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IBI Test 1 > B3.004 Innate Immunity > Flashcards

B3.004 Innate Immunity Flashcards

1
Q

pathogen

A

a microbe that is causing disease

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2
Q

necrotic

A

dead cells or tissue from injury or disease

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3
Q

apoptosis

A

cell death as a normal and controlled part of an organism’s growth and development

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4
Q

cytokines

A

soluble proteins important in cell signaling

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5
Q

chemokine

A

cytokine that attracts a particular cell into an environment

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6
Q

opsonization

A

coating a microbe with molecules that can be recognized by receptors on a phagocyte

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7
Q

phagocytosis

A

process by which a cell engulfs a solid particle

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8
Q

roles of the immune system

A 
defense against infections
defense against tumors
injure cells
induce pathogenic inflammation
recognize and respond to tissue grafts and newly introduced proteins
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9
Q

overview of innate immunity

A

natural or native immunity
present in all individuals at birth
immediate response upon infectious encounters
restricted response without memory
receptors encoded in germline
does not react against host in normal circumstances

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10
Q

innate immunity defense at the site of microbial entry

A

epithelium of skin, GI tract, and respiratory tract

-physical barrier, antimicrobial molecules, lymphoid cells

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11
Q

innate immunity defense in tissues where microbes breach

A

macrophages, dendritic cells, and mast cells secrete cytokines
-initiation of inflammation
phagocytes destroy microbes, eliminate damaged cells

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12
Q

innate immunity defense in blood

A

plasma proteins (complement) promote microbial destruction

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13
Q

innate immunity defense in viruses

A

induce production of interferons from infected cells to inhibit infection of other cells
induce killing by NK cells

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14
Q

process of innate immunity microbial recognition

A

recognize structures shared by classes of microbes not present on host cells
enhanced function through the adaptive immune system

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15
Q

PAMPs

A

pathogen-associated molecular patterns
microbial molecules, shared by microbes of the same type
not on normal host cells
stimulate innate immune response

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16
Q

4 classes of PAMPs essential for survival/infectivity

A

LPS endotoxin- gram - bacteria
peptidoglycans - bacteria
terminal mannose residues - opportunistic infections
unmethylated CG-rich DNA - intracellular viral infections

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17
Q

DAMPs

A

damage associated molecular patterns
released from damaged or necrotic host cells
present in injury or infection

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18
Q

PRRs

A

pattern recognition receptors

innate immune receptors that recognize PAMPs and DAMPs

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19
Q

where are PRRs expressed?

A

phagocytes
dendritic cells
others

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20
Q

why are cellular receptors present on different cellular compartments?

A

cell surface to detect extracellular microbes
vesicles where microbes are ingested
cytosol to sense cytoplasmic microbes

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21
Q

what are TLRs and what do they bind?

A

toll like receptors
extracellular microbes: proteins, lipids, and polysaccharides on cell surfaces
endosomes: nucleic acids

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22
Q

how do TLRs function?

A

activate transcription factors to stimulate expression of genes encoding cytokines, enzymes, and other proteins
-NFKB family promotes other items involved in fighting infections

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23
Q

extracellular TLRs

A 
1 - bacterial lipopeptides
2 - lipopeptides, peptidoglycans
4 - LPS
5 - flagellin
6 - lipopeptides
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24
Q

intracellular TLRs

A

3- dsRNA
7- ssRNA
8- ssRNA
9- CpG DNA

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25
Q

run through the steps involved in TLR signaling

A
  1. TLR engagement by bacterial or viral molecules
  2. recruitment of proteins that activate transcription (NFKB and IRFs)
  3. increased expression of cytokines, adhesion molecules, co-stimulators
  4. production of type I interferon (IFN alpha and beta)
  5. generate inflammation
  6. stimulate adaptive immunity
  7. antiviral activity
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26
Q

what are NLRs and what do they bind?

A

NOD-like receptors
family of cytosolic receptors that sense DAMPs and PAMPs in the cytoplasm that contain:
-central NOD (nucleotide oligomerization domain)
-different N-terminal domains

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27
Q

NOD-1 and NOD-2

A

contain N-terminal CARD (caspase related domains)

  • bacterial peptidoglycans in the cell wall
  • activated NFKB
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28
Q

NLRP-3

A

recognizes microbial products, substances associated with cell damage, and endogenous substances in cells in large quantities
enhances production of IL-1b

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29
Q

what is the inflammasome?

