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Immunology > Panic > Flashcards

Panic Flashcards

1
Q

What 2 things do phagosomes fuse to?

A

Lysosomes and granules

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2
Q

What three ways can phagosomes use to kill pathogens?

A

Enzyme degradation, antimicrobial peptides, toxic effects of reactive oxygen and nitrogen free radicals

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3
Q

How many TLRs are in mice and humans?

A

13

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4
Q

What part of the TLR dimers bind PAMPs and DAMPs?

A

The extracellular leucine rich repeats (LRRs)

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5
Q

Where are TLRs located?

A

In lysosomes/endosomes and surface bound

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6
Q

What pathways do TLRs trigger?

A

NF-kB transcription factor production
Interferon regulating factor (IRF) pathways
MAP kinase downstream transcription factors such as AP-1

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7
Q

Are C-type lectin receptors (CLRs) a heterozygous or homozygous population of surface PRRs?

A

Heterozygous

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8
Q

What part of the cell do CLRs recognize?

A

Cell wall components, such as the sugars/polysaccharides of bacteria/fungi

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9
Q

What is the structure of RLRs and where are they located in the cell?

A

RNA helicases and they are cytosolic PRRs

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10
Q

What type of molecules do RLRs recognize?

A

Double stranded viral RNAs

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11
Q

What signalling pathways do RLRs activate?

A

Interferon regulatory factors (IRFs) to trigger antiviral interferon responses
NF-kB transcription factor

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12
Q

Where are NOD-like receptors located in the cell?

A

Cytosolic PRRs

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13
Q

What does the NOD-like receptor activate?

A

Caspase-1 protease

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14
Q

What does caspase 1 cleave? Why is this important?

A

IL-1 and IL-18. Important because IL-1B is the major cytokine for inflammation

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15
Q

What 5 main things does signalling of PRRs activate the expression of (particularly in macrophages)?

A

Antimicrobial peptides
Cytokines (inflammatory IL-1, TNF-a, and IL-6)
Chemokines
Type 1 interferons (potent antiviral activity)
Enzymes (iNOS and COX2)

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16
Q

What are acute phase responses (APRs)?

A

Detectors of systemic inflammation.

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17
Q

When do acute phase responses occur?

A

After injury, trauma, or infection of a tissue.

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18
Q

What induces acute phase responses?

A

Proinflammatory cytokines (IL-1, TNF-a, and IL-6).

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19
Q

What category of cytokines do macrophages and blood monocytes secrete (generally)?

A

Pro-inflammatory

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20
Q

What is the purpose of acute phase proteins?

A

Prevent ongoing tissue damage and activate the repair process.

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21
Q

When do fever and leukocytosis occurs?

A

Systemic acute inflammation

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22
Q

What is the mechanism behind acute phase responses?

A

Increases synthesis/secretion of antimicrobial proteins from the liver (MBL, CRP, and complement components).

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23
Q

What two cytokines induce fever?

A

IL-1 and IL-6

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24
Q

What two functions do NK cells perform?

A

Kill altered self-cells

Produce cytokines that induce adaptive responses against the altered self cell.

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25
Q

During the first stages of the immune response for viruses, which cytokines and which cells do we primarily rely on?

A

IFN and NK cells.

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26
Q

What is the Fc receptor on NK cells called?

A

CD16

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27
Q

What two molecules do NK cells release into the lytic synapse?

A

Perforin and granzymes

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28
Q

What are NETs stimulated by?

A

PAMPs and cytokines

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29
Q

What two main mechanisms connect the innate and adaptive immune responses?

A

Opsonisation and complement activation

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30
Q

What are TLRs on lymphocytes used for?

A

Costimulation receptors

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31
Q

What are the three groups of PRRs?

A

Extracellular
Cell surface
Intracellular

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32
Q

What is LPS recognized by?

A

TLRs

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33
Q

What TLR recognizes bacterial parasites? What about viral dsRNA?

A

TLR2/1 and TRL3/3

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34
Q

Describe what happens during TLR signalling (in detail).

A

A PAMP or DAMP binds the LRR of the TLR dimer which causes a conformational change -> association of MyD88 to TIR domain of the TLR -> assembly of IRAK1/IRAK4 complex -> IRAK 4 phosphorylates IRAK1 -> creates docking site for TRAF6 -> IRAK1-TRAF6 complex dissociates and activates the TAK1 protein kinase complex -> leads to activation of 2 different pathways:

  • > phosphorylates IKK -> phosphorylates IkB-> siddociation of NF-kB -> translocation to nucleus to activate NF-kB dependent genes
  • > phosphorylates/activates component of the MAP kinase pathway -> MAP kinase cascade leads to transcriptional activators translocating to the nucleus and activating MAPK dependent genes (like AP-1).
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35
Q

Describe what happens during TLR signalling in general.

