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PCB3233 Immunology > Exam 2 Study Guide (Chapters 3 and 4) > Flashcards

Exam 2 Study Guide (Chapters 3 and 4) Flashcards

1
Q

How can you tell the difference between cytokines and chemokines?

A

Chemokines initiate acute-phase reactions and anaphylactic responses (ex. C3a and C5a)

Cytokines induce anti-inflammatory factors.

ALL chemokines are cytokines but not all cytokines are chemokines.

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2
Q

Which leukocyte is generally responsible for producing and releasing cytokines?

A

Macrophages

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3
Q

What does PRR stand for?

A

Pattern Recognition Receptors

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4
Q

What does PAMPS stand for?

A

Pathogen Associated Molecular Patterns

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5
Q

What recognizes which? (PRR and PAMPS)

A

PRRs recognizes PAMPS

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6
Q

Which is found on leukocytes?

A

PRRs (Pattern Recognition Receptors)

PRRs on leukocytes bind to PAMPS on pathogens

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7
Q

Which is found on pathogens?

A

PAMPS (Pathogen Associated Molecular Patterns)

PRRs on leukocytes bind to PAMPS on pathogens

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8
Q

When a macrophage acts as a phagocyte, what events are involved? (Hint: receptor-mediated endocytosis)

A

Binding of phagocytic receptors. Pathogen becomes enveloped and is turned into a phagosome vesicle, joined by a lysosome-phagosome, lysosome contains enzymes and toxic substances to destroy pathogen.

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9
Q

The four Gram-positives & Gram-negatives

A

Gram Positives: Bacillus, Staphylococcus aureus, Streptococcus, Mycobacterium (kinda)

Gram Negatives: LPS (lipopolysaccharide), E. coli, Pseudomonas, Salmonella, Shigella

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10
Q

When the mannose receptors are engaged, what mechanism is initiated in a phagocyte?

A

Activates Lectin complement cascade, binds to particular carbohydrates NOT found on human cells.

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11
Q

When the CR3 and CR4 receptors are engaged, what mechanism is initiated in a phagocyte?

A

Recognize iC3b and LPS (gram negative bacteria).

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12
Q

When the scavenger receptors are engaged, what mechanism is initiated in a phagocyte?

A

Preferences for neg. charged molecules, such as: Nucleic acids, gram positive bacteria, and gram negative bacteria

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13
Q

When TLR receptors are engaged, what mechanism is used in a macrophage?

A

Signals macrophages to secrete cytokines

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14
Q

What does TLR-3 bind to?

A

Double strand viral RNA

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15
Q

What does TLR-7 bind to?

A

single strand viral RNA (remember Seven starts with an S for Single)

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16
Q

What does TLR-4 bind to?

A

LPS (lipopolysaccharide)

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17
Q

What does TLR-5 bind to?

A

bacteria flagella (remember Five starts with an F for Flagellum)

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18
Q

What type of microorganism(s) does TLR-3 recognize?

A

recognizes double stranded viral RNA

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19
Q

What type of microorganism(s) does TLR-7 recognize?

A

recognizes single strand viral RNA

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20
Q

What type of microorganism(s) does TLR-4 recognize?

A

recognizes gram negative bacteria

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21
Q

What type of microorganism(s) does TLR-5 recognize?

A

recognizes bacteria

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22
Q

What location of the cell are TLR-3 receptors found?

A

inside the cell, on endosomes

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23
Q

What location of the cell are TLR-7 receptors found?

A

inside the cell, on endosomes

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24
Q

What location of the cell are TLR-4 receptors found?

A

outside the cell, on plasma membrane.

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25
Q

What location of the cell are TLR-5 receptors found?

