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ANBI 470 > Midterm 2- key concepts > Flashcards

Midterm 2- key concepts Flashcards

1
Q

defensins

A

animal specific immune responses that make holes in bacterial membrane so bacteria can flow out

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2
Q

lysosome

A

kill bacteria, concentration is closer to cell layer where there is more risk of bacteria entering

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3
Q

interferons

A

bind to receptors on a cell to prevent transcription & translation of a virus = stop infection
- induces non-viral state in neighbouring cells also so virus cannot replicate

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4
Q

complement

A

produces a cascade where serum proteins are activated that leads to opininization, chemotaxis, and killing of bacteria

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5
Q

classical pathway

A

adaptive immune system, antibodies might bind to something on bacteria then get complement cascade

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6
Q

alternative pathway

A

bacteria will be recognized by L3

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7
Q

lectin pathway

A

mannose binds to lectin = starts cascade

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8
Q

which of the 3 pathways are part of the adaptive vs innate immune systems?

A

innate- alternative & lectin
adaptive - classical (b/c activated by antibodies)

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9
Q

3 common components of all complement cascade pathways

A

1) C3- always in blood, spontaneously combusts into c3a & b
2) C3a- chemotaxic protein -> directs movement
3) C3b - for opsonization & macrocytosis

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10
Q

opsinization

A

coating pathogens to promote phagocytosis

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11
Q

how does phagocytosis work

A

1) phagocyte receptors bind to complement
2) receptors bind to bacteria
3) recognition of bacteria
4) englufs bacteria & kills it

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12
Q

2 main opsonins

A

1) C3b of complement system
2) antibodies

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13
Q

chemotaxis

A

leukocytes follow chemical gradient of chemotactic molecules to site of infection

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14
Q

the 3 chemotactic agents

A

1) C3a
2) bacterial components
3) chemokines/ecosinoids

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15
Q

how does chemotaxis work

A

1) neutrophils eat bacteria
2) C3b binds to bacteria = activates complement = produce more C3b = more C3a
3) C3a goes towards capillary & diffuses out
4) increase blood flow to site of infection to bring white blood cells
5) chemokines follow chemical gradient from low->high concentration to start eating the bacteria

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16
Q

epithelial cell function

A

sense infection & signal secretion of chemokines

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17
Q

mast cell function (2)

A
  • induce vasodilation to increase blood flow
  • signalling using histamine /eicosinoids
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18
Q

anti-histamine function

A

binds histamine & prevents it from causing inflammation & diapedesis

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19
Q

what are the 4 acute phase proteins

A

1) C-reactive protein
2) serum amyloid A
3) haptoglobin
4) fibrinogen

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20
Q

polynmorphonuclear neutrophils

A

eat bacteria to control infection, does not secrete anything

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21
Q

how is danger detected

A

pattern recognition receptors bind MAMPs & initiate inflammation

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22
Q

MAMPs

A

pathogens have structures that we do not have, these act as flags that immune system is constantly looking out for

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23
Q

Toll-like receptors (TLR)

A

each recognize a diff molecule that is not present in the mammalian world = indicator of infection
- when binding = activate intracellular signalling pathways to activate immune response

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24
Q

how might neutrophils sense bacteria? (2)

A
  • sense pathogen recognition receptors
  • if chemokines -> can sense without touching
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25
Q

innate immune response cascade steps

A

1) pathogen breaks physical barrier
2) pattern recognition receptors activated on immune cells (neutrophils) and non-immune cells (epithelial cells)
3) release of inflammatory mediators
ex. eicosanoids, cytokines, chemokines & histamine
4) vasodilation through capillary wall
5) C3 breaks apart to C3A & C3B
6) bring more complement & cells to cite of infection
7) fever, pain & appetite suppression

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26
Q

MHC I

A
  • found on all nucleated cells
  • intracellular
  • partially degraded & presented on cell surface
  • viral, tumor surveillance
  • cytotoxic T cells
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27
Q

MHC II

A
  • found on antigen presenting cells
  • extracellular
  • proteins are degraded & presented on MHC II
  • viral particles, bacteria
  • T helper cells
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28
Q

B cell function

A

recognize extracellular antigens via transmembrane antibodies
- 1 B cell only has 1 specificity

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29
Q

variable region

A

binds to antigen, determines antigen specificity

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30
Q

constant region

A

tells what the antibody isotype is to know what antibody we are making

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31
Q

VDJ region

A

unique coding sequences for every naive B cell

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32
Q

T helper cells

A

recognize MHC II
- secrete cytokines
- activate B cells, cytotoxic T cells, macrophages & neutrophils

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33
Q

cytotoxic T cells

A

recognize MHC I
- kill infected cells
- can differentiate viruses

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34
Q

3 types of antigen presenting cells (APCs)

A

1) macrophages/dendritic cells
2) B cells
3) MHC II bearing cells

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35
Q

how can B cells act as APCs?

