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Immuno > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

Is innate immunity specific or non-specific? Fast or slow?

A

Non-specific, fast

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2
Q

Is adaptive immunity immediate or later? Specific or not?

A

Slow, specific

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3
Q

What are the cells that are involved in innate immunity?

A
  1. Phagocytes
  2. Neutrophils
  3. Natural killer T cells
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4
Q

What are the cells that are involved in adaptive immunity?

A

T and B lymphocytes

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5
Q

What are the cell receptors in innate immunity?

A

Fc & complement receptors, lectins (Non-polymorphic), Pattern recognition receptors

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6
Q

What are the cell receptors in adaptive immunity?

A

B and T cell receptors (diverse)

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7
Q

What are the circulating molecules in innate immunity?

A

Complement (non- polymorphic)

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8
Q

What are the circulating molecules in adaptive immunity?

A

Immunoglobulins (diverse)

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9
Q

What are the soluble mediators of innate immunity?

A

Macrophage-derived cytokines, other acute phase reactants, systemic effects, inflammation

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10
Q

What are the soluble mediators of adaptive immunity?

A

Lymphocyte-derived factors (local growth and regulation)

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11
Q

What is the recruitment mechanism in innate immunity?

A

Recruitment

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12
Q

What is the recruitment mechanism in adaptive immunity?

A

Clonal expansion

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13
Q

Which type of immunity has memory?

A

Adaptive

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14
Q

Which type of immunity it variable within indiiduals?

A

Adaptive–innate response is largely the same

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15
Q

What are PAMPs?

A

pathogen-associated molecular patterns (e.g single stranded DNA, RNA etc).

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16
Q

What is lipopolysaccharide (LPS, endotoxin)?

A

A pattern expressed by gram negative bacteria

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17
Q

What are damage associated molecular patterns?

A

endogenous molecules that are produced by, or released from damaged and dying cells, activating the innate immunity

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18
Q

What are toll-like receptors?

A

A subset of pattern recognition receptors

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19
Q

What is TLR4?

A

Toll-like receptor that binds to LPS, a gram negative protein

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20
Q

Where are PRRs found?

A

in different cellular locations; some are on the cell membrane, others in endosomes, and others in the cytoplasm

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21
Q

What does PAMP/TLR activate?

A

NFkB and IRFs which leads to inflammation antiviral state

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22
Q

What are inflammasomes?

A

Hyperactivation of the inflammasome results in autoinflammatory syndromes which can be treated with IL-1 antagonists.

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23
Q

True or false: The receptors of the innate immune system are encoded in germline DNA and recognize conserved patterns on pathogens

A

True

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24
Q

What is the complement system?

A

a system of non-polymorphic soluble proteins that form a proteolytic cascade important in clearance of a variety of pathogens

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25
Q

What are cytokines?

A

soluble molecules that form a mechanism for communication in the immune system. They can facilitate innate and adaptive immunity.

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26
Q

How does recruitment of lymphcytes occur? Leukocytes?

A

Lymphocytes - clonal expansion of specific lymphocyte populations

Leukocytes - Recruitment of leukocytes to sites of infection

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27
Q

Which type of immunity improves over time?

A

Adaptive

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28
Q

What are pattern recognition patterns (PRRs)?

A

Structures that a on leukocytes that recognize microbial pathogens

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29
Q

What are Pathogen-associated molecular patterns (PAMPs)?

A

molecular structures that are produced by microbial pathogens

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30
Q

PAMPs are ligands for what?

A

PRRs

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31
Q

What is the example of a PAMP used in class?

A

Lipopolysaccharide (LPS, endotoxin), which is on Gram-negative bacteria

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32
Q

What allows the innate immune system to recognize damaged self cells?

A

Damage associated molecular patterns (DAMPs). These are expressed by cells consitutively, so long as there is no damage to the cell

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33
Q

What are Toll-like receptors?

A

A protein recognition receptor on leukocytes that enables recognize specific PAMPs

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34
Q

What is the function of TLR4?

A

Recognizes the LPS molecule on Gram-negative bacteria, resulting in production of pro-inflammatory cytokines from monocytes and macrophages.

