1
Q
biotechnology =?
A
exploitation of biological processes or organisms to produce goods or services
2
Q
before genetic engineering:
- random mutations, screen for desired traits
- spontaneous mutations
- artificial mutagenesis
A
random mutations, screen for desired traits
- repeated crossbreeding + selection
spontaneous mutations
- natural DNA dmg, DNA repair errors
artificial mutagenesis
- UV, Xray, chemicals
3
Q
limitations before genetic engineering
A
- LONG time
- undesired mutations
4
Q
DNA mutations may result in…
a) Loss of gene function
b) Restoration of gene function lost previously
c) Modification of gene function
d) None of the above
A
a
b
c
5
Q
examples of biotechnology before genetic engineering! what is this called?
A
- corn
- bananas
- carrots
NOT genetic engineering! artificial selection!
6
Q
what did brassica make w artificial selection? (6)
A
cabbage
brussels sprouts
kohlrabi
kale
broccoli
cauliflower
7
Q
is this genetic engineering or artificial selection:
“phenotypic testing to select strains with best antibiotic resistance traits for antibiotic production”
A
also artificial selection :)
8
Q
molecular biotechnology AKA? =?
A
aka genetic engineering!
- deliberate modification of an organism’s characteristics by manipulating specific sequences of its genome
9
Q
HOW can we do molecular biotechnology
A
- modify existing gene seq
- remove genes
- add genes from other organisms
10
Q
adding genes from other organisms is called?
A
transgenic
11
Q
Q: What are the benefits of genetic engineering over artificial selection?
a) Faster results.
b) More precision.
c) Don’t have to rely on natural random mutations.
d) More versatile.
A
a b c d!
12
Q
4 examples of transgenic usage
A
- HPV vaccine (viral proteins expressed in yeast)
- glofish (fluorescent proteins)
- rainbow papaya; ringspot virus protein expression
- transgenic mice for research :]
13
Q
transgenic plants and animals rely on ___
A
microbiology
14
Q
how do we make transgenic plants and animals using microbiology? steps & gen explanation
A
- genetic material assembled in microbes first
-> using enz from microbes - then transferred to plant/animal cells
plasmid in bacterium, REs, insert DNA of interest
-> genetically modified bacterium
- then add to ex. fish
15
Q
Q: Like Darwinian evolution, biotechnology can only modify what already exists
a) True
b) False
A
False!!!!
16
Q
function of promoter, mutation effects
A
promoter controls WHEN, WHERE, & HOW MUCH protein is made
- mutation: change timing, location (cell type), or amount of protein
17
Q
function of coding region, mutation effects
A
coding region determines WHICH protein is made
- can include SIGNAL SEQ that targets locations inside or outside cell
- mutation: changes protein, protein func, localization of protein
18
Q
Q: A mutation in the promoter region of a gene might have the following effect(s)…
a) Change in the protein product.
b) Change in the function of the protein product.
c) Change in the rate of transcription.
d) Transcription occurring in cell types that don’t normally transcribe the given gene.
e) Change in the localization of a protein product.
f) None of the above
A
c d
19
Q
Q: A mutation in an exon of a gene might have the following effect(s)…
a) Change in the protein product.
b) Change in the function of the protein product.
c) Change in the rate of transcription.
d) Transcription occurring in cell types that don’t normally transcribe the given gene.
e) Change in the localization of a protein product.
f) None of the above.
A
a b e
20
Q
site-directed mutagenesis =?
A
creates a specific mutation, instead of relying on chance
21
Q
site-directed mutagenesis process steps
A
- plasmid with wt DNA
- oligonucleotide with desired DNA, still mostly complementary to wt DNA
- oligonucleotide binds to wtDNA, acts as primer to polymerase
- ds plasmid made -> insert into cells, replicate
- screening
22
Q
molecular cloning explanation, gen steps
A
- assembling recombinant DNA, having them replicate in host cells
- recombinant plasmid inserted -> microbe
- microbe reproduces, reproducing plasmid
23
Q
how to make recombinant plasmid
A
plasmid digested with REs, insert gene of interest, DNA ligase -> recombinant plasmid
24
Q
purpose of selectable marker in plasmids
A
lets us kill cells without plasmid
ex. Amp
25
purpose of lacZ'
blue-white screening
26
purpose of MCS (also stands for?)
multiple cloning site
- allows insertion of DNA w diff REs
27
purpose of ori
origin of DNA replication
- independent replication of plasmid in host cell
28
Q: What would happen if you used a plasmid with no origin of replication in a cloning experiment?
a) The cells you insert the plasmid into would not be able to replicate
b) The plasmids would not be able to replicate within the cells
c) The plasmids would not be able to replicate outside of the cells
d) All of the above
b
29
how do we get DNA into bacteria (2)? describe steps
chemical transformation
- salty sol (neutralize charges), incubate, heat shock
electroporation
- electric shock
30
purpose of chemical transformation and electroporation; how efficient?
make them take up DNA (leaky membranes)
- not efficient at all!
