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Immunology > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

dWhen are commensal bacteria acquired?

A

Starting at birth and the development of the immune system is influences by the microbiota

->1000 species of bacteria inhabit the human gut

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2
Q

What hydrophobic proteins are involved in host defense?

A

SP-A and SP-D

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3
Q

What pathogens induce phagocytosis by alveolar macrophages?

A

Agglutinate pathogens

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4
Q

What is unique about viruses compared to other pathogens?

A

Can replicate and assemble and kill host cell

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5
Q

What is the complement system?

A

a system of plasma proteins that mark pathogens for destruction

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6
Q

Where are soluble proteins produced in?

A

liver

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7
Q

Where are plasma proteins found?

A

found in blood, lymph, and extracellular fluids and they coat the surface of pathogens-targets for destruction

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8
Q

What does the cleavage of C3 form?

A

C3a and C3b

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9
Q

What bond is exposed after cleavage of C3b protein?

A

thioester bond

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10
Q

What happens when the thioester bond ofd C3 is attacked by water?

A

a soluble C3 protein is formed

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11
Q

What happens when the C3 protein is attacked by a carboxyl group or amine group?

A

C3 protein becomes insoluble and bounds to the pathogen surface

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12
Q

What is the first complement pathway to act and what does it do?

A

Alternative pathway and the pathogen surface creates local environment conducive to complement activation

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13
Q

What is the second complement pathway to act?

A

Lectin pathway; mannose binding lectin binds to pathogen surface

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14
Q

What is the last complement pathway to act?

A

Classical pathway; C-reactive protein or antibody binds to specific antigen on pathogen surface

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15
Q

What is the result of complementation?

A

cleavage of C3 into C3a and C3b

C3b covalently bounds to surface components of pathogen

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16
Q

what are the three fates of the complement system?

A

recruitment of inflammatory cells
opsonization of pathogens, facilitating uptake and killing by phagocytes
perforation of pathogen cell membranes

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17
Q

What inititiates the alternative pathway?

A

formation and action of the soluble C3 convertase iC3Bb

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18
Q

Is iC3Bb soluble or insoluble?

A

soluble

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19
Q

Is C3b soluble or insoluble?

A

insoluble

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20
Q

What reaction occurs between C3 and iC3?

A

spontaneous hydrolysis

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21
Q

What enzyme is responsible for the possible positive feedback?

A

iC3Bb convertase

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22
Q

What are used to control the alternative pathway?

A

regulatory proteins, they determine the extent and site of C3b deposition

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23
Q

What does properdin do?

A

Binds C3bBb, preventing degradation

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24
Q

What does Factor H do?

A

binds C3b and induces cleavage to iC3b by factor I-decreases amount of C3b on pathogen surface

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25
Q

What does DAF do?

A

binds C3b and causes dissociation and inactivation Bb fragment

MCP-binds C3b and makes it susceptible to cleavage by factor I

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26
Q

What does DAF and MCP do?

A

disrupt C3 convertase C3bBb

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27
Q

What is opsonization?

A

coating of a pathogen with protein that facilitates phagocytosis

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28
Q

Why is phagocytosis necessary?

A

Phagocytois by macrophages provides a first line of cellular defense against invading microorganisms

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29
Q

What is CR1 and why is it unique?

A

the receptor on macrophages that bind to C3b protein to initiate phagocytosis.

CR1 protects expressing cells-makes C3b susceptible to cleavage by Factor I

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30
Q

What is a Phagolysosome?

A

A fusion of lysosome and phagosome

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31
Q

How do complement proteins lyse pathogens?

A

The terminal complement proteins lyse pathogens by forming membrane pores

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32
Q

What is C5 and why is it important?

A

involved in lysing of pathogens and binds to the C3b2Bb protein on the pathogen surface

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33
Q

How is the alternative C5 convertase formed?

A

C3b binds the alternative C3 convertase= alternative C5 convertase

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34
Q

What is C5b?