A

Detects PAMP -> signalling through adaptor proteins -> recruitment of ubiquitin, ligases, and kinases -> phosphorylation and ubiquitination -> activation of nuclear factors -> inflammatory gene expression

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36
Q

What does NFkB stand for?

A

Nuclear factor kappa-light-chain-enhancer of activated B cells

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37
Q

What does activation of NFkB and AP-1 lead to?

A

Expression of most immune genes

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38
Q

What does IRF do?

A

Regulates type 1 (IFNa and IFNB) antiviral interferon genes.

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39
Q

What cytokines does TLR signalling produce?

A

TNF, Pro-IL1, and anti-viral cytokines (IFNa and IFNB)

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40
Q

What does ITAM stand for?

A

Immunoreceptor tyrosine-based activation motif

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41
Q

How do CLRs signal and what is the result of the signalling?

A

Signal via ITAMs ->leads to activation/modulation of NFkB and AP-1

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42
Q

What receptor does HIV use to infect T cells?

A

CLR

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43
Q

What signalling pathways do RLRs trigger?

A

IRFs to trigger antiviral interferon responses.

NF-kB transcription factor

44
Q

What is the main purpose for RLR signalling?

A

Interfere/ shut down viral replication using interferons (interferon = interfere with viral replication)

45
Q

How does influenza avoid RLR signalling?

A

Binds and sequesters dsRNA to inhibit RLR activation

Interacts directly with RIG-I to prevent activation

46
Q

How does the Ebola virus prevent RLR signalling?

A

Inhibits IRF phosphorylation which inhibits RIG-I pathway signalling

47
Q

How does PRR signalling impact antigen presenting cells?

A

Increases MHC levels on APCs

48
Q

True or false: PRR signalling can cause complement activation?

A

True: this is stimulated by extracellular PRR binding (MBL through the lectin pathway)

49
Q

Where are CAMs/ICAMs expressed?

A

Endothelium and leukocytes

50
Q

What two molecules make up CAMs?

A

Selectins and integrins

51
Q

What are CAMs

A

Proteins on the cell surface that bind with other cells or the ECM in adhesion.

52
Q

What are the sour families of CAMs?

A

Selectins
Mucin-like
Integrins
Ig superfamily

53
Q

What is Sialyl Lewis?

A

E-selectin ligand carbohydrate

54
Q

Where is Sialyl Lewis expressed?

A

Granulocytes, activated Th1 cells, and monocytes

55
Q

What is the purpose of Sialyl Lewis?

A

Partner for selectins that bind leukocytes and endothelial cells; important in leukocyte tethering and rolling.

56
Q

Where are integrins expressed? Give an example of an integrin.

A

Expressed on leukocytes. LFA-1

57
Q

What do integrins bind to?

A

ICAMs (Ig superfamily)

58
Q

Where are ICAMs expressed?

A

Endothelium

59
Q

What provides the activating signal to neutrophils during extravasation?

A

IL-8 from the endothelium

60
Q

What is leukocyte extravasation analogous to in lymphocytes?

A

T cell migration into the lymph node

61
Q

List the steps involved in leukocyte extravasation

A

Tethering (slow down, contact) recognition of inflamed tissue -> rolling -> activation -> conformational change in leukocyte integrins -> strong adherence to ICAMs/Ig superfamily on endothelium (arrest and adhesion) -> trans endothelial migration

62
Q

Where do lymphocytes extravasate specifically?

A

High endothelial venues (HEV)

63
Q

Where in the lymph node do dendritic cells pick up most of the antigens?

A

Subcapsular sinus (SCS

64
Q

What integrins and chemokine receptors do T cells moving to the intestine have?

A

LPAM, LFA-1, and CCR9

65
Q

What chemokine receptors and integrins fo T cells moving to the skin express?

A

CLA, LFA-1, CCL1, CCL17, and CCL27

66
Q

What induces mast cells and basophils during inflammation?

A

Activated complement proteins

Histamine-releasing proteins made by WBCs

Inflammatory cytokines (IL-1 and IL-8)

In hypersensitivity reactions, by binding of soluble IgE to the FcR

67
Q

True or false: endothelial cells contain histamine receptors that activate endothelium and increase vascular permeability

A

True

68
Q

True or false: mast cells are key mediators of inflammation.

A

True

69
Q

True or false: Eicosinoids act on targets far away from the site of formation?

A

False

70
Q

What produces eicosanoids (specifically)?

A

Endothelium, granulocytes, macrophages, platelets

71
Q

What do prostaglandins do?

A

Promote vascular permeability/dilation, platelet aggregation and increased pain sensitivity

72
Q

What do leukotrienes do?

A

Promote vascular permeability and chemotaxis.

73
Q

What are the 3 main mediators of inflammation-induced activation of coagulation?

