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Exam 1 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

opsonization

A

the process of locating a microbe with molecules that can be recognized by receptors on phagocytes, which proceed to engulf and kill microbes

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2
Q

sites of microbial entry

A

epithelium of skin, GI tract, and respiratory tract

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3
Q

cells that show up at site of microbial entry

A

macrophages, dendritic cells, mast cells, phagocytes

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4
Q

plasma proteins

A

complement proteins that circulate in the blood promoting microbial destruction

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5
Q

cardinal feature of adaptive immunity

A

memory response, somatic rearrangement of gene segments during lymphocyte development leading to clonal expansion of B and T lymphocytes

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6
Q

innate microbial recognition

A

structures shared by classes of microbes not present on host cells are recognized

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7
Q

adaptive microbial recognition

A

lymphocytes express receptors (antibodies) on their cell surface that recognize specific antigens, activating phagocytosis, an innate property

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8
Q

PAMPs

A

microbial molecules shared by microbes of the same type that are not on normal host cells, that stimulate immune responses

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9
Q

examples of PAMPs

A

lipopolysaccharides (gram - bacteria), peptidoglycans (bacteria), terminal mannose residues (opportunistic infections), and unmethylated CG rich DNA (viruses)

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10
Q

DAMPs

A

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

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11
Q

PRRs

A

pattern recognition receptors, recognize PAMPs and DAMPs, present on phagocytes, dendritic cells, and others

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12
Q

PRRs can be located in different places in the cell

A

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

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13
Q

Toll-Like Receptors are PRRs detecting microbial components located

A

extracellularly, recognizing proteins, lipids, and polysaccharides on cell surfaces, and in endosomes, recognizing nucleic acids

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14
Q

What do toll-like receptors do

A

activate transcription factors to stimulate the expression of genes encoding cytokines, enzymes and NF kappa B, which promotes other infection-fighting agents

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15
Q

what is the result of a defect in TLR signaling

A

recurrent and highly severe infections

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16
Q

which toll-like receptors are found extracellularly and what do they find

A

1,2,4,5,6 look for proteins, lipids, and polysaccharides on microbial membranes

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17
Q

which toll-like receptors are found intracellularly in endosomes and what do they find

A

3,7,8,9 look for nucleic acids, both single and double stranded RNA and CG rich DNA (viruses)

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18
Q

how do toll-like receptors signal inflammatory responses

A

engage with bacteria or virus on leucine-rich repeats, signaling domain recruits transcription factors NF kappa B and interferon regulatory factors, which lead to increased expression of inflammatory cells and antiviral cells

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19
Q

what does NF kappa B do

A

transcription factor, increases expression of cytokines, adhesion molecules, and costimulators, leading to acute inflammation and the stimulation of adaptive immunity

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20
Q

what do interferon regulatory factors do

A

transcription factor, increases expression of type 1 interferons IFN alpha and beta, which lead to the antiviral state

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21
Q

what is the role of NOD-like receptors

A

sense DAMPs and PAMPs in cytoplasm containing nucleotide oligomerization domain, and different N-terminal domains

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22
Q

Nod1 and Nod2

A

contain N-terminal caspase related domains (CARD), found in bacterial peptidoglycan in cell wall, activated NF kappa B

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23
Q

NLRP3

A

recognizes microbial products, substances associated with cell damage, and endogenous substances in too large of quantities e.g. crystals, enhances production of IL1b beta, which leads to fever

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24
Q

genetic defect in NLRP3

A

enhances production of IL1b beta, leads to periodic fever syndrome

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25
Q

how do patients with gout get a “fever” in their toe

A

NLRP3 oligomerizes with inactive form of caspase 1 inflammasome in response to crystal buildup, activating caspase 1, which cleaves IL1 beta precursor, which gets activated and generates fever locally

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26
Q

chemical barrier on epithelium

A

peptide antibiotics like defenses and cathelicidins which kills some microbes locally

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27
Q

intraepithelial lymphocytes

A

limited diversity, lymphocytes embedded in barrier kill microbes before they breach epithelium

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28
Q

chemokines

A

call leukocytes to cell surface and to the site of injury

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29
Q

selectins

A

allow for leukocyte to slow down and adhere to cell surface in process known as rolling

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30
Q

integrin

A

allows for stable adhesion of leukocytes to cell wall

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31
Q

PMNs

A

polymorphonuclear leukocytes, or neutrophils, most abundant leukocyte in the blood, rapidly increase in number during infection, first responders, dominant cell of inflammation, phagocytose microbes in blood and tissue and remove debris leading to pus formation

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32
Q

Band Neutrophils

A

immature neutrophils, unsegmented nucleus, released prematurely indicating desperate situation

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33
Q

oxidative burst

A

PRR recognizes microbe and phagocytosis occurs, membrane closes and forms phagosome, fuses with lysosome forming phagolysosome, phagocyte oxidase converts O2 to superoxide and ROS, works with lysosomal proteases to destroy microbes

