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PM3 - Infection and immunity > Innate immunity > Flashcards

Innate immunity Flashcards

1
Q

Definition inflammation

A

Local accumlation of fluid, plasma proteins and leukocytes
caused by infection, injury or chemical irritation

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2
Q

Signs of inflammation

A

RCDT
rubor (redness)
calor (heat)
dolor (pain)
tumor (swelling)

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3
Q

pro-inflammatory cytokines

A

IL-1, IL-6 and TNF-alpha

adhesion. chemokines, immune cells, luid, proteins
fever, acute phase proteins, leukocyte production
septic shock

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4
Q

Effect: IL-1 and TNF-alpha

A
  • adhesion molecules on EC upregulated (permeability)
  • vasodilation in combination with other mediators (histamine, prostaglandine from mast cells)
  • chemokine expression induced
  • recruitment of immune cells, fluid and plasma proteins
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5
Q

Effect of IL-1, IL-6 and TNF-alpha

A

PROTECTIVE:
- fever: immune cell activity up, growth rate down, rest
- acute phase protein synthesis: opsonisation, complement activation

PATHOGENIC:
- systemic TNF-alpha leads to septic shock
–> HR down, permeability and vasodilation up –> BP DOWN
–> systemic blood coagulation and impaired perfusion leads to multi-organ failure

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6
Q

types of antimirobial products

A

Lysozymes
Defensins
Cathelicidins
Histatins

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7
Q

Lysozymes

A

cleave bacterial peptidoglycan in gram-positive bacteria

present in saliva, tears, paneth cells (intestinal crypts) and phagocytes

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8
Q

Defensins

A

form pores in cell membranes of microbes (e.g. gramnegative bacteria, viruses)

hydrophobic and hydrophilic end, positive charge –> allignment within the membrane and pore formation

can also bind e.g. glycoproteins and PREVENT VIRAL ENTRY

in mucosa, skin, paneth cells and phagocytes

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9
Q

Cathelicidins

A

skin, GIT and respiratory tract, phagocytes

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10
Q

Histatins

A

saliva

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11
Q

cell-associated membrane bound PRR

A

SIGNALLING: TLR, N-formyl met-leu-phe receptors

PHAGOCYTOTIC: CLR, scavenger

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12
Q

cell associated
membrane bound + signalling

A

TLR
N-formyl met-leu-phe receptors

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13
Q

cell associated
membrane bound + phagocytotic

A

CLRs
scavenger receptors

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14
Q

cell associated cytosolic PRRs

A

RLRs
STING pathway
NLRs

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15
Q

TLRs
types
activation pathway and effect

A

cell associated, membrane bound and signalling

cell surface -> 1, 2, 4, 5 and 6 -> bacterial and fungal cell wall
endosomal -> 3, 7, 8 and 9 -> nucleic acid (viral, bacterial)

Ligand binding -> dimerization -> TIR domain recruits MyD88 or TRIF -> TRAF6 activation -> inflammatory and antiviral genes

cell surface -> NFkB and AP-1 -> inflammatory genes
endosomal -> IRFs > antiviral genes

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16
Q

cell surface TLRs

A

1, 2, 4, 5 and 6
detect bacterial infections and activate NFkB and AP-1

expression of pro-inflammatory cytokines TNF-alpha, IL1 and IL6
chemoines
endothelial adhesion molecules
costimulatory molecules for adaptive immunity

Acute Inflammatory Response
Atimulation Of Adaptive Immunity

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17
Q

endosomal TLRs

A

3, 7, 8 and 9
detect viral infections
activate IRFs and expression of antviral genes

Type I IFNs –> alpha and beta

induction of the Antiviral Response

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18
Q

N-formyl met-leu-phe receptors

A

call associated
membrane bound signalling

on plasmamembranes of phagocytes

recognize peptides containing N-formyl-methionyl residues (= first AA in bacterial peptides)

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19
Q

CLRs

A

cell associated
membrane bound phagocytosing

on phagocytes
binds mannose and fructose on carbohydrates

  • Type I: DEC-205
  • Type II: dectins, DC-SIGN
  • soluble
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20
Q