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35
Q

Where are PRRs found? Why is this significant?

A

some are on the cell membrane, others in endosomes, and others in the cytoplasm.

This is significant because both intracellular and extracellular pathogens can activate PRR.

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36
Q

What are NOD-like receptors?

A

Cytosolic PRR that trigger activation of innate immunity

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37
Q

What is the NLRP family

A

a subfamily of NLR that are important in generation of the proinflammatory cytokine IL-1 via activation of the inflammasome

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38
Q

What are inflammasomes?

A

Proteins that are responsible for activation of the inflammatory process

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39
Q

What are the three mechanical barriers the body has to prevent infection?

A
  1. Epithelial cells
  2. Longitudinal flow of air
  3. Movement of mucus
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40
Q

What type of junctions are between epithelial cells?

A

Tight junctions

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41
Q

What are the two families of antimicrobial peptides that epithelial cells produce?

A
  1. Defensins

2. Cathelicidins

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42
Q

What is the mechanism of action of Defensins/cathelocidins?

A

These molecules are directly toxic to microbes and also activate leukocytes to promote inflammation

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43
Q

What prevent colonization of microbes in the GI and GU tract?

A

Low pH

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44
Q

What are lysozomes?

A

antimicrobial enzymes that break down bacterial cell walls

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45
Q

What is the commensal bacteria that normally reside in/on epithelial barriers

A

The microbiome

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46
Q

What is the benefit of the presence of a microbiome on human epithelial cells?

A

Prevents the colonization of the epithelial tissue by other microbials

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47
Q

What are the three professional phagocytic cells?

A

Neutrophils
Monocytes/macrophages
Dendritic cells

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48
Q

Where do the professional phagocytes originate from?

A

Bone marrow

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49
Q

What are the first cells that are present in the sites of infection?

A

Neutrophils

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50
Q

What percent of circulating leukocytes are neutrophils?

A

59%

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51
Q

How long do neutrophils live for?

A

24-48 hours

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52
Q

What differentiates monocytes from macrophages?

A

Monocytes are circulating cells, whereas macrophages are the cells when they are present in tissues, where they differentiate

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53
Q

How long do macrophages live for?

A

Months

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54
Q

Where are macrophages found?

A

In all tissues

55
Q

How are macrophages named?

A

Based on their location (microglia, alveolar macrophages etc)

56
Q

What is the first step in the generation of an immune response?

A

Phagocytosis of an antigen by professional phagocytes

57
Q

What are intraepithelial lymphocytes?

A

lymphocytes found in the epithelial layer of mucosal linings, such as the gastrointestinal (GI) tract and reproductive tract. However, unlike other T cells, IELs do not need priming. Upon encountering antigens, they immediately release cytokines and cause killing of infected target cells. In the GI tract, they are components of gut-associated lymphoid tissue (GALT)

58
Q

What is phagocytosis needed for, beside the immune system?

A

Development and tissue homeostasis

Also eat dead neutrophils

59
Q

What are polymorphonuclear-leukocytes (PMNs)?

A

Neutrophils

60
Q

Where are sinusoidal macrophages found?

A

In the spleen

61
Q

What happens after microbes bind to phagocyte receptors?

A

Actin is rearranged to engulf microbe

62
Q

What are dendritic cells? What is their function?

A

Phagocytic cells that exists in tissues.

Their main function is to process antigen material, and present it on the cell surface to the T cells of the immune system in lymph nodes. They act as messengers between the innate and the adaptive immune systems.

63
Q

What are opsonins?

A

Soluble proteins that recognize phagocytic targets and are then recognized by specific receptors on phagocytics cells

64
Q

What are the two major classes of opsins?

A

Complement and antibodiy

65
Q

What are the two specific opsins discussed in class?

A

C3 -complement

IgG - antibody

66
Q

What is the receptor molecule for IgG?

A

Fc(gamma)RI

67
Q

What is the intracellular vesicle formed following engulfment of a particle ?

A

Phagosome

68
Q

What happens to the phagosome once it is inside the cytoplasm?

A

Fuses with a lysosome

69
Q

What is the pH of lysosomes?

