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LECOM Microbiology MS1 > Innate Immunity (Exam 1) > Flashcards

Innate Immunity (Exam 1) Flashcards

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1
Q

What two things does innate immunity use to eliminate viruses

A

interferons and NK cells

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2
Q

How does innate immunity eliminate microbes

A

inflammation

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3
Q

What are the two branches of the immune system

A

adaptive

innate

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4
Q

What is innate immunity

A

native, natural

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5
Q

What is adaptive immunity

A

acquired, specific

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6
Q

What are the mechanisms of innate immunity

A

physical barriers
physiological barriers
cellular responses

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7
Q

What is an example of physical barrier innate immunity

A

skin

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8
Q

What is an example of physiological barrier innate immunity

A

stomach acid

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9
Q

What is an example of cellular response innate immunity

A

phagocytosis and inflammation

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10
Q

What are the components of acquired immunity

A

B and T cells

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11
Q

How are innate and adaptive immune responses connected

A

both use cytokines that help the opposite system

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12
Q

What are anatomical and chemical barriers of adaptive immunity

A

lymph nodes
spleen
MALT

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13
Q

What are anatomical and chemical barriers of innate immunity

A 
skin
mucosa
chemicals
pH
Temperature
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14
Q

What are blood proteins of innate immunity

A

complement

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15
Q

What are blood proteins of adaptive immunity

A

antibodies

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16
Q

What are the cells of innate immunity

A

phagocytes

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17
Q

What are the cells of adaptive immunity

A

lymphocytes

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18
Q

What are the phagocytic cells

A

neutrophils
macrophages/monocytes
dendritic cells

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19
Q

What phagocyte offers a prolonged defense

A

monocytes and macrophages

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20
Q

What causes neutrophils to die

A

contacting a pathogen

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21
Q

What are the two major types of monocytes and macrophages

A

M1

M2

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22
Q

What is the M1 macrophage function

A

plays a role in inflammation

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23
Q

What is the M2 macrophage function

A

tissue repair and control of inflammation

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24
Q

What molecule induces M2 macrophages

A

IL-4 and IL-13

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25
Q

When will monocytes differentiate into macrophages

A

once they leave the blood and enter the tissue

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26
Q

WHat are the two major functions of dendritic cells

A

initiate inflammatory response and the adaptive immune response

antigen processing and presentation

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27
Q

What type of phagocytes are involved in acute inflammation

A

neutraphils

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28
Q

What type of phagocytes are involved in chronic inflammation

A

macrophages

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29
Q

What is the brief process of phagocytosis

A 
extension of pseudopodia
formation of phagosome
fusion with lysosome to form phagosome
digestion
exocytosis
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30
Q

What receptors can LPS bind to

A

CD14 or TLR-4

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31
Q

Where are toll receptors found

A

macrophages and neutrophils

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32
Q

What do Toll like receptors recognize

A

sequences among different pathogens

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33
Q

Where is CD14 found

A

macrophages and neutrophils

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34
Q

What does CD14 bind

A

LPS

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35
Q

What do Pattern recognition receptors recognize

A

pathogen associated molecular patterns (PAMPs) or damage associated molecular patterns (DAMPs)

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36
Q

What are examples of the toll receptors

A

CD14 and TLR-4

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37
Q

What are examples of pattern recognition receptors

A

Toll receptors
NOD receptors
RIG receptors
CR3 and CR4 complement receptors

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38
Q

What is the downstream effect of NLRP-3

A

NOD like receptor that initiates inflammation through an inflammasome

Generates IL-1 beta

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39
Q

What is the pathogen target of TLR-4

A

LPS

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40
Q

Where are higher numbered TLR found

A

intracellular

recognize viral components

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41
Q

What is the purpose of opsonization

A

enhances phagocytosis by binding to a pathoge and directly delivering it to a phagocytic cell

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42
Q

What are the 2 opsonisn

A

IgG and C3b

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43
Q

What receptor do IgG and C3b bind to in order to activate opsonization

A

CD16

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44
Q

Where is CD16 found

A

on the membrane of phagocytes

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45
Q

What will be seen in an individual with an Ig deficiency

A

only innate complement pathways are working

recurrent bacterial infections that are severe due to lack of opsonization

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46
Q

What will be seen in an individual with a deficiency in oxygen-dependent killing

A

severe immunodeficiency

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47
Q

What type of killing is most powerful

A

oxygen-dependent killing

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48
Q

What are the 3 phagocytic killing mechanisms

A

oxygen-dependent
oxygen-independent
engulfment

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49
Q

How is NO generated in phagocytic and non-phagocytic cells

A

inducible nitric oxide synthetase (iNOS)