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34
Q

patients who can’t produce ROS

A

can’t properly destroy microbes using the phagolysosome, experience chronic granulomatous disease

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35
Q

Mononuclear phagocytic system

A

monocytes differentiate into macrophages in the tissues, found in all connective tissue and organs, ingest microbes, clear dead tissues, initiate repair

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36
Q

some macrophages are derived from

A

the yolk sack or fetal liver during development, particularly those in the brain (microglial cells), liver (kupffer cells), spleen (sinusoidal macrophages), and lungs (alveolar macrophages)

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37
Q

Classical macrophage activation

A

toll-like receptor ligands and interferon gamma lead to production of phagolysosomal killing of bacteria and fungi

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38
Q

alternative macrophage activation

A

IL13 and IL4 lead to macrophage production of IL10, which is anti-inflammatory and TGF beta, which leads to tissue repair

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39
Q

role of dendritic cells

A

antigen presenting cells, activated by cytokines, move through lymphatic vessels, connect to and activate t cells in lymph nodes, bridge between innate and adaptive immunity

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40
Q

role of mast cells

A

contain vasoactive granules i.e. histamine, which increase capillary permeability at site of injury, and synthesize and secrete prostaglandins and cytokines (TNF), which stimulate inflammation

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41
Q

where do mast cells reside

A

skin and mucosal epithelium

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42
Q

role of natural killer cells

A

combat intracellular microbial infections by identifing infected or stressed cells and killing them by emptying their cytoplasmic granules in the extracellular space nearby, which enter the cell and induce apoptosis, also secrete IFN gamma to activate macrophages

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43
Q

what activates natural killer cells

A

cytokines from macrophages and dendritic cells, particularly IL 15 and IL 12

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44
Q

IL 15

A

develops and matures natural killer cells

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45
Q

IL 12

A

enhance natural killer cell killing function, as well as type I interferons alpha and beta

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46
Q

inhibitory role of natural killer cells

A

block signaling by receptor activation specific for “self” MHC I molecules, protect healthy cells

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47
Q

ITIMs

A

inhibitory receptors of natural killer T cells, blocking ITAMs, preventing NK activation

48
Q

CD94/NKG2 lectin subunit

A

block NK cell activation

49
Q

KIRs

A

killer cell immunoglobulin-like receptors, block NK cell activation

50
Q

NK cell ADCC

A

antibody-dependent cellular cytotoxicity, antibodies recognize viral glycoproteins on cells infected with enveloped viruses, leads to killing of antibody-coated cell

51
Q

NKT cells

A

shares properties of both NK cells and T cells, recognizes lipids on CD1 molecule, not adaptive immunity

52
Q

B-1 B cells

A

B lymphocytes in the peritoneal cavity and mucosal tissue that produce IgM, not adaptive immunity

53
Q

complement system: alternative pathway

A

activated complement proteins on microbial surface are uncontrolled due to lack of regulatory proteins, innate immunity

54
Q

complement system: classical pathway

A

antibodies bound to antigens, adaptive immunity, C3a and C5a are inflammatory, C3b is responsible for opsinization

55
Q

complement system: lectin pathway

A

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

56
Q

3 main functions of complement system

A

opsonization and phagocytosis (C3b), inflammation (C3a and C5a), and cell lysis via membrane attack complex

57
Q

complement membrane attack complex formation

A

C5 cleaved to C5b, binds with C6,7,8 and multiple C9, forms a pore in membrane, influx of water and ions, cell death

58
Q

collectins

A

plasma proteins including mannose binding lectin and surfactant

59
Q

mannose binding lectin

A

recognizes microbial carbohydrates, coats them for phagocytosis, activation of lectin complement system, not clinically relevant

60
Q

surfactant

A

soap like protective coating on lung against infectious microbes, important in premature babies

61
Q

c-reactive protein

A

binds phosphorylcholine on microbes, opsonizes them for phagocytosis, activates classical complement pathway proteins, can be measured in blood to prove active infection

62
Q

interleukins

A

soluble proteins cause cell signaling to generate immune/inflammatory reactions, stimulated by infection, produced by, activated, and act on leukocytes

63
Q

interleukin role in innate immunity

A

communicate with mast cells, dendritic cells, and macrophages

64
Q

interleukin role in adaptive immunity

A

communicate with helper T lymphocytes

65
Q

cytokines responsible for monocyte/neutrophil recruitment

A

TNF, IL1, and chemokines

66
Q

cytokines responsible for fever

A

TNF and primarily IL-1b

67
Q

cytokines responsible for acute phase response protein synthesis in liver

A

IL6, leads to production of C-reactive protein and fibrinogen

68
Q

cytokines responsible for hypotension

A

TNF, at high concentrations

69
Q

cytokines responsible for septic shock

A

TNF at high concentrations, IL12 from dendritic cells and macrophages, in response to LPS and other microbial molecules