A

present antigen & respond to antigen

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36
Q

activation of naive T cell steps (6)

A

1) antigen presenting cells recognize extracellular antigen
2) antigen is ingested
3) antigen is broken down in endosome
4) MHC II + antigens fuse
5) cleave antigens
6) antigen expressed on cell surface through MHC II
7) dendritic cell goes to lymph node to find its T cell receptor
8) T

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37
Q

TH1 subset

A

immunity to intracellular pathogens

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38
Q

TH2 subset

A

immunity to parasites, allergy responses

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39
Q

TH17

A

extracellular pathogens, fungi & bacteria

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40
Q

Treg

A

maintain tolerance to bacteria so we are not responding to the microbiome all the time
- important in small intestine

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41
Q

T helper cell activation of humoral immunity steps

A

1) B cell goes to lymph node to find its T cell match using T cell receptors
2) T cell & B cell bind and send messages to each other
3) T cell secretes cytokines to tell B cell what antibodies to make
4) B cell is now activated
5) B cell can undergo clonal expansion to make plasma cells or can make memory cells

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42
Q

antibody vs humoral immunity

A

antibody- differentiate based on effector functions
humoral- make antibodies that bind to proteins & cells

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43
Q

activation of cellular immunity

A

forms 3 cell cluster
- clonal expansion of T helper & cytotoxic T cells
- produce effector cytotoxic T cells

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44
Q

3 cell cluster components

A

1) APC
2) T helper cell
3) Cytotoxic T cells

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45
Q

activation of cytotoxic T cells in the 3 cell cluster

A

cytotoxic t cell has its own T cell receptor that is specific for antigen & MHC I
1) T cell meets with its antigen = T helper cell is activated
2) activated T helper cell can activate B cells & cytotoxic T cells
3) secreted cytokines activate the cytotoxic T cell
4) proliferation = effector & memory cells produced

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46
Q

antigen specific immune response steps

A

1) activated cytotoxic T cells look for foreign antigens
2) T cell receptor binds MHC I & its antigen
3) secretes perforins
4) secrete granzymes
5) infected cells are killed but neighbouring, uninfected cells are not

47
Q

what MHC class do T helper & cytotoxic T cells recognize?

A

helper- MHC II
cytotoxic- MHC I

48
Q

4 functions of antibodies

A

1) neutralization
2) opsonization
3) bind complement
4) can cross placenta for maternal antibody transfer

49
Q

cytokines

A

give instructions on what to do/become

50
Q

peyers patches function & components

A

areas highly concentrated in diff types of immune cells to try survey antigen
- M cells sample antigen
- IgA response
- tolerance -> not responding to everything

51
Q

how does coupling of self antigen to a large carrier molecule overcome mechanisms of self/non-self discrimination?

A

if carrier is next to self antigen, it learns to recognize this antigen
- the B cell will recognize the large carrier & T cell together = always respond to it

52
Q

8 characteristics of the ideal vaccine

A

1) safe for all individuals -> little to no replication
2) induces appropriate protective response -> targets what we want, broad cross protection against variants
3) long lasting
4) overcomes maternal immunity
5) easily administered
6) single dose
7) inexpensive
8) stable

53
Q

antigenic drift

A

b/c viruses replicate fast, they do not have ability to recognize a mistake so if it is mutated, antibody will not recognize it = vaccines does not work anymore

  • mutated virus = antibody won’t recognize it = vaccine doesn’t work anymore
54
Q

antigenic shift

A

when brand new viruses are made

55
Q

what must be done to make new vaccines for more variants?

A

make new antibodies that hopefully the virus does not escape against

56
Q

is neutralizing antibodies enough for vaccine development?

A

no, we should also focus on cytotoxic T cells

57
Q

what is the most safe vaccine?

A

subunit vaccines, but has least immunogenicity

58
Q

advantage & disadvantage to killed vaccines

A

A:
- relatively safe (cannot replicate)
- longer shelf life b/c more it is more stable

D:
- proteins can be changed on the virus
- no cell mediated immunity (no cell mediated immunity)
- requires adjuvant

59
Q

adjuvant

A

slow release of antigen to activate antigen presenting cells
-> give boost to immune system

60
Q

3 things that adjuvants improve

A

1) more antigen presentation
2) T/B cell activation
3) memory immune response

61
Q

cellular vs humoral immunity-> what cytokine responses do they want?