Scavenger receptor

A

cell associated
membrane bound and phagocytosing

on plasmamembranes of phagocytes
binds microbial diacylglycerides

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21
Q

RLRs

A

cell associated
cytosolic signalling

recorgnizes viral RNA -> recognized intracellular viruses

RIG-1 (uncapped RNA) and MDA-5 (dsRNA)

contain CARD domain (caspase -> apoptosis and IRF)
ROBUST ANTIVIRAL RESPONSE

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22
Q

STING pathway

A

cell associated
cytosolic signalling

stimulator of IFN-genes in response to cytoslic DNA

cGAS binds DNA -> produces cGAMP -> activates STING on ER -> IRF3 and NFkB mediated type I IFN (a&b) production

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23
Q

RIG-1

A

RLR
(cell associated, cytosolic signalling)

binds short uncapped ss or dsRNA

CARD domain -> apoptosis and IRFs
ROBUST ANTIVIRAL RESPONSE

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24
Q

MDA-5

A

RLR
(cell associated, cytosolic signalling)

binds dsRNA

CARD domain -> apoptosis and IRFs
ROBUST ANTIVIRAL RESPONSE

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25
Q

NLRs

A

cell associated
cytosolic signalling

recognizes bacterial cell wall
Leu-rich repeats for ligand bindig, NOD-domain and variable N-terminal domain

CARD in NOD receptors, PYR in NLRP3

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26
Q

NOD 1&2

A

IkB degradation and NFkB activation
NOD2 lof mutation -> Chron’s disease

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27
Q

NLRP3

A

recognizes bacterial products and DMAPs
oligomerization and adaptors and caspase 1 form inflammosome
Casp1 cleaves pro-IL1b -> IL1b -> acute inflammation

contributes to Gout, Alzheimers, atherosclerosis, autoinflammatoric syndromes

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28
Q

Type I IFN and viruses

A

produced via IFR genes -> TLRs, RLRs and STAT
via NFkB -> NLRs, STING

induces ANTIVIRAL STATE
- induction of antiviral enzymes
- activate adoptive IS (MHC I upregulation)

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29
Q

receptors activating IFR genes

A

TLRs
RLRs/STAT

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30
Q

receptors activating NFkB

A

NLRs
STING

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31
Q

Antiviral state

A

induced via type I IFN
(induced by IRF or NFkB)

antivral enzymes
- PKR reduces viral protein sythesis
- 2’5’ oligo A synthesase degradation of viral RNA
- Mx proteins reduce gene expression and viral assembly

activate adapive IS via MHC I upregulation -> CD8+ activation

32
Q

antiviral enzymes

A

PKR -> reduces viral protein synthesis

2’5’ oligoA synthesis -> degradation of viral RNA

Mx proteins -> reduces gene expression and virion assembly

33
Q

Adaptive IS activation by IFN via

A

MHC I upregulation -> CD8+ activation

34
Q

solubel PRRs

A

bind microbial structures in blood and extracellular fluids

opsonization
increase in inflammatory response
killing

acute phase proteins
complement system

35
Q

acute phase protein

A

soluble PRR
produced by liver

acute phase response initiated by IL1, Il6 and TNF alpha

e.g. CRP: C-reactive protein, opsonin and activates complement, diagnostic factor for inflammations

36
Q

CRP

A

C reactive protein
produced by the liver
acute phase protein
induced by IL1, IL6 and TNFa (acute phase response)

opsonin, activates complement, diagnostic factor for inflammation

37
Q

Complement system
Function

A

soluble PRR
> 30 proteins synthesized mainly by liver

circulate inactive -> proteolytic cleavage in presence of pathogens (activation) -> cascade -> MAC formation

OPSONIZATION (C3b)
INFLAMMATION (C3a, C5a)
KILLING (C5b activates cascade -> 6,7,8,9 -> MAC)

38
Q

Complement system
Activation

A

soluble PRR
> 30 proteins synthesized mainly by liver

circulate inactive -> proteolytic cleavage in presence of pathogens (activation) -> cascade -> MAC formation