70
Q

type 1 interferon role in viral infection

A

binds to the virus, blocks enzymes necessary for viral replication, preventing protein synthesis, degrading viral RNA, and inhibiting gene expression

71
Q

TNF produced from

A

macrophages, T cells, and mast cells

72
Q

TNF effect on endothelial cells

A

inflammation and coagulation

73
Q

TNF effect on neutrophils

A

activation

74
Q

TNF effect on hypothalamus

A

fever

75
Q

TNF effect on liver

A

synthesis of acute-phase proteins

76
Q

TNF effect on muscle/fat

A

cachexia

77
Q

Tissue types/cells effected by TNF

A

endothelial, neutrophils, hypothalamus, liver, muscle/fat

78
Q

Interleukin 1 produced by

A

macrophages, dendritic cells, endothelial cells, epithelial cells, mast cells (MDEEM)

79
Q

Tissue/cell types effected by interleukin 1

A

endothelial cells, hypothalamus, liver, and T cells

80
Q

Interleukin 1 effect on endothelial cells

A

inflammation coagulation

81
Q

Interleukin 1 effect on hypothalamus

A

fever, particular IL1b

82
Q

Interleukin 1 effect on liver

A

synthesis of acute-phase proteins

83
Q

Interleukin 1 effect on T cells

A

Th17 differentiation

84
Q

Th17

A

produces IL17, pro inflammatory cells, found in joints of arthritis patients

85
Q

chemokines produced by

A

macrophages, dendritic cells, endothelial cells, T cells, fibroblasts, platelets

86
Q

tissue/cell types effected by chemokines

A

leukocytes

87
Q

chemokine effect on leukocytes

A

increased integrin affinity, chemotaxis, activation

88
Q

Interleukin 12 produced by

A

dendritic cells, macrophages

89
Q

tissue/cell types effected by interleukin 12

A

NK cells, T cells

90
Q

effect of interleukin 12 on NK cells

A

interferon gamma production, increased cytotoxic activity

91
Q

effect of interleukin 12 on T cells

A

interferon gamma production, increased cytotoxic activity, Th1 differentiation

92
Q

interferon gamma produced by

A

NK cells and T lymphocytes

93
Q

interferon gamma role

A

activates macrophages, stimulates some antibody response

94
Q

type 1 interferons produced by

A

alpha: dendritic cells and macrophages, beta: fibroblasts

95
Q

type 1 interferon role

A

antiviral state, increased class I MHC expression, activates natural killer cells

96
Q

interleukin 10 produced by

A

macrophages, dendritic cells, T cells

97
Q

interleukin 10 effects which cells?

A

macrophages and dendritic cells

98
Q

role of interleukin 10

A

inhibition of cytokine and chemokine production, reduced expression of costimulators and class II MHC molecules

99
Q

interleukin 6 produced by

A

macrophages, endothelial cells, t cells

100
Q

interleukin 6 effects which tissue/cell types?

A

liver and B cells

101
Q

interleukin 6 effect on liver

A

synthesis of acute-phase proteins

102
Q

interleukin 6 effect on B cells

A

proliferation of antibody-producing cells

103
Q

interleukin 15 produced by

A

macrophages

104
Q

interleukin 15 role

A

promote proliferation of NK cells and T cells

105
Q

interleukin 18 produced by

A

macrophages

106
Q

interleukin 18 role

A

cause NK cells and T cells to produce interferon gamma

107
Q

TGF beta produced by

A

many cell types

108
Q

role of TGF beta

A

inhibition of inflammation, leads to tissue repair

109
Q

chronic granulomatous disease

A

defective production of ROS leads to inability to produce phagocytic oxidase, leading to low immunity, many infections, mostly skin and some pulmonary

110
Q

leukocyte adhesion deficiency

A

defective leukocyte adhesion-dependent functions leads to high WBC count in patients

111
Q

complement C3 deficiency

A

can prevent the full cascade, other times it’s just defective and slow

112
Q

Chediak-Higashi syndrome

A

defective lysosomal function in neutrophils, macrophages, dendritic cells, and defective granule function in NKs, diagnosed very early, patients have silver hair, effects phagocytosis, bad long-term infections

113
Q

HSV1 encephalitis

A

mutation in toll-like receptor 3 leads patients with HSV1 to have defective CNS antiviral effects

114
Q

Positive selection of reactive cells

A

check to see if the T cells are able to interact with MHC, if they are, they will survive and move on to maturity

115
Q

negative selection of reactive cells

A

check to see how capable the T cells are of binding with self, if it’s too strong, cell will be told to undergo apoptosis, way to prevent autoimmunity

Exam 1 (7 decks)

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