A

initiates the formation of a membrane attack complex

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35
Q

What does C6 do?

A

binds to and stabilizes C5b. Forms a binding site for C7

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36
Q

What does C7 do?

A

Binds to C5b6 and exposes a hydrophobic region that permits attachment to the cell membrane

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37
Q

What does C8 do?

A

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

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38
Q

What does C9 do?

A

Polymerization on the C5b678 complex forms a membrane-spanning channel that disrupts the cell’s integrity and can result in cell death

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39
Q

What is CD59?

A

protein that binds to the C5b678 complex and prevents the recruitment of C9 to form a pore in human cells

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40
Q

What is a protectin and example?

A

protein that prevents destruction of cell integrity (eg CD59, HRF)

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41
Q

What is paroxysmal nocturnal hemoglobinuria?

A

disorder where patients cannot prevent against cell death through membrane pores

42
Q

What do small peptides do during complement activation?

A

induce local inflammation

43
Q

What are anaphylatoxins?

A

act on blood vessels to increase vascular permeability

44
Q

What leads to an increase in release of histamine and other vasoactive substances

A

contraction of smooth muscle and degranulation of mast cells and basophils

45
Q

What increase phagocytic capacity?

A

Chemoattractant for phagocytes

46
Q

What does increased permeability allowed?

A

allows increased fluid leakage from blood vessels and extravasation of complement and the plasma proteins at the site of infection

-migration of monocytes and neutrophils from blood into tissue is increased. microbicidal activity of macrophages and neutrophils is also increased

47
Q

what is the importance of alpha 2-macroglobulin and protease?

A
  1. ) the protease cleaves bait region, causing a conformational change
  2. ) alpha 2 macroglobulin enshrouds the protease and is covalently bonded to it

after conformational change, the complex will bind receptors on hepatocytes, fibroblasts, and macrophages and be cleared

48
Q

How do antimicrobial peptides kill pathogens?

A

by perturbing their membranes

  • they are amphipathic
  • charged and uncharged regions
  • secreted at mucosal surfaces-epithelial cells and neutrophils
49
Q

What are the main source of defensin in the intestine?

A

Paneth cells

50
Q

What brings defensins together?

A

electrostatic attraction and the transmembrane electric field

51
Q

What do defensins do?

A

form pores to destroy cell membrane

52
Q

What are pentraxins?

A

plasma proteins of innate immunity that bind microorganisms and target them to phagocytes

  • ‘antibodies” of the innate immune system
  • bridging molecules that bind pathogens to human cells (phagocytes)

Long Pentraxin
eg. PTX3 from monocytes, macrophages, dendritic cells, endothelial cells, epithelial cells

Short Pentraxin
eg. Serum amyloid P component from liver hepatocytes

53
Q

What are the stages of immediate innate immune response (0-4 hours)?

A
  1. ) pathogen invades tissue and proliferates
  2. ) pathogen is recognized by preformed soluble effector molecules and resident effector cells in the infected tissue
  3. ) pathogen is eliminated and infection ends
  4. ) very minor tissue damage is repaired
54
Q

What are the stages of induced innate immune response (4 hours to 4 days)?

A
  1. ) pathogen invades tissue and proliferates
  2. ) activation of cells resident in the infected tissue. Recruitment of effector cells to the infected tissue. Inflammation, fever, the acute phase response
  3. ) soluble effector molecules and effector cells recruited to the infected tissue recognize and attack the pathogen
  4. ) pathogen is eliminated and infection ends
  5. ) minor tissue damage is soon repaired
55
Q

What are the stages of the adaptive immune response (4 days until death of the pathogen, defeat of the host, or the truce of chronic disease)?