A

3.5-4.5

70
Q

How is TB able to survive the acidic phagosome?

A

prevent fusion of the phagosome and lysosome and inhibit acidification of the phagosome

71
Q

What are the ROS that the body uses in defense?

A 
superoxide
hydrogen peroxide
singlet oxygen
hydroxyl radical
Hypohalite (OCl)
72
Q

How have bacteria evolved to avoid the ROS that the body produces?

A

expression of enzymes like catalase

73
Q

How is superoxide produced in the body?

A

Via NADPH oxidase

74
Q

What happens when individuals lack NADPH oxidase?

A

Developed chronic granulomatous disease (CGD), where they are more susceptible to bacterial infections

75
Q

What type of cells express NADPH oxidase?

A

PMNs (neutrophils)

76
Q

How are toxic nitrogen oxides produced?

A

from activated macrophages especially following macrophage activation with proinflammatory cytokines such as TNF.

77
Q

What is the enzyme that is produced by both macrophages and epithelial cells that breaks down bacterial cell walls?

A

Lysozyme

78
Q

What are cytokines? What is the effect on macrophages?

A

Cell signalling molecules

Upregulates NO production, and the killing capacity of macrophages

79
Q

What is IL-12?

A

a cytokine released by macrophages that activates otherc ells types, such and lymphocytes

80
Q

What are natural killer cells?

A

Large granular lymphocytes that are important in killing of virally infected cells and tumor cells

81
Q

When are natural killer cells particularly important?

A

early stages of viral infection prior to induction of adaptive immune response

82
Q

NK cell inhibitory receptors bind to what molecules?

A

MHC class I

83
Q

What are MHC Class I molecules?

A

A molecule that is expressed on all healthy nucleated cells, and prevents killing by natural killer cells

84
Q

What happens to MHC Class I molecules as a cell becomes infected?

A

Downregulated, leading the virally infected cell or tumor cell susceptible to killing by NK cells

85
Q

What is Fcγ receptor III (CD16)?

A

A receptor for natural killer cells that binds to antibody (IgG) that binds to target cells

86
Q

What is the process through which natural killer cells kill infected cells?

A

antibody dependent cell mediated cytotoxicity (ADCC)

87
Q

What is perforin?

A

A protein found in NK cell granules that is released when prompted, and kills target cells

88
Q

What are granzymes?

A

Granule proteins that translocate into the cytosol of a NK cell’s target, and cause programmed cell death

89
Q

What is cytokine IL-2?

A

A cytokine that activated NK cells to kill, turning them into lymphocyte activated killer cells (LAK)

90
Q

What are lymphocyte activated killer cells (LAK)?

A

NK cells that have been activated by IL-2, and kill tumor cells

91
Q

What is cytokine IL-12?

A

Cytokine produced by activated macrophages, and stimulates NK cells to produce interferon γ which is the most potent macrophage activating cytokine

92
Q

How do NK cells cells facilitate macrophage activation and killing of phagocytosed micro-organisms?

A

Via interferon γ

93
Q

What are the three types of innate lymphoid cells?

A

ILC1, 2, and 3

94
Q

What is the function of innate lymphoid cells?

A

Produce specific cytokines

95
Q

What are the three main effector functions of complement?

A

Opsonization
Leukocyte migration
Lysis of pathogens

(Therefore, when a microbe enters the body, the complement system facilitates clearance of the microbe by enhancing phagocytic clearance, recruiting additional leukocytes to the site of infection, and directly killing the pathogen. )

96
Q

The complement opsonins are large proteolytic fragments of what?

A

complement components C3b and C4b

97
Q

What is the function of C3b and C4b?

A

covalently attach to the surface of pathogens via a reactive thioester bond to opsinify it

98
Q

Do NK cells specifically recognize antigen that causes disease?

A

No–only the virus infected cells

99
Q

What stimulates keuocyte migration?

A

Chemicals called chemokines

100
Q

What are the complement chemokines?

A

Anaphlyatoxins

101
Q

What is C3a?

A

A chemokine that triggers leukocyte recruitment

102
Q

What is C3b?