ALTERNATIVE -> recognizes micorbes directly
CLASSICAL -> Ab
LECTIN -> mannose-binding lectin PRRS (CLRs)

39
Q

Complement system
Receptors

A

soluble PRR
> 30 proteins synthesized mainly by liver

CR1: rec. C3b, on all immune cells (innate and adaptive)
CR3: iCRb (opsonin), on APCs
CR4: iC3b, on APCs but mainly DCs
CR2: C3dg & C3d (opsonin), on B cells and follicular T cells -> germline centers!

40
Q

C3b function & receptors

A

Opsonization
recognized by CR1, CR3 and CR4 (iC3b)
CR2 recognizes C3dg & Cd also opsonins and recognized by B and FDCs (germline centers)

41
Q

C3a

A

promotes inflammtion
increased permability and chemoatraction for phagocytes

42
Q

C5a

A

promotes inflammtion
increased permability and chemoattrction for phagocytes

43
Q

C5b

A

activates killing cascade -> C6-9
C9 essential for MAC formation and cell lysis

44
Q

alternative pathway

A

complement activation via direct recognition of microbes

45
Q

classical pathway

A

complement activation via recognition of Ab

46
Q

lectin pathway

A

complement activtion via mannose-binding PRRs (CLRs)

47
Q

CRP

A

acute phase protein
opsonin
activates complement
diagnostic factor for inflammation (1000x elevated)

48
Q

mast cells

A

innate immune cells
tissue resident
contain granules with pro-infl mediators
express FceR1 -> bind IgE -> SENSITIZING
multivalent Ag can cross-link bound IgE -> Granule content release

crucial in ALLERGIC REACTIONS and their diagnosis (wheal and flare in prick test)

49
Q

FceRI

A

recognizes IgE
expressed by mast cells
contributes to sensitizing of mast cells by IgE binding and triggering of granule release upon multivalen Ag-mediated cross-linking

50
Q

cell essential for allergic reactions

A

mast cells via FceRI-IgE mediated sinsitization

51
Q

granulocytes

A

innate immune cells
eosinophils, neutrophils and basophils

eosinophils: circulating, migration to infection and release of granule content, toxic to helminths!

basophils: circulate and migrate, otherwise similar to mast cells

neutrophils: phagocytosis and killing, NETosis, ADCC, regulation of T cells, …

52
Q

basophils

A

innate immune cell, grnaulocyte

basophils: circulate and migrate, otherwise similar to mast cells

53
Q

eosinophils

A

innate immune cells, granulocytes

circulating, migration to infection and release of granule content, toxic to helminths!

54
Q

neutrophils

A

innate immune cell, phagocyte and granulocyte

phagocytosis and killig of bacteria
NETosis
cell-cell contact with adaptive immune cells
degranulation and cytokine release effects T cells activating or suppressive
contain different ytpes of granule

55
Q

phagocytes

A

innate immune cells
neutrophils and macrophages

recruited via IL1 and TNFa (by tissue-resident MO)

PRODUCTION of PRO-INF CYTO- and CHEMOKINES (IL1, IL6 and TNFa)
release chemokines -> integrin activation, chemoattraction

PHAGOCYTOSIS and KILLING: have phagocytotic PRRs (CLRs, scavenger), opsonin recognition (IgG, C3b, CRP) and killing via phagolysosome (oxidative burst)

bacterial resistance to phagolysis or destruction

56
Q

phagocytes
recruitment

A

IL1 and TNFa by tissue-MO
activate nedothelial cells -> upregulation of ICAM-1 and selectins
bound by LFA-1 and carbohydrates on phagocytes
extravasation
migration along chemokine gradient

57
Q

phagocytes
function

A

2 main functions
PRODUCTION of PRO-INF CYTO- and CHEMOKINES (IL1, IL6 and TNFa)
release chemokines -> integrin activation, chemoattraction

