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IHO Week 1 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Major Functions of Innate immunity

A

Complement activation, inflammation, cell activation (cytokine and chemokine production, phagocytosis and other killing of microbes), priming of adaptive immune response

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2
Q

Innate immune response recognizes 3 things:

A

PAMPs
DAMPs
Absence of certain “self” marker molecules (by NK cells)

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3
Q

TLRs

A

transmembrane proteins that are PRRs

bind to and are activated by PAMPs and DAMPs

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4
Q

TLR1

A

Triacyllipopeptides (mycobacteria and gram-negative bacteria)
Heterodimer w/ TLR 2 –>
MyD88 –>
NF-kB –> antimicrobials, cytokines and chemokines
& MAP kinase –> AP-1 –> IFN-b and a (and above)

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5
Q

TLR2

A

Peptidoglycans (Gram +), GPI-linked proteins (trypanosomes), Lipoproteins (mycobacteria and other), Zymosan (yeast and other fungi), phophatidylserine (schistosomes)
Heterodimer w/ TLR 1 –>
MyD88 –>
NF-kB –>
& MAP kinase –> AP-1 –> IFN-b and a & antimicrobials, cytokines and chemokines

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6
Q

TLR 3

A 
Homodimer
ds RNA (viruses) - endosome
PI3K/TRIF/TRAM --> 
IRF7/3 --> IFN-b, a
PI3K --> MAP Kinase pathway --> AP-1 -->
Also TAK1 --> MAP kinase and NF-kB -->  IFNb, a & antimicrobials, cytokines, and chemokines
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7
Q

TLR 4

A

LPS (gram -), F-protein (RSV), mannans (fungi) on cell membrane AND endosome
homodimer
–> TAK1 & IRF7/IRF3
TAK1 –> MAP kinase –> AP1 & TAK1 –> NF-kB
–> IFNb/a and proinflammatory cytokines

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8
Q

TLR6

A

heterodimer with TLR2
TLR6 - diacyllipopolypeptides (mycobacteria and gram +) & zymosan (yeasts and other fungi)
signalling unknown (likely TAK1)

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9
Q

TLR 7

A 
homodimer
endosome - viral ssRNA
MyD88
TAK1 --> MAP k and NF-kB
also IRF7

IFN b/a
proinflam

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10
Q

TLR8

A

viral ssRNA - signalling unknown

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11
Q

TLR 9

A 
homodimer
CpG DNA/hemozoin/herpes byproducts 
endosome
MyD88 --> TAK1 and IRF7
MAP k and NF-kB
IFNb/a and proinflammatory cytokines
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12
Q

TLR 1 PAMPs

A

triacylllipopeptide (mycobacteria and gram - bacteria)

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13
Q

TLR 2 PAMPs

A 
Peptidoglycans (Gram +)
GPI-linked proteins (trypanosomes)
Lipoproteins (mycobacteria and other)
Zymosan (yeast and other fungi)
Phosphatidylserine (schistosomes)
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14
Q

TLR 3 PAMPs

A

dsRNA (viruses)

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15
Q

TLR 4 PAMPs

A

LPS (gram -)
F-protein (RSV- virus)
Mannans (fungi)

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16
Q

TLR 5 PAMPs

A

Flagellin (bacteria)

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17
Q

TLR 6 PAMPs

A

Diacyllipopolypeptides (mycobacteria and gram +)

Zymosan (yeasts and other fungi)

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18
Q

TLR 7 PAMPs

A

ssRNA (viruses)

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19
Q

TLR 8 PAMPs

A

ssRNA (Viruses)

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20
Q

TLR 9 PAMPs

A

CpG unmethylated dinucleotides (bacterial DNA)
Dinucleotides
Herpes virus components
Hemozoin (malaria)

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21
Q

TLR 1 signaling

A 
heterodimer with TLR 2
MyD88
TAK 1 --
MAP kinase
NF-kB
--
AP-1
NF-kB
--
IFNa/b and proinflammatory cytokines
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22
Q

TLR 2 signaling

A 
heterodimer with TLR 1 OR 6
MyD88
TAK 1 --
MAP kinase
NF-kB
--
AP-1
NF-kB
--
IFNa/b and proinflammatory cytokines
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23
Q