A

an opsonin that stimulate phagocytosis

103
Q

What is C3?

A

Precursor to C3a/b, and is central to all complement pathways

104
Q

What is the mechanism by which lysis of pathogens can be brought about?

A

The terminal components of complement: C5, C6, C7, C8 and C9 form a pore in the membrane of pathogens (mostly Gram-negative bacteria) resulting in lysis of pathogens

105
Q

What are the three pathways through which complement is activated?

A
  1. Classical
  2. Alternative
  3. Lectin
106
Q

What is the result of all three complement activation pathways?

A
  1. opsonization
  2. leukocyte recruitment
  3. pathogen lysis
107
Q

Where do the three pathways of complement activation converge? What happens next?

A

At C3, which is cleaved by C3 convertase into C3a and C3b

108
Q

C3b also associates with the C3 convertase to form what?

A

a C5 convertase which cleaves C5 into C5a and C5b

109
Q

What is the function of C5b?

A

C5b remains associated with the microbial surface to form the membrane attack complex

110
Q

What is the classical complement activation pathway?

A

Initiated by antibodies to produce C1.

111
Q

What is C1?

A

The complement activating protein in the classical pathway,consisting of the recognition component, C1q, and two molecules each of the serine proteases C1r and C1s.

112
Q

How it the lectin pathway initiated?

A

Sugar residues on microbes are recognized and start the pathway, leading to

113
Q

Will free antibodies activate the complement cascade?

A

No

114
Q

Which is more effective at activating the classical pathway, IgM or IgG?

A

IgM

115
Q

What is the initiation component of the classical complement pathway?

A

C1

116
Q

Where does the alternative complement pathway take place? When does it occur?

A

On the microbial surface

Happens constitutively, but the C3 will be degraded if there are no bacteria around

117
Q

What is the effect of the regulator protein CD59?

A

prevents the binding of C9 such that the membrane attack complex cannot form

118
Q

What is the effect f decay accelerating factor?

A

dissociates the C3 convertases to prevent all effector functions of complement

119
Q

What is paroxysmal nocturnal hemoglobinuria? What causes it?

A

A condition where there is intravascular lysis of red blood cells by complement.

This is caused by deficiencies in either CD59, or decay accelerating factor

120
Q

What is the inhibitor for the classical complement activation?

A

C1 inhibitor

121
Q

What is the activator protein for the alternative pathway?

A

C3

122
Q

What are the activator proteins for the lectin pathway?

A

MASP1 and 2

123
Q

What is hereditary angioneurotic edema (HAE?) What causes it?

A

A condition where there is swelling of skin and larynx which can be potentially life threatening.

This is caused by a deficiency in C1 inhibitor

124
Q

Deficiencies in C1, C2, C4 or other early classical complement pathway components leads to what?

A

Autoimmune diseases, like lupus

125
Q

Deficiencies in early components of the lectin pathway results in what?

A

increased susceptibility to bacterial infection

126
Q

Deficiency in Factor D and Factor P, early components of the alternative pathway leads to what?

A

increases susceptibility to infection with pyogenic bacteria and Neisseria

127
Q

Deficiency in C3 affects all three complement pathways and leads to what?

A

increased susceptibility to pyogenic bacteria and Neisseria

128
Q

Deficiency in the terminal components of complement, C5b- 9, results in what?

A

The inability to generate the membrane attack complex and increased susceptibility to Neisseria infection.

129
Q

Can cytokines act at a distance?

A

Yes

130
Q

What is the main method of communication in the immune system?

A

Cytokines

131
Q

What is IFNγ?

A

Cytokine produced by activated T-cells to promote macrophage activation

132
Q

What is IL-12?

A

A cytokine produced from activated macrophages that causes NK cells to make more IFNγ

133
Q

Type 1 interferon (IFN) is composed of  and  IFN and is produced in response to viral infection. What are its effects? (3)

A
  • Inhibit viral replication via a paracrine action.
  • Enhance the cytolytic capability of NK cells
  • Increase cellular expression of class I MHC molecules (Class I MCH is important for host defense against viral infection.)

Immuno (16 decks)

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