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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
Q

TLR 3 results

A

IL-12 –> Th1 –> IFN gamma

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26
Q

TLR 4 signalling

A

homodimer
cell membrane: MyD88
endosome: TRIF/TRAM

TAK 1 and IRF 7/3 –> IFN a/b and proinflamm

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27
Q

TLR 4 results

A

IL-12 –> Th1 –> IFN gamma

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28
Q

TLR 5 signalling

A

Homodimer
MyD88 –> TAK1

IFN ab and proinflamm

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29
Q

TLR 6 signaling

A 
Heterodimer with 2 
MyD88
TAK 1 --
MAP kinase
NF-kB
--
AP-1
NF-kB
--
IFNa/b and proinflammatory cytokines
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30
Q

TLR 2/6 results

A

IL-10, RA, TGF-b –> Treg –> IL-10, TGF-beta

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31
Q

TLR 7 signalling

A

Homodimer
MyD88 (endosome)
TAK 1 and IRF7

IFN b/a and proinflamm

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32
Q

TLR 8 signaling

A

unknown

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33
Q

TLR 9 signaling

A

homodimer
MyD88 (endosome)
TAK1 and IRF7

IFN b/a and proinflamm

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34
Q

TLR 7 results

A

IL-12 –> Th1 –> IFN gamma

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35
Q

TLR 9 results

A

IL-12 –> Th1 –> IFN gamma

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36
Q

Which PRRs are TLRs?

A

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
Q

Hallmarks of inflammation

A

Influx of fluid (edema)
Increased temperature (hyperthermia)
Decreased oxygenation (local hypoxia)
Influx of white blood cells (extravasation)

38
Q

Triggers of Inflammation

A

C5a stimulation of basophil/mast cell degranulation and activation
Macrophages
NK cells

39
Q

Histamine

A

increase vascular permeability

40
Q

PGE2

A

Vasodilation, increased vascular permeability

41
Q

LTD2

A

Neutrophil chemotaxis, increased vascular permeability

42
Q

LTD4

A

Increased vascular permeability

43
Q

What do macrophages do to trigger inflammation

A

TNF
IL-1
IL-8

44
Q

TNF

A

cause fever, stimulated expression of E-selectin

45
Q

IL-1

A

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
Q

IL-8

A

chemotaxis

47
Q

NK cells and inflammation

A

IFN gamma - activation of phagocytic cells and Nk cells

48
Q

3 principle changes in tissue during acute inflammation

A

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
Q

acute inflammation phases

A

recruit / activate leukocytes, eliminate the pathogen, resolve the damage, disappearance of leukocytes from the tissue, regenerate tissue function.

50
Q

Chronic inflammation during infection

A

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
Q

What cells are in acute inflammation

A

neutrophils and activated helper T cells

52
Q

what cells are in chronic inflammation

A

macrophages, cytotoxic t cells and b cells

53
Q

Important inflammatory cytokines

A

TNF-a, IL-1, IFN gamma

54
Q

Important molecules in leukocyte adhesion and diapedesis

A

CD15 on cell attaches to E-selectin on endothelium
Chemokines (IL-8)
Integrins

55
Q

Inflammatory response

A
  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
Q

What role tissue cells in inflammation

A

when infected or damaged, can send signals to immune system to call for help (interferons, cytokines)
Also make defensins and cathelicidins

57
Q

Neutrophils role in tissue inflammation

A

Primary phagocytic cell sin blood
First cells to migrate to site of inflammation/infection
Phagocytize bacteria and viruses
Can recognize antibodies

58
Q

Neutrophil differentiation

A

IL3 + GM-CSF (myeloid progenitor) –> G-CSF = neutrophil

59
Q

Eosinophils role

A 
Phagocytosis 
Granules contain major basic protein
vs helminths
induce histamine release from mast cells
activate neutrophils and platelets
activated by complement to degranulate
60
Q

Eosinophils differentiation

A

IL-3 + GM-CSF (myeloid progenitor) –> +IL-5 = Eosinophil

61
Q

Mediators of delayed reaction of allergic response

A

Eosinophils, Th1 and basophils

62
Q

Basophils role

A

Have IgE on surface
Mediators of delayed reaction of allergic respnse
Release histamine when IgE finds antigen
activated by complement to degranulate

63
Q

Basophils differentiation

A

IL-3 + GM-CSF (myeloid progenitor) –> IL-4 = basophil

64
Q

Monocytes role

A

Differentiate to form macrophages in peripheral tissues where they are first line of defense against microbial invasion

65
Q

kupfer cells

A

liver

66
Q

microglia

A

brain

67
Q

monocytes differentiation

A

IL3 + GM-CSF (myeloid progenitor) –> M-CSF (monocyte)

68
Q

macrophage role

A

late migrators to sites of inflammation (effector cells of chronic inflammation)
Major producers of cytokines and lymphokines
Phagocytosis
APCs

69
Q

What cytokines/lymphokines macrophages release

A

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
Q

IFNa

A

antiviral

71
Q

IL1b, IL-6, TNF-a

A

fever

72
Q

IL-8

A

chemotaxis of PMNs, basophils, T cells

73
Q

IL-12

A

activation of NK cells and CD4 Th1 cells

74
Q

Macrophage differentiation

A

(IL3 + GM-CSF) (myeloid progenitor) –> (IL-3 + GM-CSF + M-CSF) (monocyte) –> (GM-CSF + M-CSF) (macrophage)

75
Q

Dendritic cells role (myeloid)

A

Classical - process and present foreign protein antigens to T cells

76
Q

Follicular dendritic cells

A

passively present foreign antigen in form of immune complexes to B cells in lymphoid follicles

77
Q

DCs differentiation

A

IL3 + GM-CSF (myeloid pro) –> M-CSF –> GM-CSF + IL-4

78
Q

NK cells role

A

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
Q

NK cells differentiation

A

IL-7 (lymphoid progenitor) –> IL-2

80
Q

important markers of NK cells

A

CD16 (FcgammaRIII) and CD56 (NCAM)

81
Q

cytokines that activate NK cells

A

IFN

IL-12, TNFalpha

82
Q

Severe congenital neutropenias

A

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
Q

Chronic granulomatous disease

A

Inability to produce hydrogen peroxide and hypochlorous acid

Inability to kill phagocytosed bacteria

84
Q

Chediak-Higashi Syndrome

A

Defect in gene LYST (CHS1), a lysosomal trafficking gene that affects lysosomes and melanosomes
Increased susceptibility to bacterial infections

85
Q

Leukocyte adhesion deficiency

A

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
Q

What important products of complement activation are also chemotactic factors and what do they increase migration of

A

C3a, C4a, C5a ***

PMNs and macrophages

87
Q

What important products of complement are deposited on surfaces with exposed amine or hydroxyl (ie bacteria)

A

C3b and C4b –> opsonins, further cleave C3

88
Q

what’s C5b’s role in complement

A

bind microorganisms, act as focal point for membrane attack complex

IHO Week 1 (9 decks)

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