A

NLRP-3 oligomerizes with inactive form of caspase 1

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30
Q

what causes the creation of the inflammasome?

A 
pathogenic bacteria
extracellular ATP
bacterial products
crystals
K+ efflux
ROS
viral DNA
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31
Q

what is the function of the inflammasome?

A

once activated, the caspase 1 cleaves an IL-1 B precursor leading to activation of IL-1 B and thus generation of fever

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32
Q

what are some results of inflammasome dysregulation?

A

gout- urate crystal deposits

auto-inflammatory syndromes (periodic fever syndrome if inflammasome is always active)

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33
Q

what are the 4 primary goals of innate immunity

A
  1. accumulation/activation of leukocytes and plasma proteins at the site of infection or injury
  2. kill extracellular microbes
  3. eliminate damaged tissues
  4. defend against intracellular infected cells
    - NK cells
    - cytokines (type 1 interferons) block viral replication in host cells
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34
Q

components of innate immunity

A 
epithelial barrier
phagocytes (neutrophils and monocytes/macrophages)
dendritic cells
mast cells
innate lymphoid cells
NK cells
lymphocytes w limited diversity
complement
plasma proteins 
cytokines
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35
Q

what are the functions of the epithelial barrier?

A
  1. mechanical barrier of tightly adherent cells
  2. produce mucous to trap and expel pathogens
  3. chemical barrier that produces peptide antibiotics such as defensins and cathelicidins
  4. intraepithelial lymphocytes kill microbes
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36
Q

what are the basic steps of leukocyte recruitment?

A
  1. rolling (selectins)
  2. stable adhesion by integrin binding
  3. migration through endothelium (diapedesis)
  4. recruitment to injury by chemokines
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37
Q

most abundant leukocyte in blood

A

neutrophils

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38
Q

why do neutrophils increase in number rapidly during infection?

A

stimulated by cytokines secreted by other cells during infections causing hematopoietic stem cells to proliferate and mature neutrophil precursors

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39
Q

first cell to respond to infections

A

neutrophils

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40
Q

dominant cell of inflammation

A

neutrophils

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41
Q

how long to neutrophils live?

A

only a few hours in tissues

dead ones form pus

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42
Q

2 goals of neutrophils

A

phagocytose microbes in blood and tissues to destroy them

dominant cell of inflammation

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43
Q

what is a band neutrophil?

A

immature neutrophil

increase in number when the immune system is overwhelmed

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44
Q

describe the steps of an oxidative burst

A
  1. microbe is recognized by PRRs and phagocytosis occurs
  2. membrane closes forming a phagosome
  3. phagosome fuses with lysosome forming phagolysosome
  4. phagocyte oxidase converts molecular oxygen into several enzymes: superoxide anions and free radical ROSs
  5. ROSs work with inducible nitric oxide synthase and lysosomal proteases to destroy microbes
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45
Q

chronic granulomatous disease

A

cant produce ROS, so you can’t fight infection despite the presence of neutrophils

46
Q

what cells differentiate into macrophages in the tissues?

A

monocytes

47
Q

where are monocytes found?

A

all connective tissues and organs

48
Q

how long to monocytes live?

A

prolonged survival in tissues

49
Q

what are the functions of monocytes?

A

ingest microbes in blood and tissues
clear dead tissues
initiate tissue repair

50
Q

what are the functions of macrophages?

A

cytokine production that regulates and induces inflammation
phagocytose microbes because of recognition of cell surface receptors
clear dead tissues
initiate repair process
activated by PRRs
respond to cytokines

51
Q

what is classical macrophage activation?

A

macrophages activated by immune signals such as TLRs and cytokine IFN-gamma
activated macrophages destroy microbes and induce inflammation (ROS, NO, lysosomal enzymes, IL-1,12,23

52
Q

what is the alternative macrophage activation pathway?

A

activation by cytokines IL-4 and IL-13

activated macrophages incite tissue repair and termination of inflammation (IL-10 and TGF-B)

53
Q

what are dendritic cells and how do they function?