A

C: TH1
H: TH2

62
Q

what is a subunit vaccine

A

only contains 1 or a few components of the infectious agent

63
Q

advantages & disadvantages for subunit vaccines

A

advantage:
- safe
- longer shelf life
disadvantages:
- multiple doses required b/c antigens have poor immunogenicity
- poor cell mediated immunity
- requires adjuvant
- time consuming to identify which subunit is protective

64
Q

live attenuated vaccines

A

a live infectious agent from which virulence has been reduced
- can still infect, but not cause same disease

65
Q

2 ways to create live attenuated vaccines

A

1) culture/mutagenization-> expose to environment where they struggled to grow
2) molecular methods -> cut out important protein = does not have ability to cause disease now

66
Q

advantages & disadvantages of live attenuated vaccines?

A

advantages:
- rapid immunity
- single dose
- no adjuvants
- induce cell mediated immunity
- long last immunity

disadvantages:
- risk of reversion to virulence
- shedding into environment
- less stable

67
Q

DNA/RNA vaccines

A

take a code for protein & put that inside the vaccine
- cells will transcribe this & make protein = expressed on cell surface = immune response

68
Q

live recombinant vaccines

A

vectors deliver information into your DNA & tell body to form immune response

69
Q

advantages & disadvantages of live recombinant vaccines

A

A:
- cell mediated immunity
- 1 dose

D:
- can become virulent again
- pre-existing immunity to vaccine carrier = get rid of vector before immune response message
- limited vector use (ex. salmonella, will not work on people exposed to it)

70
Q

DNA/RNA vaccines advantages & disadvantages

A

A:
- cannot revert to virulence
- easy to switch out AA
- do not need to make protein in bacteria -> the mRNA will look like mRNA

D:
- need to identify protective antigen = time consuming
- expensive
- RNA vaccines are not stable
- DNA difficult to get nuclear localization

71
Q

mRNA vaccines

A

make it look like the real mRNA so the immune system can go through MHC I processing & end up on cell surface for cell mediated immune response
- our bodies do the work for protein creation

72
Q

4 types of live vaccines

A

1) fully virulent
2) heterlogous
2) attenuated
4) live recombinants

73
Q

4 types of killed vaccines

A

1) killed
2) metabolic products
3) DNA/RNA
4) subunit vaccines

74
Q

problems with genetically modified bacteria (4)

A

1) need signal sequences to signal transcription
2) proper protein activity
3) how much protein can we recover from bacteria
4) prokaryotes have diff codon systems than eukaryotes -> need more sequences onto this transgene

75
Q

5 methods of how transgenic animals can be produced

A

1) recombinant DNA
2) genetic cloning
3) gene expression
4) genomic mapping
5) CRISPR-Cas 9

76
Q

promotor sequence

A

signals to get RNA polymerase & transcription factors to bind on promotor sequence to start making RNA

77
Q

gene expression requires what 3 things

A

1) regulatory mechanisms
2) promotor sequences
3) enhancers

78
Q

enhancer role on gene expression

A

stimulate RNA transcription & incorporated into germ line so it passes on this genome

79
Q

how to increase efficiency rates of microinjection (4)

A

1) decrease size of needle
2) small concentration of DNA
3) increase experienced people
4) ensuring proper egg development & quality

80
Q

retroviral infection steps

A

1) transfer RNA into infected host
2) DNA will be made from RNA via reverse transcription
3) double stranded DNA integrates into genome
4) recombinant retroviruses that are replication defective are produced

81
Q

advantages & disadvantages of viral replication

A

a- easy, can be done at diff stages, effective
d- integration is random, limitation to gene size, mosiacisim = some cells have transgene, others do not

82
Q

embryonic stem cell mediated gene transfer

A

1) grow embryonic stem cells in culture
2) put transgene in
3) allow cells to be transfected via chemicals
4) put into surrogate

83
Q

advantages & disadvantages of embryonic stem cell insertion

A

A- easy, can differentiate into any cell, can study all pathways

D- chimeras result, harder to find embryonic stem cell lines for livestock

84
Q

epigenetics

A

describes changes in a phenotype that are not coded in the DNA
- effect of the environment

85
Q

3 factors that epigenetics can change

A

1) how tightly DNA is coiled around histones
2) methylation of DNA
3) imprinting

86
Q

monozygotic twins

A

identical DNA but may differ in phenotype based off environmental factors
- ex. twins separated at birth

87
Q

what stage has lots of epigenetic factors? Why?