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50
Q

What are the different mechanisms of oxygen independent killing

A

Capthepsin G
Lactoferrin
Lysozyme
Defensins

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51
Q

What does capthepsin G use to kill cells

A

neutral proteas

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52
Q

What does Lactoferring use to kill cells

A

iron

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53
Q

What is the function of Lysozyme

A

breaks down peptidoglycan

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54
Q

What is the function of defensins

A

punches holes in cells

55
Q

What is the effectiveness of oxygen independent killing

A

not very effective

56
Q

Where will oxygen independent killing occur

A

lysosome

57
Q

WHere will oxygen dependent killing occur

A

phagosome

58
Q

What is the function of NADPH oxidase in oxygen dependent killing

A

takes molecular oxygen and converts it to superoxide radicals (Hydrogen peroxide)

59
Q

What is the importance of the radicals created by NADPH

A

radicals are unstable and will degrade to kill a pathogen within the phagolysosome

60
Q

Where will H2O2 be produced in oxygen dependent killing

A

NADPH oxidase or by a bacteria once it enters phagosome

61
Q

What is the function of myeloperoxidase

A

takes hydrogen peroxide and converts it to bleach

62
Q

When is myeloperoxidase used

A

if NADPH oxidase isn’t working

63
Q

What causes chronic granulomatous disease

A

deficiency in NADPH oxidase, x chromosome

64
Q

What are the results of chronic granulomatous disease

A

frequent infections with catalase positive bacteria and fungi (these organisms can break down H2O2)

65
Q

Why will an individual with CGD not have recurrent catalase negative infections

A

catalase negative organisms will produce H2O2 which can be converted into bleach

66
Q

How will a myeloperoxidase deficiency present

A

mild or asymptomatic as NADPH oxidase will kill organisms

67
Q

What assembles an inflammasome

A

NLRP-3, an adaptor, and inactive caspase

68
Q

What occurs to the caspase as a result of the inflammasome

A

activates the caspase

69
Q

What does the activation of the caspase result in

A

expression of active caspase (converts from Pro-IL1 to active form to initiate inflammation)

70
Q

What is produced by an inflmmasome

A

IL-1 and IL-18

71
Q

What are IL-1 and IL-18

A

potent inflammatory cytokines

72
Q

What will occur in a gain of function mutation of an inflammasome

A 
inflammatory diseases 
(gout, atherosclerosis, type 2 dm)
73
Q

What will be the effect of mutation in signaling molecules affecting TLRs

A

recurrent severe bacterial infections (pneumonia)

74
Q

What will be the effect of NOD-2 mutations

A

IBD

75
Q

A patient presents with recurrent infections of mycobacterium. What is likely mutated in this patient’s innate immune system

A

IL-12 and IFN gamma receptor deficiencies

76
Q

Activation of what induces inflammation

A

macrophages

77
Q

What is diapedesis

A

cells leaving blood and entering tissue

78
Q

How will activation of macrophages lead to inflammation

A

production of cytokines
recruitement of neutrophils
phagocytosis

79
Q

What is acute inflamamtion

A

inflammation in which cells are going to a specific site

80
Q

What are the steps of inflammation

A 
recruitment of WBC
rolling
adhesion
tight binding
diapedesis 
migration
81
Q

What molecules are involved in rolling adhesion

A

selectins and muscins

82
Q

On vascular epithelium, what are the selectins

A

P-selectin

E-selectin

83
Q

On neutrophils what is the muscins

A

sialyl lewis carbohydrates

84
Q

What molecules are involved in tight binding

A

integrins
ICAM-1
CD18

85
Q

What will occur during transendothelial migration

A

molecules such as histamine will increase space in junction of tissue allowing neutrophils to cross, causes fluid to leak into tissue causing swelling and vasodilation

86
Q

What causes an infected area to become warm and red

A

histamine, prostaglandins, leukotrienes causing vasodilation

87
Q

What is absent in leukocyte adhesion deficiency and what does this prevent

A

CD18 is absent

prevents leukocytes from migrating from blood into tissues

88
Q

What are signs of leukocyte adhesion deficiency

A

Ophalitis
recurrent chornic bacterial infections
no abscess or pus formation
excess neutrophils in the blood