A

outside the cell, on plasma membrane

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26
Q

Extracellular components of TLR-4 signaling mechanism

A

LBP, LPS, CD14, MD2, and TLR4

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27
Q

Order of TLR-4 signaling mechanism

A

LPS –> LBP –> CD14 –> MD2 –> TLR-4

*Note: If Weigel asks about what the TLR4 complex is it is TLR4, MD2 and CD14

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28
Q

Intracellular components of TLR-4 signaling mechanism

A

MyD88, IKK, IκB, and NFκB

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29
Q

MyD88

A

adaptor protein. Is what allows assembly of (see above) cascade to commence.

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30
Q

IKK

A

inhibitor of KappaB Kinase. Leads to phosphorylation of inhibitor KappaB which leads to degradation of IkB.

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31
Q

NFkB

A

translocation of TF nuclear factor kB from cytoplasm—>to nucleus for inflammatory cytokines.

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32
Q

What type of bacteria (Gram-pos. or Gram-neg.) would the tissue be infected with?

A

Gram negative

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33
Q

What is the general term given to these 5 gene products? (Hint: two-part name; includes what they result in, along with what type of molecules they are)

A

General term: inflammatory cytokines

IL-6, IL-12, TNF-A, CXCL8 and CCL2 (are chemokines)

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34
Q

What are the 5 genes that are transcribed as a result of TLF-4 recognition?

A

IL-6, IL-12, TNF-A, CXCL8 and CCL2 (are chemokines)

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35
Q

Effects of IL-6

A

signals hepatocytes (liver) to produce acute-phase reactants (MBL and CRP) + increase body temp.

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36
Q

Effects of IL-12

A

produces IFN-gamma which activates macrophages (when a NK cell is activated near IL-12)

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37
Q

Effects of TNF-alpha

A

Raise temp, increased permeability; so effector cells can enter infected tissues.

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38
Q

Effects of CXCL8

A

Recruits neutrophils to the site of infection. NK cells follow gradient in order to find infection.

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39
Q

Effects of CCL2

A

Recruits macrophages to the sit of infection, NK cells follow gradient in order to find infection.(Does exactly the same thing as CXCL8 but recruits macrophages instead of neutrophils)

40
Q

What genes of the 5 that are transcribed as a result of TLR-4 recognition are CHEMOKINES?

A

CXCL8 and CCl2 are chemokines because of the double C’s in name. They direct traffic in a concentration dependent way from weakest—>strongest.

41
Q

What are the four major characteristics of inflammation?

A

Pain, swelling, heat and redness

42
Q

What is the cellular location of NOD-like receptors (NOD-1 and NOD-2)?

A

Cytoplasm

43
Q

What does NOD-1 recognize?

A

Degradation of product of gram NEGATIVE bacteria.

44
Q

What does NOD-2 recognize?

A

Degradation of most bacteria

45
Q

How do these receptors (NOD-1 and NOD-2) complement the membrane bound TLRs? (Hint: what part of the cell is being recognized?)

A

Detects products derived from the intercellular degradation of phagocytosed pathogens.

46
Q

Which is long-lived? Which is short-lived? (Macrophages and Neutrophils)

A

Macrophages are long-lived

Neutrophils are short-lived

47
Q

Where do macrophages reside?

A

In tissues

48
Q

Where do neutrophils reside?

A

In blood

49
Q

What is considered the most abundant leukocyte?

A

Neutrophils

50
Q

Which is first to appear at the site of infection, macrophages or neutrophils?

A

Macrophages are the first to appear at the site of infection

51
Q

Do macrophages recognize the cell-surface carbohydrates of bacterial cells, human cells, or both?

A

Macrophages recognize the cell-surface carbohydrates of BACTERIAL CELLS

52
Q

Are macrophages unique to innate immunity, adaptive immunity, or both?

A

Macrophages are involved in BOTH innate and adaptive immunity

53
Q

What cellular process are macrophages notable for enhancing and how? (Hint: involves their surface receptors)

A

Enhances phagocytosis by using surface receptors.

54
Q

What other name are neutrophils also known by? (Hint: think about their morphology)

A

Polymorphonuclear leukocytes (PMNs)

55
Q

Three primary jobs of neutrophils (their roles/responsibilities during an innate immune response)

A

Recognition, Phagocytosis, and Destruction

56
Q

Are neutrophils included in healthy tissues or are they excluded from them? Why might this be?

