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Immunology > Module 2 Lectures and Chapter 2 > Flashcards

Module 2 Lectures and Chapter 2 Flashcards

1
Q

What are the four kinds of anatomic barriers?

A
  • Structural
  • Mechanical
  • Chemical
  • Microbiological
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2
Q

What are the five symptoms of inflammation?

A
  • Redness
  • swelling
  • heat
  • pain
  • loss of function.
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3
Q

What are the five categories of innate immunity?

A
  • Anatomic barriers
  • inflammation
  • phagocytosis
  • compliment system
  • cell mediated toxicity.
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4
Q

Why does inflammation cause pain?

A

The sensitization of local nerve endings.

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5
Q

What causes the redness and heat of inflammation?

A

Mast cells and macrophages that stimulate capillary endothelial cells to dilate the blood vessels and increase blood flow.

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6
Q

What are four benefits of acute inflammation?

A
  • Delivery of O2 and clotting factors that heal wounds
  • Infiltration of phagocytes that destroy pathogens
  • Sensitization of the nervous system that alerts host to the infection
  • Initiation of the adaptive response
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7
Q

What are two consequences of acute inflammation?

A

Pain and loss of function

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8
Q

What are four risks of acute inflammation?

A
  • Permanent tissue damage
  • Widespread inflammation leading to death
  • Hypersensitivity induced pathology
  • Autoimmunity and allergies
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9
Q

What is phagocytosis?

A

The process by which microorganisms and debri are engulfed in phagocytosis vesicles, fuse with lysosomes and are degraded.

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10
Q

What are the four leukocytes that are also phagocytic?

A

Neutrophils, monocytes, macrophages and dendritic cells

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11
Q

Which leukocyte is the most prolific of the phagocytes?

A

Neutrophils

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12
Q

How many circulating protein sets make up the compliment system?

A

30

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13
Q

What are the three activation pathways of the complement system?

A

Alternative, lectin and classical

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14
Q

What are the three key effector functions of the complement system?

A

Cytolysis of target cells
Enhanced phagocytosis
Induction of inflammation

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15
Q

What is cytolysis of target cells?

A

Membrane attack complex (MAC) forms pores on target cell causing them to burst.

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16
Q

What is enhanced phagocytosis?

A

Opsonization, where products of the complement system coat the pathogen surface.

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17
Q

How is inflammation induced?

A

Anaphylatoxins induce the response

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18
Q

What is cell mediated cytotoxicity?

A

When cells kill other cells

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19
Q

What is the difference between direct and indirect cell mediated cytotoxicity?

A

Direct destruction of a pathogen vs self induced death through apoptosis

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20
Q

How do the cells of the innate immune response recognize pathogens?

A

By carrying a fixed set of non variable receptors that recognize the general structure of microorganisms.

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21
Q

What are PAMPs?

A

Pathogen associated molecular patterns that alert immune cells to destroy the pathogen.

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22
Q

What are PRRs?

A

Pathogen recognition receptors that are used by the innate immune cells to detect bacteria and viruses.

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23
Q

What three classes of pathogen recognition receptors (PRRs)?

A
  • Toll like receptors (TLRs)
  • RIG I like receptors (RLRs)
  • NOD like receptors (NLRs)
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24
Q

What are DAMPs?

A

Danger associated molecular patterns that are released by damaged or dying self cells and activate the innate immune response.

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25
Q

How was the Toll gene originally discovered?

A

A fruit fly in a German lab studying fruit fly development

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26
Q

What does the Toll gene do?

A

Recognizes fungal pathogens

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27
Q

How are Toll Like Receptors (TLRs), expressed?

A

Through the plasma membrane where they can detect microbial surface molecules or endosomal receptors where they can detect microbial DNA or RNA.

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28
Q

How many Toll Like Receptors (TLRs) are there in humans?

A

At least 10

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29
Q

How is the specificity and diversity of antigen specific receptors developed in the adaptive immune system?

A

Gene rearrangement during B and T cell development

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30
Q

Where do antibodies come from?

A

They are secreted B cell receptors (BCR) that come from B cells

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31
Q

What are antibodies made up of?

A

Four polypeptide chains, two heavy and two light, with two identical antigen binding sites at the end of each light chain.

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32
Q

What are the two steps of Ag (antigen) recognition for TCRs (T cell receptors)?

A
  1. Antigen processed into small pieces that serve as peptide antigens
  2. Peptide antigens presented in MHC molecules on antigen presenting cells active T cells
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33
Q

What are the two types of Major Histocompatibility complex (MHC) molecule?

A 
MHC class 1: presents antigens to cytotoxic T cells
MHC class 2: presents antigens to helper T cells
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34
Q

What are the two premises that underlie global selection?

A
  1. Each B and T cell is unique to Ag

2. Specificity is determined before contact with Ag

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35
Q

What is the process of clonal selection?