TLR 2/1 result

A

IL-10 –> Th2 –> IL-4, IL-5, IL-13

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24
Q

TLR 3 signalling

A 
homodimer TLR 3/3
endosome
NOT MyD88
But get TAK1 and MAP kinase
Also IRF7 and IRF3 
IFN a/b and proinflamm
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25
TLR 3 results
IL-12 --> Th1 --> IFN gamma
26
TLR 4 signalling
homodimer cell membrane: MyD88 endosome: TRIF/TRAM TAK 1 and IRF 7/3 --> IFN a/b and proinflamm
27
TLR 4 results
IL-12 --> Th1 --> IFN gamma
28
TLR 5 signalling
Homodimer MyD88 --> TAK1 IFN ab and proinflamm
29
TLR 6 signaling
``` Heterodimer with 2 MyD88 TAK 1 -- MAP kinase NF-kB -- AP-1 NF-kB -- IFNa/b and proinflammatory cytokines ```
30
TLR 2/6 results
IL-10, RA, TGF-b --> Treg --> IL-10, TGF-beta
31
TLR 7 signalling
Homodimer MyD88 (endosome) TAK 1 and IRF7 IFN b/a and proinflamm
32
TLR 8 signaling
unknown
33
TLR 9 signaling
homodimer MyD88 (endosome) TAK1 and IRF7 IFN b/a and proinflamm
34
TLR 7 results
IL-12 --> Th1 --> IFN gamma
35
TLR 9 results
IL-12 --> Th1 --> IFN gamma
36
Which PRRs are TLRs?
Some PRRs that recognize PAMPs do not activate phagocytosis but rather trigger cell signaling leading to gene transcription events to combat the foreign material. These are the TLRs.
37
Hallmarks of inflammation
Influx of fluid (edema) Increased temperature (hyperthermia) Decreased oxygenation (local hypoxia) Influx of white blood cells (extravasation)
38
Triggers of Inflammation
C5a stimulation of basophil/mast cell degranulation and activation Macrophages NK cells
39
Histamine
increase vascular permeability
40
PGE2
Vasodilation, increased vascular permeability
41
LTD2
Neutrophil chemotaxis, increased vascular permeability
42
LTD4
Increased vascular permeability
43
What do macrophages do to trigger inflammation
TNF IL-1 IL-8
44
TNF
cause fever, stimulated expression of E-selectin
45
IL-1
Induction of local inflammation. Activates endothelial cells to express adhesion molecules. Induces the production of chemokines to recruit leukocytes. Also plays a role in systemic effects such as fever, the acute phase response, and the stimulation of neutrophil production.
46
IL-8
chemotaxis
47
NK cells and inflammation
IFN gamma - activation of phagocytic cells and Nk cells
48
3 principle changes in tissue during acute inflammation
Increased blood supply to the affected area. Increase capillary permeability (allows for large serum molecules to enter the tissue). Increase in leukocyte migration into the affected tissue.
49
acute inflammation phases
recruit / activate leukocytes, eliminate the pathogen, resolve the damage, disappearance of leukocytes from the tissue, regenerate tissue function.
50
Chronic inflammation during infection
Most pathogenic organisms have developed systems to deflect immune responses that would eliminate them. In this case the body often tries to contain the infection or minimize the damage it causes. Persistent antigenic stimulus and the cytotoxic effects of the unresolved infection leads to ongoing chronic inflammation.
51
What cells are in acute inflammation
neutrophils and activated helper T cells
52
what cells are in chronic inflammation
macrophages, cytotoxic t cells and b cells
53
Important inflammatory cytokines
TNF-a, IL-1, IFN gamma
54
Important molecules in leukocyte adhesion and diapedesis
CD15 on cell attaches to E-selectin on endothelium Chemokines (IL-8) Integrins
55
Inflammatory response
1. Tissue damage/bacteria --> resident sentinel cells to release chemoattractants and vasoactive factors to trigger local increase in blood flow/permeability 2. Allow influx of fluid and cells 3. Neutrophils and other phagocytes migrate to site of inflammation (chemotaxis) 4. Phagocytes and antibacterial substances destroy bacteria
56
What role tissue cells in inflammation
