelial cells) and this causes neutrophil cells to bind and "roll" along endothelium surface
79
what stimulates expression of selectin on endothelium
cytokines = IL-1 and TNF produced by activated macrophages
80
strength of SLIG - selectin interaction
weak : not strong enough to secure the neutrophils to the infection site
81
INT
integrin
82
SLIG
selectin - ligand
83
stimulation of INT expression on neutrophil
at inflammation site = C5a and LSP, activate expression of integrin on neutrophil surface
84
strength of INT - ICAM interaction
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
how neutrophils recognise bacteria
mammalian cells = methionine bacteria cells = formyl-methionine (f-Met) difference in N-terminal amino acid
86
key facts on neutrophils
- once activated = become extremely phagocytotic | - produce cytokines (TNF) to activate other immune cells
87
what is pus
mainly dead neutrophils
88
The Natural Killer cell
the assisted suicide cell
89
difference in lineage between NK cells compared to macrophage and neutrophils
NK cells = lymphoid | macrophage/neutrophils = myeloid
90
where are NK cells produced
bone marrow
91
where are NK cells mostly found
blood, liver and spleen
92
what cytokines do NK cells produce
IFN-y and IL-2 and destroy infected cells
93
NK cells ligand
Fas ligand to bind to target cells
94
NK cells suicide enzyme
perforin protein to inject granzyme B into cell = kills cell

IMS Immunology (4 decks)

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