A

antigen presenting cells
production of cytokines
bridge innate and adaptive immunity by presenting to T-cells

54
Q

what is present within mast cells

A

abundant cytoplasmic and vasoactive granules

55
Q

where are mast cells found

A

skin and mucosal epithelial

56
Q

how mast cells activated?

A 
microbial products binding to TLRs
antibody dependent (allergic reactions)
57
Q

how do mast cells impact inflammation?

A

release vasoactive amines (histamine and tryptase)
-increase capillary permeability
synthesize and secrete lipid mediators and cytokines
-stimulate inflammation

58
Q

what is the function of NK cells?

A

identify infected and stressed cells and kill them

  • empty cytoplasmic granules into the extracellular space near the infected cell
  • granules enter the cell and activate enzymes to induce apoptosis
59
Q

what type of infections to NK cells fight?

A

intracellular microbial infections

60
Q

what do NK cells secrete?

A

IFN-gamma to activate macrophages

61
Q

how are NK cells activated?

A

by cytokines from macrophages and dendritic cells
IL-15 - development and maturation of NK cells
IL-12 and type I IFNs- enhance NK cell killing function

62
Q

describe ITIMs and their mechanism of action

A

immunoreceptor tyrosine-based inhibitory motifs (ITIMs)
become phosphorylated on tyrosine residues when receptors bind MHC I (self molecule)
counteract ITAMs blocking NK cell activation

63
Q

describe the mechanism of action of ITAMs

A

immunoreceptor tyrosine-based activating motifs (ITAMs)
become phosphorylated on tyrosine residues and recognize their activating ligands
promote activation of cytosolic protein tyrosine kinase
activate other substrates involved in downstream signaling pathways causing cytotoxic granule exocytosis and production of IFN-gamma

64
Q

when do NK cells act against tumor cells?

A

when they have stress from DNA damage and malignant transformation

65
Q

describe NK cell ADCC (antibody dependent cellular cytotoxicity)

A

antibodies recognize viral glycoproteins expressed on the surface of cells infected w enveloped viruses
NK cells recognize antibodies and kill antibody coated cell
therapeutic intervention in treating tumor cells

66
Q

alternative pathway of the complement system

A

triggered when activated complement proteins on microbial surfaces are uncontrolled due to lack of regulatory proteins
innate immunity

67
Q

classical pathway of the complement system

A

triggered by antibodies bound to microbes/antigens

adaptive immunity

68
Q

lectin pathways of the complement system

A

mannose binding lectin binds to terminal residues on microbial cell surface glycoproteins
innate immunity

69
Q

3 main functions of complement system

A
  1. opsonization and phagocytosis
  2. inflammation
  3. cell lysis
70
Q

describe the formation and function of the MAC

A

C5 convertase causes proteolysis of C5 to C5b
C5b binds with C6-9
forms a pore in the cell membrane
causes and influx of water and ions and cell death

71
Q

what is the acute phase response?

A

plasma proteins of innate immunity increase rapidly with infection

72
Q

collectins

A

mannose binding lectins (MBLs)
-recognize microbial carbs, and coat them for phagocytosis
-activation of complement by the lectin pathway
surfactant
-soap like substance in the lung protective from infectious microbes

73
Q

C-reactive protein (CRP)

A

binds phosphorylcholine on microbes, opsonizes them for phagocytosis by macrophages
activated classical complement pathway proteins

74
Q

what are interleukins?

A

cytokines of innate immunity

soluble proteins that cause signaling to generate immune and inflammatory reactions - stimulated by infection

75
Q

cytokines responsible for recruitment of neutrophils and monocytes

A

TNF
IL-1
chemokines

76
Q

cytokines responsible for fever by acting on hypothalamus

A

TNK

IL-1 (predominant)

77
Q

cytokines responsible for acute phase response protein synthesis from the liver (CRP and fibrinogen)

A

IL-6

78
Q

cytokines responsible for thrombus formation

A

TNF at high conc

79
Q

cytokines responsible for hypotension

A

TNF at high conc

80
Q

cytokines responsible for septic shock

A

high TNF

IL-12 from dendritic cells and macrophages

81
Q

type 1 interferon

A

important in viral infections
binds to the virus
blocks enzymes necessary for viral replication

82
Q

how does type 1 interferon block viral replication?