A

Neutrophils are excluded from healthy tissues, the release of inflammatory cytokines by macrophages is what attracts them.

57
Q

How do neutrophils carry out and achieve phagocytosis?

A

Fc receptors bind to antibodies and complement components bind to the complement to make opsonins. Neutrophils bind and engulf bacteria and destroy them. Ultimately being phagocytosed by macrophages.

58
Q

The names of granules (they contain antimicrobials)

A

Primary (azurophilic)
Secondary (specific)
Tertiary (gelatinase)

59
Q

Understand what the “Inflammatory Response” is, why it happens, and how it happens.

A

The inflammatory response is what occurs when an infection is taking place. It causes increase in vasodilation and permeability so soluble molecules can enter the tissues and try to halt the pathogen from spreading any further (caused by the release of cytokines).

60
Q

Four classes of leukocyte adhesion molecules:

A

Selectins, Vascular addressins, Integrins, and Immunoglobulin superfamily

61
Q

What classes of leukocyte adhesion molecules bind to each other?

A

Selectins and Vascular addressins

Integrins and Immunoglobulin superfamily

62
Q

What do L-selectins bind to?

A

CD34
GlyCAM-1
MAdCAM-1

63
Q

What does LFA-1 bind to?

A

ICAM-1

64
Q

Four steps of extravasation

A

Rolling adhesion –> Tight binding –> Diapedesis –> Migration to infection site

65
Q

Overall purpose/goal of extravasation

A

Basically, it’s the movement of leukocytes out of the circulatory system and into the site of infected tissue.

66
Q

What cytokines/chemokines are involved in extravasation?

A

Cytokines: IL-1, TNF-alpha

Chemokines: CXCL8 (of neutrophils) CCL2 (of monocytes)

67
Q

Are leukocyte adhesion molecules involved in extravasation?

A

Yes; LFA-1 and ICAM-1

68
Q

Understand why neutrophils utilize respiratory burst and how it arises.

A

Respiratory burst increases oxygen consumption so the pH of the phagosome is raised. This in turn will cause neutrophils to release granules and activate itself so it can kill the pathogen.

69
Q

Respiratory burst (definition)

A

Transient increase in oxygen consumption = purpose is to raise the pH of the phagosome so the granule contents can become active to kill pathogen

70
Q

What enzymes are involved in respiratory burst?

A

NADPH oxidase = NADPH + O2

Superoxide dismutase = 2H+ + 202

Catalase = 2H2O2

71
Q

How is potential damage from the process of respiratory burst limited?

A

We transform hydrogen peroxide into water +oxygen = 2H2O2 —catalase—> 2H2O +O2

72
Q

What is Netosis?

A

a way neutrophils die that leads to capture and destruction of the pathogen

Neutrophils nucleus swells and ruptures, leaving behind granules, DNA, and histones (sticky part). This will trap anything that comes through and allows for defensins to bind and poke holes in the pathogen.–> Nets

73
Q

NET’s (neutrophil extracellular traps)

A

The neutrophil’s nucleus swells and leads to the cell bursting (netosis) leaving behind all the antimicrobial components of the granules as well as DNA and histones that serve to trap the pathogen.

74
Q

What cytokines/chemokines are involved in acute phase response?

A

Cytokines: IL-1 beta, IL-6, TNF-alpha (slide 47)

Chemokines: CXCL-8 and CCL-2

75
Q

Know the acute phase proteins we discussed (exclude serum amyloid A). What two major things are these proteins able to do/perform?

A

*MBL and *CRP

Both act as opsonins regardless of its complement activity and initiate complement activation .

76
Q

What is the role of hepatocytes? What stems their activation?

A

Their role is to produce acute-phase reactants. Il-6 increases temp + activates hepatocytes.

77
Q

What cell(s) can produce interferon?