31
What would happen if we skipped this initial growth phase before plating on antibiotic-containing medium?
Give cells time to express antibiotic gene!
So might see no growth
32
Q: You perform a cloning experiment, but don’t have access to any antibiotic to add to your medium. The plasmid you used contains an ampicillin resistance gene, but you do not include ampicillin in the medium you plate your transformation mix onto. What could you expect?
a) No colonies will form
b) Many colonies will form, but many will be made of cells with no plasmids
c) All colonies that grow will come from cells with plasmid
d) Any of the above is a likely scenario
b
33
Q: You add a DNA segment of interest to a cloning vector and transform E. coli cells with the vector. After transformation, you add growth medium, incubate for an hour, then plate the mixture on medium containing an antibiotic for which resistance is encoded on the plasmid. What result should you expect?
a) No bacterial growth.
b) Colonies formed of plasmid with no bacteria.
c) All colonies will contain cells with plasmid and insert.
d) All colonies will contain cells with plasmid, but some will have insert and others won’t.
e) No colonies will contain plasmid.
d
34
what is the purpose of blue-white screening?
check for inserts in the plasmids within cells
35
how does blue-white screening work?
intact lacZ gene makes beta-galactosidase!
-> break down X-gal substrate to galactose & blue product
-> usual func is to break down lactose into galactose & glucose
functional beta-galactosidase can't be made with free floating plasmids or colonies lacking plasmids
36
why can't free-floating plasmids or cells w/o plasmids make functional beta-galactosidase?
lacZ gene needs:
- LacZ alpha from plasmid
- LacZ omega from host
37
what colour indicates a successful insertion in blue-white screening? selective/differential?
white! differential!
38
Q: You add a DNA segment of interest to a cloning vector and transform E. coli cells with the vector. The cloning vector and E. coli strain are designed for blue-white screening. After transformation, you add
growth medium, incubate for an hour, then plate the mixture on medium containing an antibiotic for which resistance is encoded on the plasmid and x-gal. What result should you expect?
a) No bacterial growth.
b) Colonies formed of plasmid with no bacteria.
c) All colonies will contain cells with plasmid and insert.
d) All colonies will contain cells with plasmid, but some will have insert and others won’t.
e) No colonies will contain plasmid.
d
39
Q: You add a DNA segment of interest to a cloning vector and transform E. coli cells with the vector. The cloning vector and E. coli strain are designed for blue-white screening. After transformation, you add growth medium, incubate for an hour, then plate the mixture on medium containing an antibiotic for which resistance is encoded on the plasmid and x-gal. Which type of colony should you pick to propagate?
a) A blue colony
b) A white colony
c) Any colony
b!
40
expression plasmid:
what are P, O, SD, TS; what do they do?
P - promoter
O - operator (turn on/off transcription)
-> allows transcription proteins to attach to DNA seq
SD - Shine-Dalgarno seq (ribosomes bind here + AUG, & perform translation)
TS - terminator seq (stop transcription)
41
Q: An expression vector is a cloning vector that enhances the transcription and translation of recombinant genes.
a) True
b) False
True
42
Q: Why would you ever want to use a cloning vector instead of an expression vector?
a) You only want to propagate the DNA.
b) The gene product is toxic.
c) You want to verify or modify the DNA sequence.
d) You are not interested in a lot of protein product.
e) You are interested in a lot of protein product.
a b c d
43
inducible expression with an expression plasmid; what? why?
inducer binds to regulatory protein on the operator -> dissociation
- makes protein/product!
why delay?
- antibiotics or toxic substance production;
- wait until we have LOTS of cells, then start producing (will inhibit growth)
44
how do we express eukaryotic genes in bacteria (hint what is diff?)
bacteria can't process most introns!
get translated mRNA, then reverse transcription! (only exon info) w reverse transcriptase
45
what is cDNA?
mRNA reverse transcribed into DNA
46
where is reverse transcriptase from?