A

A large number of lymphocytes are made and circulated. Most remain silent and die. Those that interact with an antigen proliferate and make memory cells.

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36
Q

What happens during primary response activation in the adaptive immune system?

A

The response is delayed and weak. Clonal proliferation happens, B cells are activated, antibodies will be secreted and live for a few weeks. Memory cells made that live for years.

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37
Q

What happens during a secondary innate immune response?

A

Memory cells that are made from primary response become activated, differentiate and the response is rapid and more intense.

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38
Q

What are the three regions of epithelial tissues that serve as physical barriers against pathogens?

A

Digestive, respiratory and urogenital tracts

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39
Q

Which serves as a larger/richer habitat for microbes. The mucosal surface or skin?

A

Mucosal surface

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40
Q

What is a pathogen?

A

A collection of organisms that exploit the human body.

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41
Q

How are extracellular infections addressed by the immune system?

A

They are attacked by the solvable secreted molecules of the immune system between cells.

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42
Q

How are intracellular infections addressed?

A

The immune system kills the host cells and exposes the pathogen to the soluble secreted molecules.

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43
Q

Where are the soluble proteins of the complement system made?

A

The liver

44
Q

Where is the complement system present?

A

Blood, lymph and extracellular fluids

45
Q

What does complement do?

A

Coats the surface of pathogens for easy phagocytosis

46
Q

What kinds of pathogens are most resistant to phagocytosis?

A

Bacteria with thick polysaccharide capsules

47
Q

What are zymogens?

A

Functionally inactive complement components

48
Q

What family of enzymes do the complement system belong to?

A

Serine proteases, which includes digestive enzymes chymotrypsin and trypsin

49
Q

Which of the 30 complement proteins is most important?

A

C3, without it host suffers successive severe infections

50
Q

What kind of bond is stabilized in the hydrophobic interior of C3?

A

High-energy thioester bond

51
Q

What do all three complement pathways have in common?

A

All trigger C3 to cleave into C3a and C3b, and C3b to bind to the pathogen’s surface for phagocytosis and effector recruitment

52
Q

What order were the complement pathways discovered in?

A

Classical
Alternative
Lectin

53
Q

What order do the complement pathways work in?

A

Alternative
Lectin
Classical

54
Q

Where are the soluble proteins of the complement system made?

A

The liver

55
Q

Where is the complement system present?

A

Blood, lymph and extracellular fluids

56
Q

What does complement do?

A

Coats the surface of pathogens for easy phagocytosis

57
Q

What kinds of pathogens are most resistant to phagocytosis?

A

Bacteria with thick polysaccharide capsules

58
Q

What are zymogens?

A

Functionally inactive complement components

59
Q

What family of enzymes do the complement system belong to?

A

Serine proteases, which includes digestive enzymes chymotrypsin and trypsin

60
Q

Which of the 30 complement proteins is most important?

A

C3, without it host suffers successive severe infections

61
Q

What kind of bond is stabilized in the hydrophobic interior of C3?

A

High-energy thioester bond

62
Q

What do all three complement pathways have in common?

A

All trigger C3 to cleave into C3a and C3b, and C3b to bind to the pathogen’s surface for phagocytosis and effector recruitment

63
Q

What order were the complement pathways discovered in?

A

Classical
Alternative
Lectin

64
Q

What order do the complement pathways work in?

A

Alternative
Lectin
Classical

65
Q

How do the two classes of complement control proteins regulate C3d deposition?

A

One class compounded plasma proteins that interact with C3b attached to cell surfaces

The other includes membrane proteins on human cells that prevent fixation

66
Q

What does Pepperdine (factor P) do?

A

Increases speed/power of complement activation by binding C3 convertase C3bBb on pathogen surface and prevents degradation by proteases

67
Q

How does factor H counter the effect of properdin?

A

It decreases C3 by binding to C3b and causing plasma serine protease factor I to cleave and form iC3b which cannot assemble a C3 convertase

68
Q

How does decay-accelerating factor (DAF) regulate complement?

A

DAF binds to C3b part of alternative C3 convertase casting dissociation and inactivation

69
Q

How does membrane cofactors protein (MCP) regulate complement?

A

MCP functions similar to DAF and factor H but binds to C3b and causes cleavage and inactivation by factor I

70
Q

How do some bacteria hide from complement?

A

By covering themselves in suspicion acid to mimic human cells - when C3b is deposited it is inactivated by factor H binding to the bacterial suspicion acid

71
Q

What are made of complement control protein (CCP) modules?

A

DAF, MCP and Factor H, all in varying numbers of CCP modules

72
Q

What is a complement control protein (CCP) module made up of?

A

60 amino acids folded into a sandwich made of two slices of beta-pleated sheets stabilized with two conserved disulfide bonds

73
Q

What are regulators of complement activation (RCA)?

A

DAF, MCP and Factor H, all proteins made of CCP modules

74
Q

What is the result of regulatory proteins determining C3b deposition?