A

inhibition of protein synthesis
degradation of viral RNA
inhibition of viral gene expression

83
Q

source of TNF

A

macrophages
T cells
mast cells

84
Q

source of IL-1

A 
macrophages
dendritic cells
endothelial cells
some epithelial cells
mast cells
85
Q

source of chemokines

A 
macrophages
dendritic cells
endothelial cells
T lymphocytes
fibroblasts
platelets
86
Q

sources of IL-12

A

dendritic cells

macrophages

87
Q

sources of IFN-gamma

A

NK cells

T lymphocytes

88
Q

sources of Type 1 IFNs

A

IFN alpha: dendritic cells, macrophages

IFN beta: fibroblasts

89
Q

sources of IL-10

A

macrophages
dendritic cells
T cells

90
Q

sources of IL-6

A

macrophages
endothelial cells
T cells

91
Q

sources of IL-15

A

macrophages

others

92
Q

sources of IL-18

A

macrophages

93
Q

sources of TGF-beta

A

many cell types

94
Q

principal targets and effects of TNF

A 
endothelial cells: activation (inflammation, coagulation)
neutrophils: activation
hypothalamus: fever
liver: synthesis of acute phase proteins
muscle, fat: catabolism (cachexia)
many cell types: apoptosis
95
Q

principal targets and effects of IL-1

A

endothelial cells: activation
hypothalamus: fever
liver: synthesis of acute phase proteins
T-cells: Th17 differentiation

96
Q

principal targets and effects of chemokines

A

leukocytes: increased integrin affinity, chemotaxis, activation

97
Q

principal targets and effects of IL-12

A

NK cells and T cells: IFN-gamma production, increased cytotoxic activity
T cells: Th1 differentiation

98
Q

principal targets and effects of IFN-gamma

A

activation of macrophages

stimulation of some antibody responses

99
Q

principal targets and effects of type 1 IFNs

A

all cells: antiviral state, increased MHC 1 expression

NK cells: activation

100
Q

principal targets and effects of IL-10

A

macrophages/dendritic cells: inhibition of cytokine and chemokine production, reduced expression of costimulators and class 2 MHC molecules

101
Q

principal targets and effects of IL-6

A

liver: synthesis of acute phase proteins

B cells: proliferation of antibody producing cells

102
Q

principal targets and effects of IL-15

A

NK cells: proliferation

T cells: proliferation

103
Q

principal targets and effects of IL-18

A

NK cells and T cells: IFN-gamma synthesis

104
Q

principal targets and effects of TGF-beta

A

inhibition of inflammation

T cells: differentiation of Th17, regulatory T cells

105
Q

deficiencies associated with chronic granulomatous disease

A

defective production of ROS

mutations in genes encoding components of the phagocyte oxidase enzyme

106
Q

deficiencies associated with leukocyte adhesion deficiency-1

A

absent or deficient expression of B2 integrins causing defective leukocyte adhesion dependent function
mutations in gene encoding B chain of B2 integrins

107
Q

deficiencies associated with leukocyte adhesion deficiency-2

A

absent or deficient expression of leukocyte ligands for endothelial E and P selectins, causing failure of leukocyte migration into tissues
mutations in gene encoding a protein required for synthesis of E and P selectin ligands

108
Q

deficiencies associated with complement C3 deficiency

A

defect in complement cascade activation

mutations in C3 gene

109
Q

deficiencies associated with complement C2,C4 deficiency

A

deficient activation of classical pathway of complement leading to failure to clear immune complexes and development of lupus like disease
mutations in C2 or C4 gene

110
Q

deficiencies associated with Chediak-Higashi syndrome

A

defective lysosomal function in neutrophils, macrophages, and dendritic cells, and defective granule function in NK cells
mutation in a gene encoding a lysosomal trafficking regulatory protein

111
Q

deficiencies associated with HSV-1 encephalitis

A

defective antiviral immunity in CNS

mutations in TLR3 gene

112
Q

deficiencies associated with recurrent pyogenic bacterial infections

A

defective innate immune responses to pyogenic bacteria

mutations in MyD88 gene

IBI Test 1 (15 decks)

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