RNA viruses
47
Q: Expression vectors increase production of recombinant molecules by…
a) Using specific and customized promoters for optimum gene expression.
b) Having multiple sites to insert the gene of interest.
c) Having multiple origins of replication, allowing for rapid replication and increased biomass production.
d) Being selected to grow well under large batch conditions.
a
48
explain natural genetic engineering by Agrobacterium tumefaciens; why/how do they do this?
- A. tumefaciens bacteria infects plant
- transfer DNA into plant cells
- DNA inserts into plant genome
- expresses hormones & opines
- hormones lead to tumour/crown gall formation
- opines used by bacteria for energy, C, N
49
how do humans use Agrobacterium tumefaciens to our advantage?
- modify the bacterial plasmid to insert genes of interest into plants
50
51
Q: What natural component of the Agrobacterium tumefaciens life cycle is exploited to create transgenic plants?
a) The ability of the bacterium to insert its genes into the plant genome.
b) The ability of the bacterium to take over the metabolism of a plant cell.
c) The ability of the bacterium to cause plant tumors.
d) The ability of the bacterium to induce the production of plant hormones
a
52
CRISPR stands for?
clustered regularly interspaced short palindromic repeats
53
T/F CRISPR naturally exists in bacteria
true
54
how does CRISPR work naturally?
- explain Cas1-Cas2, spacers, Cas9
Cas1-Cas2 = part of adaptive immune response
- look for foreign DNA (e.g., phage DNA), clip it, integrate into chromosome
spacers = foreign DNA
Cas9 = molecular scissors
- spacers bind to Cas9, cuts complementary DNA (reinfection from same phage)
55
how do researchers use CRISPR instead? (specific steps)
cut genomic DNA wherever they want!
- engineered guide RNA binds DNA of interest
- introduce guide RNA and Cas9 genes into cell
- insert new seq w/ homology-directed repair
56
Q: Which of the following is a benefit of the CRISPR-Cas genome edition system?
a) Highly adaptable.
b) Allows for efficient gene editing.
d) Only works in bacteria.
e) Involves plasmids, which are inexpensive.
a b
57
define "normal" microbiota for humans
microbes that live on or within human tissues
- normally do not cause disease
- can protect against certain health problems
- incl euk!
58
59
60
61
61
62
define pathogenic microbes!
compare primary vs opportunistic pathogens
pathogenic microbes = commonly associated with disease
primary pathogens: cause disease readily in healthy hosts (not part of natural microbiome)
opportunistic pathogens: only causes disease when displaced to an unusual site OR in weakened immune system
63
Q: Which of the following statements best distinguishes normal microbiota, primary pathogens, and opportunistic pathogens?
a) Normal microbiota always cause disease, while primary and opportunistic pathogens do not.
b) Primary pathogens only cause disease in immunocompromised individuals, whereas opportunistic pathogens infect healthy individuals.
c) Opportunistic pathogens are harmless in all situations, while normal microbiota and primary pathogens always cause disease.
d) Normal microbiota typically do not cause disease under normal conditions, primary pathogens can cause disease in healthy hosts, and opportunistic pathogens cause disease mainly when host defenses are compromised.
e) There is no meaningful difference between these groups; all microbes have equal potential to cause disease.
d) Normal microbiota typically do not cause disease under normal conditions, primary pathogens can cause disease in healthy hosts, and opportunistic pathogens cause disease mainly when host defenses are compromised.
64
example of an opportunistic pathogen
microbes in the "wrong" place
ex. E. coli causing UTIs
65
Q: A patient undergoing chemotherapy develops a bloodstream infection caused by Staphylococcus epidermidis, a bacterium commonly found on the skin of healthy humans. How would this microorganism best be classified in this scenario?
a) Normal microbiota
b) Primary pathogen
c) Opportunistic pathogen
d) Obligate pathogen
e) Mutualistic symbiont
c
66
how do microbes cause disease? (5)
- ENTER host
- ATTACH to and invade cells/tissues
- EVADE defenses
- OBTAIN nutrients
- EXIT host
(often damages cells in this process)
67
what are virulence factors? what can they help with? examples
products made by pathogens that enhance their ability to cause disease
may help w:
- gain access to tissues/cells
- evade host defenses
- obtain nutrients
ex. tail fibers, biofilm, toxin production, flagella, cilia
68
adhesins =?
bacterial molecules used for binding and colonizing host tissues
- also used for biofilm formation!