A

Distinguishing self from non-self by ensuring deposition on pathogens and not human cells.

75
Q

What are macrophages?

A

Mature forms of circulating monocytes that have moved from the blood to tissue. Phagocytes that are a part of innate and adaptive immunity.

76
Q

What are Kupffer cells?

A

Phagocytic macrophage cells found in the liver to help in processing red blood cells.

77
Q

What is opsonization?

A

Improved phagocytosis through the process of costing the pathogen with proteins.

78
Q

What does complement receptor 1 (CR1) do?

A

Some protect the cell by distrusting C3 convertase by making C3b susceptible to factor I and the rest engage C3b fragments on the pathogen to facilitate opsonization.

79
Q

What do complement receptor 3 (CR3) and complement receptor 4 (CR4) do?

A

They serve as ligands for CR3 and CR4 to facilitate phagocytosis by binding to iC3b fragments on microbial surface.

80
Q

How do complement receptors work best?

A

CR1, CR3 and CR4 work best together rather than individually at inducing phagocytosis.

81
Q

What is the most important product of complement activation?

A

C3b bonded to pathogen surfaces

82
Q

What are the terminal complement components that make up the membrane attack complex (MAC)?

A

C5, C6, C7, C8 and C9

83
Q

What is the function of MAC protein C5?

A

On activation, soluble C5b fragment initiates assembly of MAC

84
Q

What is the function of MAC protein C6?

A

Binds and stabilizes C5b forming the binding site for C7

85
Q

What is the function of MAC protein C7?

A

Binds to C5b6 and exposes hydrophobic region that attaches to cell membrane

86
Q

What is the function of MAC protein C8?

A

Binds to C5b67 and exposes hydrophobic region that inserts into cell membrane

87
Q

What is the function of MAC protein C9?

A

Polymerization on the C5b678 complex to form membrane-spanning channel that disrupts cell integrity and results in cell death

88
Q

How do S protein, cluster in and factor J regulate terminal complement components in human cell interactions?

A

These soluble proteins prevent C5b with C6 and C7 proteins from attaching to human cell membranes

89
Q

How do homologous restriction factors (HRF) and CD59 (protectin) regulate terminal complement component interaction with human cells?

A

These human cell surface proteins prevent C9 recruitment by complexes of C5b, C6, C7 and C8

90
Q

When C3 and C5 are cleaved into larger C3b/C5b and smaller C3a/C5a, what is the function of the smaller fragments?

A

C3a and C5a are anaphylatoxins that

  • Can cause anaphylactic shock
  • smooth muscles contract
  • degranulate mast cells and basophils
  • release histamines
  • Increase capillary permeability
91
Q

How does C5a protein work on neutrophils and monocytes?

A
  • Increases adherence to blood vessel walls
  • Chemoattractant directs migration towards complement fixation sites
  • Raises expression of CR1 and CR3 on pathogen surfaces for increased phagocytic potential
92
Q

What are antimicrobial peptides?

A

Soluble effector molecules of the innate immune system

93
Q

What are defensins

A

A major family of human antimicrobial peptides

94
Q

What are defensins made up of?

A

35-40 amino acids rich in arginine residues with three intra-chain disulfide bonds

95
Q

What are alpha defensins?

A

Defensins secreted by Panera cells of the small intestine. There are six types coded for with 2-14 alpha-defensin gene copies.

96
Q

What are beta-defensins?

A

Defensins produced by epithelial cells, respiratory tract and urogenital tract. There are four types of beta-defensins codes for by 2-12 gene copies.

97
Q

What determines the amount of defensin proteins a person makes?

A

The number of gene copies. 2-14 for alpha defensins and 2-12 for beta defensins.

98
Q

What does it mean that defensin molecular dare amphipathic?

A

That they have both hydrophobic and hydrophilic regions on its surface that help it penetrate pathogen’s membranes.

99
Q

What are the plasma proteins of innate immunity that bind and target microorganisms for phagocytes?

A

Pentraxins circulating in the blood and lymph

100
Q

What is the primary mechanism of pentraxins?

A

They serve as a bridging molecule that connects pathogens to human cell surface receptors

101
Q

What binds to the same phagocytic surface receptors as antibodies?

A

Pentraxins

102
Q

What are short pentraxins?

A

They are made by hepatocytes in the liver and represented by serum amyloid P component (SAP)

103
Q

What are long pentraxins?

A

They are made by myeloid, endothelial and epithelial cells and represented by PTX3

104
Q

What provides the larger surface are for commensal microorganisms?

A

The skin

105
Q

What is the inactive form of an enzyme that participated in complement activation?

A

Zymogen

106
Q

What is the primary role of the complement control protein that operates in the early stage of complement activation?

A

It ensures that C3b is deposited on the correct surfaces

107
Q

Where do Panera cells reside?

A

The crypts of the intestinal tract

Immunology (11 decks)

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