89
Q

What is omphalitis

A

swelling of umbilical cord stump

90
Q

What might be deficient in a newborn with omphalitis

A

CD18

91
Q

What are the pro-inflammatory cytokines

A

IL-1, IL-6, TNF alpha

92
Q

What is the function of IL-8

A

chemotaxis of neutrophils

results in the tight binding of CD18 integrin to vascular epithelium

93
Q

Where is IL-8 released from

A

macrophages

94
Q

What is the function prostaglandins and leukotrienes

A

increase vasodilation and vascular permeability

95
Q

Where are prostaglandins and leukotrienes released from

A

mast cells

96
Q

What is the function of C5a in acute inflammatory response

A

chemoctactic molecule that recruits cells from vasculature into the tissue

97
Q

What are the pro-inflammatory cytokines

A

IL-1, IL-6, TNF-alpha

98
Q

What are the effects of the pro-inflammatory cytokines systemically on the liver

A

activation of complement opsonization

99
Q

What are the effects of the pro-inflammatory cytokines systemically on the bone marrow endothelium

A

neutrophil mobilization for phagocytosis

100
Q

What are the effects of the pro-inflammatory cytokines systemically on the hypothalamus

A

increased body temperature

101
Q

What are the effects of the pro-inflammatory cytokines systemically on the fat, muscle

A

protein and energy mobilization to generate increased body temperature

102
Q

What are the effects of the pro-inflammatory cytokines systemically on the dendritic cells

A

TNF-alpha stimulates migration to lymph nodes and maturation

103
Q

What is the function of leukotriene B4

A

chemotaxis

104
Q

What is the function of C5a and C3a

A

anaphylatoxins that will cause degranulation of a mast cell and increase vasodilation and vascular permeability

105
Q

How are complement reactive proteins used clinically

A

marker of inflammation, increased in MI

106
Q

What releases complement reactive proteins

A

liver

107
Q

What is a left shift

A

increased numbers of imamture neutrophils in the blood, bone marrow cannot keep up with body’s demands

108
Q

What is an example of a systemic inflammatory response

A

fever

109
Q

Where are IFN alpha and beta produced

A

alpha: leukocytes
beta: fibroblasts

110
Q

What interferons are made in direct response to viral infections

A

IFN alpha and beta

111
Q

What is the major innate response to viruses

A

release of interferon

surrounding cells take up the interferon and shut down protein synthesis

112
Q

After the virus is gone, what occurs to cells that temporally shut down protein syntehsis

A

resume protein synthesis

113
Q

Why does interferon degrade mRNA

A

inhibits protein synthesis to prevent viral replication

114
Q

What are the functions of IFN

A

resistence to viral replication
increase MHC class I expression and antigen presentation in all cells
Activate NK cells

115
Q

What is the function of NK cells

A

kill viral infected and transformed cells

116
Q

What markers are found on NK cells

A

CD16 and CD56

117
Q

What are the two ways in which NK cells work to kill

A

degranulation

apoptosis

118
Q

What do the NK cells secrete to cause degranulation

A

perforin

119
Q

How does apoptosis occur

A

FasL on NK binds to Fas on target cell and induces target cell to commit suicide

120
Q

What is the differentiating factor between NK cells and cytotoxic cells

A

cytotoxic cells recognize the antigen through class 1 MHC

121
Q

What cells will be targeted by NK cells

A

cells with decreased MHC class 1 expression

122
Q

What are the two classes of receptors on NK cells

A

inhibitory

activating

123
Q

What are the inhibitory receptors on NK cells

A

KIR

124
Q

What are the activating receptors on NK cells

A

KAR

125
Q

What is the function of KR receptors

A

recognize MHC alpha chains

126
Q

What receptor will override the other n NK cells

A

Inhibitory overrides activation receptor

127
Q

Where will a stress molecule bind to a NK cell

A

KAR

128
Q

RBCs are anucleate and do not express class 1 MHC. Why aren’t they targeted by NKs

A

don’t bind to KAR thus they are left alone

129
Q

What type of cells will express class 1 MHC

A

nucleated cells that aren’t infected or cancerous

130
Q

Outline the collaboration of macrophages and NK cells

A

interferone gamma from NK cells stimualtes macrophages

macrophages produce IL12 that stimulates NK cells

131
Q

What are the proinflammatory cytokines

A

IL-1
IL-6
TNF alpha
IL-8

132
Q

What secretes the proinflammatory cytokines

A

macrohages

133
Q

What is the chemokine

A

IL-8

LECOM Microbiology MS1 (22 decks)

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