69
fimbria =?
attachment pilus with tip protein (adhesins)
- expression can be turned on/off
- one bacterium can express diff types
- specific interactions with host receptors
70
bacterial pathogen vs viral pathogen attachments
fimbriae can be very long!
same overall goal as viral attachment proteins, but more dynamic & variable
71
Q: Bacterial molecules that allow them to bind to host tissues are called…
a) Attachment proteins
b) Host recognition proteins
c) LPS
d) Adhesins
e) Fimbriae
d) adhesins
72
T/F: some pathogenic E. coli make their own receptors for the host cell surface
- what does this mean?
true! so that hosts will "recognize" them, like a spy infiltration
- intimin in E. coli membrane
- E. coli injects Tir in host cell, migrates to membrane
- intimin in E. coli attaches to Tir in host cell
73
what does this Tir/Intimin interaction look like at a tissue level?
E. coli cells squish down microvilli to make a pedestal (flatter)
- lowers surface areas for host cells
- lower absorption
- diarrhea
74
Q: Many bacteria adhere to host surfaces using _________, pili that are primarily used for attachment.
a) Microvilli
b) Fimbriae
c) Pedestals
d) Fibronectin-binding proteins
b) fimbriae!
75
how are capsules virulence factors?
avoid phagocytosis
- no access of receptors to opsonins
ex. Streptococcus pneumoniae encapsulated strains are virulent, strains without capsules are not
76
Q: Virulence factors assist bacteria in…
a) Causing disease
b) Attaching to host cells
c) Avoiding immune destruction
d) All of the above
e) None of the above
d) all of the above
77
Q: The presence of a ________ aids bacterial attachment and inhibits phagocytosis.
a) Outer membrane
b) Cell wall
c) Capsule
d) Capsid
e) Cell envelope
c) capsule
78
4 different ways that microbes will obtain iron, a limiting nutrient
- siderophores bind iron, take IRON from host iron-binding proteins
- proteins bind host iron-binding proteins, bring entire PROTEIN
- lower *pH* at infection site -> reduce iron-binding ability of host protein
- cytolysins lyse RBCs to release iron
79
Q: One way bacterial pathogens obtain iron is by producing their own iron-binding molecules that can scavenge iron from the host. What are these molecules called?
a) Cytolysins
b) Metabolites
c) Hemolysins
d) Siderophores
d) siderophores
80
differences between exotoxin and endotoxin
exotoxin: secreted
endotoxin: part of cell wall, triggers host inflammatory response (G-ve)
- usu when dying
81
3 types of exotoxins!
- cytotoxin
- A-B toxin
- superantigen
82
exotoxin: cytotoxin
damages hsot cells directly
83
exotoxin: A-B toxin
various mechanisms, shared structure
84
exotoxin: superantigen
excessive activation of non-specific immune response
85
Q: Which of the following correctly describes a key structural difference between endotoxins and exotoxins?
a) Endotoxins are proteins, while exotoxins are lipids.
b) Endotoxins are part of the outer membrane of bacteria, while exotoxins are proteins secreted by bacteria.
c) Endotoxins are secreted only by Gram-positive bacteria, while exotoxins remain attached to the cell.
d) Endotoxins are released only from living cells, while exotoxins are released when cells die.
e) Endotoxins are made of DNA, while exotoxins are made of RNA.
b) Endotoxins are part of the outer membrane of bacteria, while exotoxins are proteins secreted by bacteria.
86
3 types of cytotoxins:
- cytolysins
- hemolysins
- leukocidins
87
cytotoxin mechanisms (2)
pore formation
- monomers polymerize in membrane to make a pore
membrane degradation
- e.g., phospholipase breaks phospholipids of cell membrane
88
define:
- cytolysins
- hemolysins
- leukocidins
cytolysins
- cytotoxins that lyse cells
hemolysins
- cytolysins that lyse RBCs
leukocidins
- cytotoxins that dmg/kill WBCs
89
general process of pore-forming cytolysins?
ex. S. aureus
- secretes hemolysin monomer
- monomer binds to membrane receptors
- other monomers bind and oligomerize
-> inflow
- conformational change + insertion of hydrophobic segments into membrane = pore!
cell lysis and bacterial consumption of nutrients
90
A-B toxins: A and B subunits
A subunit (usu works inside host cell)
- toxic enz activity
- dmg host cells
B subunit (get inside host cell)
- binds cell receptor
(determines affected species & tissues)
- enters by endocytosis
91
Diphtheria toxin is an example of?
how does it work?