A
  1. ) pathogen invades tissue and proliferates
  2. ) secondary lymphoid tissue close to the infected tissue is made aware of the infection
  3. ) pathogen-reactive B and T cells are identified in secondary lymphoid tissue
  4. ) B and T cells proliferate and mature to become effector cells
  5. ) effector molecules (antibodies) and effector T cells travel to the site of infection
  6. ) pathogen is eliminated and infection ends
  7. ) major tissue damage is gradually repaired
56
Q

How do cells of innate immunity distinguish themselves?

A

Through receptors (over 100 receptors)

  • macrophage receptors recognize the cell-surface carbohydrates of bacterial cells but not those of human cells
  • NK cell receptors recognize changes at the surface of human cells that are caused by a viral infection
57
Q

What is unique about toll-like receptors (TLR)?

A

induces signaling while the others induce phagocytosis

58
Q

What is CTLD?

A

Carbohydrate recognition domain (C-type lectin domain)-requires calcium
-mannose receptor

59
Q

What is RTLD?

A

Ricin-type lectin domain
-recognizes sulfated galactosamine residues
mannose receptor

60
Q

What is SR?

A

scavenger receptor

- recognizes negatively charged microbial ligands

61
Q

What are toll-like receptors?

A

Family of 10 genes-TLR 1-10
TIR- toll interleukin-1 receptor
-LRR-leucine-rich repeat-20-29 aminoacids-caries-pathogen recognition domain
- Homodimer or heterodimers-TLR4 only homodimerizes

62
Q

What are allotypes?

A

proteins encoded by different alleles of the same gene

63
Q

What does TLR4 recognize?

A

LPS

64
Q

What binds LPS on the macrogphage receptor?

A

CD14

65
Q

What protein binds TLR4 and LPS?

A

MD2

66
Q

What is MyD88?

A

adaptor protein-binds TIR domain and IRAK4

67
Q

What is IRAK4?

A

autophosphorylates, then phosphorylates TRAF6

68
Q

What is IKK?

A

inhibitor of IkB- Phosphorylation releases NFkB

69
Q

What is NEMO disorder?

A

lack an IKK subunit-impaired NFkB response

abnormalities in tissues taht arisw from ectoderm

70
Q

What do NOD like receptors do?

A

recognize bacterial degradation products in the cytoplasm

71
Q

What do LRRs in NOD domain do?

A

recognize degradation products of bacteria (degraded peptidoglycan)

72
Q

What do CARDs do?

A

caspase recruitment domain

- NOD receptors DO NOT recruit caspases-recruit proteins with CARD domains

73
Q

What is RIPK2?

A

phosphorylates TAKI which phosphorylates and activates IKK-NFkB activation

74
Q

What do inflammasomes do?

A

amplify the innate immune response by increasing the production of IL-1B

75
Q

Describe the assembly of inflammasome?

A
  1. ) IL-1B binds to IL-1 R1 and IL-1 RAcP (dimerizes)
  2. ) MyD88 binds to TIR domain
  3. ) transcription and translation of IL-1B leads to pro-IL-1B
  4. ) active caspase 1 binds to pro-IL-1B
  5. ) release IL-1B

ATP release causes activation of potassium channels to decrease K+ conc. causes NLRP3 (no CARD) to bind adaptor protein with CARD -binds procaspase 1

positive feedback-loop-IL1B binds IL1R
*** adapter protein and NLRP3 and procaspase 1

76
Q

What are chemokines?

A

direct the flow of leukocytes in the body

77
Q

Where are adhesion molecules found?

A

leukocyte and tissue surface

78
Q

What is inflammation?

A

blood vessels dilate and vascular endothelial cells selectins

79
Q

What does TNF do to ICAM-1 and ICAM2?

A

increases and vascular endothial cells upregulate ICAM-1 and ICAM-2

80
Q

Describe how neutrophils attend to infected cells?