A

fetus stage, b/c cells have differentiated so can have factors here

88
Q

somatic cell nucleus cloning

A

1) take egg cells from 1 breed & remove nucleus
2) take somatic cells & grow in plate
3) fuse somatic cells to enucleated egg via electrical pulse
4) implant into surrogate

89
Q

2 reasons for cloning & example

A

possibility for cells from adult individual to repair a disease
- huntingtons

make vulnerable species more prevelant

90
Q

3 methods to get a transgenic founder

A

1) pro-nuclear injection
2) embryonic stem cells
3) nuclear transfer

91
Q

what are antisense genes made of

A

single stranded RNA complementary to mRNA

92
Q

antisense gene function

A

1) target gene we want to knockdown using complementary RNA
2) gene sequence is then inverted
3) RNA cannot be made into a protein bc the antisense gene is blocking it
4) chews up the double stranded mRNA

93
Q

gene shears

A

targets a specific sequence that you want cut = no protein made

94
Q

how are gene shears delivered

A

viral vectors in mammalian cell cultures

95
Q

RNA interference (RNAi)

A

uses microRNA that gets cut into small pieces call small interfering RNAs & take up by protein complexes = binds to target area & cuts = no protein made

96
Q

morpholino knockdown

A

synthesized oligionucletides that are complementary to a specific target, therefore blocking translation/splice sites

97
Q

2 advantages of morpholinos

A

1) not degraded by nucleases b/c they are synthesized, not natural oligionucleotides
2) do not trigger immune response

98
Q

how does morpholino knockdown work?

A

1) insert morpholino into target gene using microneedle
2) antisense to targeted DNA
3) blocks translation = no protein produced

99
Q

non-homologous end-joining

A

repair breakage of DNA through error prone pathway that results in a deletion or insertion in target gene, does not require a template

100
Q

homologous recombination

A

nucleotide sequences are exchanged between 2 similar/identical molecules of DNA during recombination
- insertion of gene/correction
- requires a template

101
Q

2 functions of neomycin

A

1) disrupts gene
2) use as indicator of effectiveness b/c if there is resistance = know transgene is inside cells

102
Q

neomycin

A

antibiotic resistance gene

103
Q

how many markers are present with 1 homologous recombination event vs 2?

A

1- both markers are still present
2- NEO present, TK lost

104
Q

insert targeting vector into embryonic stem cells

A

put targeting vector into nucleus of cell then rely on homologous recombination so it will flip inside to the genome = cross over piece put into normal genome & gene is released

105
Q

crossover must occur ( ) to ensure gene is successfully knocked out

A

2 crossover events

106
Q

zinc finger nucleases

A

recognize triple repeats & cut at a specific location between recognized sequences
- can be used for embryonic stem cells

107
Q

1 advantage & 2 disadvantages of zinc finger nucleases

A

A- can recognize 24bps to be very specific
D- not very triplet has zinc finger nuclease associated with it, and sometimes zinc fingers interact with each other = not efficient

108
Q

how does CRISPR Cas9 work

A

cells that survive infection retain a little piece of DNA in their genome. if similar virus attacks again it will recognize it & destroy it by cutting up the viral genome using cas proteins

109
Q

CRISPR Cas9 steps

A

1) virus attacks & inserts viral DNA
2) crRNA comes to tracer RNA & matches up with viral genome
3) Cas proteins cut foreign DNA

110
Q

Cas steps

A

1) single guide RNA & tracer RNA match up on genome
2) Cas9 & single guide RNA bind
3) complex binds to target sequence & cleaves target DNA
4) cleavage site is repaired by non-homologous end joining or homologous directed repair

111
Q

results of non-homologous end joining vs homologous directed pair in Cas system

A

non-homologous: results possible in gene function disruption
homologous: results in incorporation of new DNA

112
Q

3 fates of genome editing

A

1) gene insertion
2) gene correction
3) gene disruption

113
Q

3 methods of genome editing

A

1) Zinc finger nucleases
2) TALENs
3) CRISPR Cas9

114
Q

what are 4 factors we should consider before moving forward with technological advances?

A

1) applications - therapeutic, but enhancement of personal could be bad (societal standards)
2) equity & access - only for the wealthy?
3) moral, philosophical os religious concerns
- “playing god”
- “disturbing natural processes”
4) balance of risk & benefit

ANBI 470 (23 decks)

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