A-B toxin!
B subunit binds to diff cells in humans
- endocytosis
- pH change -> subunits dissociate
A subunit enters cytoplasm
- kills cell by stopping protein synthesis
92
A-B toxins are commonly the targets of ___?
vaccines!
93
what do superantigens do?
exotoxins that act on ANY helper T cells
- massive release of non-specific cytokines (signaling proteins released by immune cells)
- systematic inflammatory response
94
how is S. aureus an example of superantigens?
- exotoxins (specifically enterotoxins -> intestines); food poisoning symptoms
ex. toxic shock syndrome, food contamination + improper heating
95
Q: Which of the following correctly matches a toxin type with its main mechanism of action?
a) Cytotoxins – bind outside cells and overstimulate the immune system
b) A-B toxins – have one part that binds to the cell and another part that damages the cell internally
c) Superantigens – directly destroy cell membranes by forming pores
d) Cytotoxins – enter cells and modify ribosomes to stop protein synthesis
e) A-B toxins – only affect immune cells by causing massive cytokine release
b) A-B toxins – have one part that binds to the cell and another part that damages the cell internally
96
Impacts of viral genes in bacterial genomes
Example: Diphtheria
Caused by bacterium Corynebacterium diphtheriae, but only when infected (lysogenized) with a certain phage
- Toxin gene from phage integrated in bacterial genome
97
Q: How does the toxin involved in a Diphtheria infection differ from other bacterial toxins?
a) It is a protein whereas normal bacterial toxins are polysaccharides.
b) It is a nucleic acid derivative whereas normal bacterial toxins are proteins.
c) It is archaeal derived
d) It is viral in origin
e) None of the above
d) It is viral in origin
98
cell envelope:
- inner cell membrane
- cell wall
- outer membrane
inner cell membrane = plasma membrane
cell wall = peptidoglycan layer (G+ve)
- teichoic acid!!!! (LTA)
outer membrane (G-ve)
- lipopolysaccharides!!! (LPS)
99
G-ve LPS endotoxin structure;
components of LPS
outer membrane is composed of phospholipids in inner leaflet, and mainly LPS in outer leaflet
LPS contains:
- lipid A (causes immune response, when it dies)
- O-antigen
- core polysaccharide
*not all LPS causes endotoxic effect
100
Cell envelope
Lipoteichoic acid (LTA) (Gram +ve)
- in cell wall, anchored to cell membrane
- recognized by innate immune system
- inflammation -> tissue dmg
- acts similar to endotoxin, but doesn't count as one. kind of like G+ve variant
101
which one can be an endotoxin and which one cannot?
LPS vs LTA
LPS: endotoxin
LTA: NOT endotoxin
102
Q: Infection by a Gram negative bacterium can cause an immune response due to lipoteichoic acid, which is found in the cell membrane
a) True
b) False
False!
103
very high levels of LPS, LTA can result in?
death
- from hemorrhagic shock (septic shock) & tissue necrosis
104
Q: Why is antigenic variation beneficial for pathogenic microorganisms?
a) It allows microbes to grow faster in all environments
b) It helps microbes produce more toxins
c) It allows microbes to avoid detection by the host immune system
d) It makes microbes resistant to antibiotics
e) It allows microbes to survive without nutrients
c) It allows microbes to avoid detection by the host immune system
105
innate vs adaptive immunity
innate
- immediate response
- general response to a range of pathogens
- incl barriers, inflammation, fever
- born with this immunity
adaptive
- specific to the invading pathogen
- based on prev exposure
106
why's skin a bad env for a lot of microbes?
- keratinized dead cells make a protective top layer
- tight cell junctions
- sweat glands -> antimicrobial substances, like NaCl + lysozyme
- sebaceous glands -> toxic fatty acids
107
how does respiratory tract protect against microbes?
- tight junctions
- mucus (goblet cells) traps microbes
- cilia sweep mucus out of respiratory tract
108
Q: What characteristic makes the skin so inhospitable to most microorganisms?
a) Skin tends to have an acidic pH.
b) Skin is dry and does not have much available moisture.
c) Skin is highly keratinized, so there is little organic material available.
d) All of these choices.
d) all of these
109
Q: Mucosal membranes are effective physical barriers to infection because…
a) microorganisms can not penetrate the mucosal layer and become trapped within.
b) mucosal membranes provide a convenient place for cells of the adaptive immune response to be stored.
c) mucosal membranes are anoxic.
d) all of these choices.
a) microorganisms can not penetrate the mucosal layer and become trapped within.