A
  • CXCL8 binding leads to changes in integrins (LFA-1)-bind ICAM1
  • basement membrane-neutrophils secrete elastase to degrade laminins and collagen
  • neutrophil follows chemical trail to source of CXCL8 in tissue (macrophages)
81
Q

CRP

A

binds pathogen-opsonin-triggers the innate immune response

-may deliver pathogens to phagocytes

82
Q

Serum amyloid amyloid A

A

interacts with HDL, binds TLRs and CD36 (induces cytokines)

83
Q

What initiates the lectin pathway?

A

the mannose-binding lectin
-binds mannose containing carbohydrates on pathogens

  • mutipotent attachment is critical
  • lectin pathway of complement activation triggered
  • opsonin- induces monocytes in blood to uptake
84
Q

What cytokine induces lectin pathway and where?

A

IL-6 and the liver

85
Q

What does C-reactive proteins bind to?

A

-CRP binds phosphocholine on bacterial surfaces, acting as an opsonin and as a complement activator

86
Q

What does mannose binding lectin bind to ?

A

binds carbohydrates on bacterial surfaces , acting as an opsonin and as a complement

87
Q

Describe lectin pathway?

A

Activated MASP-2 cleaves C4 to C4a and C4b

  1. ) C4b binds covelently to the microbial surface
  2. ) Activated MASP-2 also cleaves C2 to C2a and C2b
  3. ) C2a binds to surface C4b forming the clasical C3 convertase, C4b2a
  4. ) C4b21 binds C3 and cleaves it to C3a and C3b. C3b binds covalently to the microbial surface
88
Q

What does C4a do?

A

recruits leukocytes (weaker than C3a and C5a)

89
Q

What is the C3 convertase for lectin pathway?

A

C4b2a

90
Q

What triggers the classical pathway

A

C-reactive proteins

91
Q

What does C-0reactive protein bind to on pathogen?

A

phosphocholine

92
Q

What components make up C-1 protein?

A

C1r
C1q
C1s -binds C4 protein and cleaves into C4a and C4b

93
Q

Where is TLR3 receptor located?

A

endosomes

94
Q

Where are TLR1 and 2 found?

A

membrane or endosome

95
Q

What cells have type 1 interferon?

A

all human cells

96
Q

Describe the process of detection of viral infection?

A
  1. ) Viral replication in cytoplasm produces uncapped RNA with a 5’-triphosphate
  2. ) RLR binding to viral RNA induces association with MAVS and dimerization
  3. ) dimerization initiates signaling pathways that activate IRF3 and NFkB
  4. ) IRF3 causes synthesis and secretion of type I interferons, and NFkB causes synthesis and secretion of inflammatory cytokines
97
Q

What results from interferon response?

A
  1. ) induce resistance to viral replication in all cells
  2. ) increase expression of ligands for receptors on NK cells
  3. ) Activate NK cells to kill virus-infected cells
98
Q

What are plasmacytoid dendritic cells?

A

factories for making large quantities of type I interferons

-helps to prevent the systemic spread of infection

99
Q

What are the main circulating lymphocytes that contribute to the innate immune response?

A

Natural killer cells

  • kill cells infected with virus
  • maintain/increase the state of inflammation (increase phagocytosis)
  • CD56 positive, lack CD3
  • 5-25% of blood lymphocyte population
100
Q

Describe the NK cell cytotoxicuty at the sites virus infection?

A
  1. ) virus infection of cells triggers the interferon response
  2. ) Type I interferon drives the proliferation of NK cells
  3. ) Type I interferon drives the differentiation of NK cells into cytotoxic effector cells
  4. ) Effector NK cells kill virus infected cells by inducing them to undergo apoptosis
101
Q

Describe the NK cell cytotoxicuty at the sites virus infection?

A
  1. ) virus infection of cells triggers the interferon response
  2. ) Type I interferon drives the proliferation of NK cells
  3. ) Type I interferon drives the differentiation of NK cells into cytotoxic effector cells
  4. ) Effector NK cells kill virus infected cells by inducing them to undergo apoptosis

Immunology (7 decks)

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