A

Pro-inflammatory cytokines (I’ll-1, IL-6, and TNF-a)

74
Q

What are pyrogens? List the 4 examples given in class.

A

Substances that induce fever; IL-1, Il-6, TNF-a, and LPS from bacteria

75
Q

List the 7 benefits of fever.

A

Increased lymphocyte response to mitogens

Increased bactericidal activity of neutrophils

Increased motility, activation, and proliferation of leukocytes

Increased phagocytosis

Higher production of interferon

Increased liver functions (acute phase proteins)

Active excretion of toxins

76
Q

What are the side effects of fever?

A

Functional overload of organs

Hypo hydration and blood hemolysis (blood clotting)

GI disturbance due to increased level of toxins

77
Q

Why does acute inflammation cause neutrophilia?

A

IL-1 and TNF-a promote the accelerated release of neutrophils in the bone marrow.

78
Q

What does prolonged infection cause in terms of neutrophils?

A

Causes the production of colony stimulating factor (G-CSF) which leads to the release of immature neutrophils into the blood

79
Q

True or false: acute inflammation shuts itself down passively.

A

False: active termination is required (otherwise leads to chronic inflammation).

80
Q

What are the mechanisms for shutting down acute inflammation?

A

Short half life of inflammatory mediators (ex. C3a and prostaglandins)

Production and release of anti-inflammatory cytokines (IL-10 and TNF-B) and molecules (cytokine signalling blockers that bind to the cytokine or its receptor)

Apoptosis of pro-inflammatory cells (ex. Neutrophils have short half life)

Desensitization (down regulation of pro-inflammatory receptors such as those for prostaglandins and histamine)

81
Q

How can macrophages cause tissue damage during acute inflammation?

A

Prolonged production of IL-1, IL-6, and TNF-a.

82
Q

What is fibrosis characterized by?

A

Lymphocytes and plasma cell infiltration of tissues with cell necrosis and fibrosis.

83
Q

What is affinity?

A

The strength of all the non-covalent interactions between the antigen binding site on the antibody and a single epitope

84
Q

What determines affinity?

A

The antigen-antibody fit and the number of interactions.

85
Q

True or false: the Kd changes during an immune response

A

True

86
Q

What is affinity equilibrium dialysis good for?

A

Good for determining the affinity of different antibodies for an antigen. Can be used for vaccine development for determining which antibody is the best for a particular antigen .

87
Q

What is avidity?

A

The strength of multiple interactions between an antibody and an antigen.

88
Q

What determines the strength of avidity?

A

The affinity and number of antibody-antigen interactions

89
Q

When can antibodies bind 2 different antigens?

A

When the different antigens share common epitopes, or when the epitopes are different but share similar chemical properties

90
Q

Which theory is the correct one for BCR diversity: germline theory or somatic hypermutation?

A

Trick question: both are correct

91
Q

How do enzymes know where to cut in the germ line DNA when forming BCRs?

A

The gene segments are flanked by short conserved recombination signal sequences (RSS)

92
Q

What are RSS’s comprised of?

A

A conserved heptamer

A 12 or 23 bp nonconserved spacer sequence

A conserved nonamer

93
Q

What does TdT do?

A

Adds N region nucleotides to the joints between gene segments in the Ig heavy chain and at all joints between TCR gene segments

94
Q

What is junctional flexibility?

A

Refers to the imprecise joining of VDJ gene segments

95
Q

What is the potential mechanism behind allelic exclusion?

A

Inhibition of rearrangement may be due to signalling through the pre-BCR (stops H chain rearrangement) and BCR (stops L chain rearrangement)

96
Q

What 2 signals do activated B cells need to undergo class switch recombination?

A

Cytokines and a co-stimulators signal from CD40

97
Q

What classes of IgG do IFN-y, IL-4, and mucosal tissue cytokines generate?

A

IgG subclasses, IgE, and IgA

98
Q

What part of the antibody determines the specificity on the antibody response?

A

The antigen binding site

99
Q

What part of an antibody determines the effector action of an antibody?

A

The heavy chain of the constant region

100
Q

What does class switch recombination do for an immune response?

A

Allows you to generate antibodies with the same antigen specificity but with different effector functions and distributions.

101
Q

What is the area in the variable region that is hypervariable called?

A

Complementarity determining regions

102
Q

Why are the hinge regions of antibodies flexible?

A

Rich in proline residues

103
Q

What do the cysteine residues in Ig’s do?

A

Allow for heavy chain dimerization through interchain disulfide bond formation

104
Q

How many T cells express 2 different alpha chains paired to the same beta chain from loose allelic exclusion?

A

1/3

105
Q

True or false: MHC molecules are members of the Ig superfamily

A

True

106
Q

How are MHC genes inherited?

A

In linked groups called haplotypes

Immunology (1 decks)

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