A

ALL NUCLEATED CELLS can produce interferon type 1

78
Q

What is the main cell of innate immunity activated by Type I interferon is?

A

Activates NK cells

79
Q

What two major isotypes are associated with Type I interferon?

A

IFN-alpha and IFN-beta

80
Q

What do Type I interferons interfere with?

A

Interfere with viral replication

81
Q

What are the three major functions of Type I interferons?

A

1) Interfere with viral replication
2) Alert immune system
3) Make infected cells > vulnerable to lymphatic attacks

82
Q

Type II interferons are primarily linked to activated of what cell type?

A

Macrophages

83
Q

_____ is the isotype associated with Type II interferon, secreted by what cell type?

A

IFN-gamma; IFN-gamma is the cytokine produced by NK cells. Also known as Type II interferon

84
Q

Where do NK (natural killer) cells reside?

A

NK cells reside in blood

85
Q

Where is NK migration to and when does this occur?

A

Migrate to the site of infection when called upon by macrophages.

86
Q

CD3 and CD56: NK cells express _____ but lack ______

A

NK cells express CD56 but lack CD3

87
Q

What are NK cells two effector functions?

A

*Cell killing: IF NK cells activated in presence of IFN-alpha or IFN-beta lead to them releasing cytotoxins. Induces apoptosis of infected cells.

88
Q

What interferons are involved in NK cells?

A

*Secretion of cytokines: If NK cells are activated in presence of IL-12 will activate IFN-gamma which activate macrophages.

89
Q

Know the type of infection NK cells typically fight against and what type of response will be generated as a result. (Hint: NK cell cytotoxicity)

A

Fight against intracellular (Viral) infections. This will cause the interferon response to take place; IFN alpha and IFN beta will cause cytotoxic effector function while IL-12 will cause the NK cells to produce cytokines (IFN gamma).

90
Q

NK cells secrete ______ (cytokine) to activate _______ (cell type).

A

NK cells secrete IFN-gamma (cytokine) to activate macrophages (cell type).

91
Q

Activation, proliferation, and differentiation of NK cells is driven by what cell type?

A

Type I Interferon drives: activation, proliferation and differentiation of NK cells.

92
Q

NK-cell receptors: inhibitory vs. activating

A

IFN-gamma activates NK cells to activate their cytotoxic capabilities.`
MIC-a and MIC-b are activating ligands
HLA-E are inhibitory ligands.

93
Q

What happens to virally infected dendritic cells when they’re outnumbered by NK cells?

A

When the infected dendritic cells are outnumbered by NK cells, the NK cells are cytotoxic to the dendritic cells. (Adaptive immune response not needed)

94
Q

What happens to virally infected dendritic cells when they outnumber NK cells?

A

When infected dendritic cells are outnumbered by NK cells, the NK cells signal the dendritic cells to migrate to the nearest secondary lymphoid tissue to activate the adaptive immune system.

95
Q

What proteins/molecules/enzymes are involved in the initiation step of each?

A

Alternative: Factor D cleaves Factor B Classical: C1s Lectin: MASP-2

96
Q

List the complement convertases and their components from each pathway

A

C3 convertase:
Alternative: C3bBb
Classical + Lectin: C4b2a

C5 convertase:
Alternative: C3b2Bb
Classical + Lectin: C4b2acb

97
Q

Write or draw out all 3 cascade pathways. (This will help you to remember the order of cleavage and attachment for all the components involved in each pathway.)

A

C2a and Bb no protease activity until cut. Bb cleaved by factor D. C2a cleaved by C1s or MASP-2

MASP-2 cleaves C2 and C4, leading to classical C3 convertase formation.

Classical pathway initiated by antibodies. 1 IgM or 2 IgG bound by C1q leads to C1r activation and cleaving of C1s. C1s cleaves C2 and C4 similar to MASP-2. All eventually lead to C3b. Any C3b, no matter which pathway initiates it, can become C3 convertase of the alternative pathway.

PCB3233 Immunology (4 decks)

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