when infected or damaged, can send signals to immune system to call for help (interferons, cytokines) Also make defensins and cathelicidins
57
Neutrophils role in tissue inflammation
Primary phagocytic cell sin blood First cells to migrate to site of inflammation/infection Phagocytize bacteria and viruses Can recognize antibodies
58
Neutrophil differentiation
IL3 + GM-CSF (myeloid progenitor) --> G-CSF = neutrophil
59
Eosinophils role
``` Phagocytosis Granules contain major basic protein vs helminths induce histamine release from mast cells activate neutrophils and platelets activated by complement to degranulate ```
60
Eosinophils differentiation
IL-3 + GM-CSF (myeloid progenitor) --> +IL-5 = Eosinophil
61
Mediators of delayed reaction of allergic response
Eosinophils, Th1 and basophils
62
Basophils role
Have IgE on surface Mediators of delayed reaction of allergic respnse Release histamine when IgE finds antigen activated by complement to degranulate
63
Basophils differentiation
IL-3 + GM-CSF (myeloid progenitor) --> IL-4 = basophil
64
Monocytes role
Differentiate to form macrophages in peripheral tissues where they are first line of defense against microbial invasion
65
kupfer cells
liver
66
microglia
brain
67
monocytes differentiation
IL3 + GM-CSF (myeloid progenitor) --> M-CSF (monocyte)
68
macrophage role
late migrators to sites of inflammation (effector cells of chronic inflammation) Major producers of cytokines and lymphokines Phagocytosis APCs
69
What cytokines/lymphokines macrophages release
IFNa (antiviral) IL-1b, IL-6, TNF-a: fever CXCL8 (IL-8): chemotaxis of PMNs, basophils, T cells IL-12: activation of NK cells and CD4 Th1 T cells
70
IFNa
antiviral
71
IL1b, IL-6, TNF-a
fever
72
IL-8
chemotaxis of PMNs, basophils, T cells
73
IL-12
activation of NK cells and CD4 Th1 cells
74
Macrophage differentiation
(IL3 + GM-CSF) (myeloid progenitor) --> (IL-3 + GM-CSF + M-CSF) (monocyte) --> (GM-CSF + M-CSF) (macrophage)
75
Dendritic cells role (myeloid)
Classical - process and present foreign protein antigens to T cells
76
Follicular dendritic cells
passively present foreign antigen in form of immune complexes to B cells in lymphoid follicles
77
DCs differentiation
IL3 + GM-CSF (myeloid pro) --> M-CSF --> GM-CSF + IL-4
78
NK cells role
REcognize damaged cells by a deficiency in MHC antigens Activated by IFNs IL-12 and TNFa activate NK cells to secrete cytokines, INF gamma
79
NK cells differentiation
IL-7 (lymphoid progenitor) --> IL-2
80
important markers of NK cells
CD16 (FcgammaRIII) and CD56 (NCAM)
81
cytokines that activate NK cells
IFN | IL-12, TNFalpha
82
Severe congenital neutropenias
Many causes leading to a lack in the ability to produce or maintain a normal level of neutrophils Leads to frequent bacterial infections ‘maturation arrest’ at the promyelocyte or myelocyte stage in the bone marrow
83
Chronic granulomatous disease
Inability to produce hydrogen peroxide and hypochlorous acid | Inability to kill phagocytosed bacteria
84
Chediak-Higashi Syndrome
Defect in gene LYST (CHS1), a lysosomal trafficking gene that affects lysosomes and melanosomes Increased susceptibility to bacterial infections
85
Leukocyte adhesion deficiency
Lack of integrin subunit, the common β chain Inability to recruit innate immune cells to site of inflammation Increased susceptibility to bacterial, fungal, and viral infections.
86
What important products of complement activation are also chemotactic factors and what do they increase migration of
C3a, C4a, C5a *** | PMNs and macrophages
87
What important products of complement are deposited on surfaces with exposed amine or hydroxyl (ie bacteria)
C3b and C4b --> opsonins, further cleave C3
88
what's C5b's role in complement
bind microorganisms, act as focal point for membrane attack complex

IHO Week 1 (9 decks)

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