PHAGOCYTOSIS and KILLING: have phagocytotic PRRs (CLRs, scavenger), opsonin recognition (IgG, C3b, CRP) and killing via phagolysosome (oxidative burst)

58
Q

phagocytes
disease

A

chronic granulomatose disease
mutationts in oxidase -> ROS production is impaired and therefore killing
characterized by recurrent infections

59
Q

macrophages

A

innate immune cell, phagocyte

dominate later stages of innate immune cells (arrive after neutrophils but are longer-lived)
phagocytosis, killing, cytokine production, Ag presentation

tissue resident MO develop during embryonic development
other develop out of monocytes when recruited to inflammations

M1 and M2 subset
M2 = wound-healing and repair promoting, by IL4 and IL13 (TH2 cells), also pro-tumorigenic

60
Q

macrophages
types

A

tissue resident -> produce IL1 and TNFa for phagocyte recruitment, developed in embryonic stages

other develop out of monocytes upon recruitment

M1 and M2 polarization
M2 = wound-healing and repair promoting, by IL4 and IL13 (TH2 cells), also pro-tumorigenic

61
Q

macrophages
function

A

phagocytosis and killing
cytokine production
Ag presentation

62
Q

neutrophils
function

A

phagocytosis and killing
NETosis
cell-cell contact with adaptive immune cells
degranulaton and cytokine release impacting T cells

63
Q

dendritic cells

A

innate immune cell
bridge between innate and adaptive
sentinel (capture and process) and presenting

PRRs: CLRs for Ag reouting into cell (Dectin)
TLRs, NLRs, RLRs and CDS to mature DCs

MATURATION: Ag processing and presentation, PRR signalling for co-stimulator expression, change in receptor reservoir (CCR7 upregulated for migration along CD19/21 to lymph nodes

activate naive T cells in primary immune response
activate mature T cells in secondary immune reponse

64
Q

dendritic cells
maturation

A

CLRs (dectin) mediate Ag processing and presentation
TLR, NLR, RLR and DCS recognize PAMPs and initiate maturation
(co-stimulator expression)
change in receptor reseroir -> CCR7 to migrate along CCL19/21 to lymph nodes

65
Q

dendritic cell
function

A

sentinel and presenting
Ag presentation of MHC I and MHC II -> cross-presentation by cDC1 possible

acivation of naive T cells in primary immune response
acivation of mature T cells in secondary immune response

66
Q

dendritic cell
subsets

A

pre-DC for conventintional, pre-pDC
cDC1: Ag CROSS PRESENTATION of exogenous Ag to CD8 (MHCI) and intraclelular pathogens (MHCI)
cDC2: extracellular pathogens to Cd4 on MHCII
CD3: extraclelular pathogens to CD4

pDC: plasmacytoid -> produce type I IFN -> antiviral

67
Q

cDC1

A

pre-DC
Ag CROSS PRESENTATION of exogenous Ag to CD8 (MHCI) and intraclelular pathogens (MHCI)

68
Q

cDC2

A

pre-CD
extracellular pathogens to Cd4 on MHCII

69
Q

DC3

A

pre-DC
extraclelular pathogens to CD4 (MHCII)

70
Q

pDC

A

pre-pDC
plasmacytoid -> produce type I IFN -> antiviral

71
Q

NK cells

A

innate immune cells

KILLING of virus infected, injured or tumour cells via perforin
IFNg PRODUCTION: induced by IL12 by MO -> activates MO to kill phagocytosed microbes
ADCC: Ab activate NK cells
- IgG binds target and FcgRIII on NK
- antibody bridge
- NK activation -> apoptosis

72
Q

IFNg production by NK cells

A

induced by IL12 from MO
activates MO to kill phagocytosed microbes

73
Q

NK cells
killing mechanism

A

perforin-mediated

74
Q

ADCC

A

Ab activating NK cells
IgG binding target and FcgRIII on NK cells -> Ab bridge
NK activation and apoptosis

75
Q

FcgRIII

A

on NK cells
mediates ADCC
IgG bindig target and FcgRIII

PM3 - Infection and immunity (9 decks)

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