110
what 2 molecules are associated with inflammation?
- histamine (AA derivative)
- cytokines (glycoproteins)
111
what do histamines do?
- promotes widening (redness, heat), permeability (swelling) of blood vessels
- initiates inflammation
112
what do cytokines do?
- primary cell-to-cell signaling molecules that communicate information during an immune response
- initiate cell-signaling pathways that control immune func, recruit other immune cells like leukocytes
113
Q: Cytokines are…
a) Secreted by B cells
b) Proteins with many non-polar amino acids, allowing the molecules to easily pass through the plasma membrane of target cells.
c) Immune signaling molecules.
d) All of the above.
c) Immune signaling molecules.
114
when is inflammation good vs bad?
good
- when CONTAINED to an infected site
bad
- when response is SYSTEMIC (can lead to septic shock)
- microbes escape initial site and move to other locations
- widespread inflammation
- large amts of fluids leak from circulatory sys
- big drop in bp
- vital organs don't get enough blood
115
Q: When bacteria are widespread through the body, a systemic inflammatory response known as _______ may occur.
a) Toxic shock
Result of superantigens throughout the body!
b) Septic shock
c) Super-immune response
d) Inflammation
b) septic shock
116
how are fevers good vs bad?
good
- temp restricts growth of many pathogens
- increases immune cell production
- speeds tissue repair
bad
- v high temp can denature host proteins
117
what causes fevers
pyrogens
118
Q: The benefit of fever is to…
a) Speed tissue repair.
b) Increase the production of leukocytes.
c) Restrict the growth of pathogens.
d) All of these choices.
d) all of these
119
can complement be activated by innate or adaptive immune response?
trick question its both >:)
120
what is end goal of the complement?
form membrane attack complex (MAC)
-> form pore
-> cell lysis
121
the complement can be triggered by (3)
- C1 recognize antibody attached to pathogen
- C1 binds to pathogen
- C3 binds to pathogen
122
Q: The end result of complement activation is…
a) the formation of a membrane-attack complex and target cell lyses.
b) the destruction of the target cell by macrophages.
c) turning off target cell DNA by transcription factors.
d) all of these choices.
a) the formation of a membrane-attack complex and target cell lyses.
123
what are the 2 cells of the INNATE immune system?
- phagocytes (ex. neutrophils, macrophages)
- natural killer cells
124
phagocytes vs natural killer cells
phagocytes
- destroy *extracellular pathogens
natural killer cells
- cytotoxic
- target *host cells containing intracellular pathogens
125
how do phagocytes recognize extracellular pathogens?
opsonin! collection of proteins, mostly antibodies!
- digests them in phagolysosome
- oxidative burst
- exocytosis
126
Q: Opsonization is a coating of microbial surfaces that targets the cells for the vertebrate immune system
a) True
b) False
true
127
what cells do NK cells target? what do they do?
- target cells with reduced MHC I expression
- release perforin & granzyme
128
perforin & granzyme func
perforin
- makes pores
granzyme
- enters pores, trigger apoptosis
129
Q: Which of the following is true regarding cells of the innate immune system?
a) Both phagocytes and natural killer cells recognize species-specific signals on pathogenic cells.
b) Phagocytes eliminate extracellular pathogens.
c) Natural killer cells target pathogenic bacteria directly.
d) Phagocytes expose engulfed cells to granzymes which lead to apoptosis.
b) Phagocytes eliminate extracellular pathogens.
130
Q: A critical property of the innate immune system is the ability to…
a) Completely eliminate pathogens.
b) Differentiate between one’s own cells and foreign cells.
c) Respond to pathogens in a species specific manner.
d) All of the above.
b) Differentiate between one’s own cells and foreign cells.
131
cell types of adaptive immune system
T-cell receptors & immunoglobulins recognize antigens
132
immunoglobulins =?
B-cell receptors and antibodies
133
antibodies are secreted forms of ____
B-cell receptors
134
Q: Any component that can be bound by a T-cell receptor or an immunoglobulin is termed…
a) An antibody
b) A ligand
c) An antigen
d) A BCR
c) An antigen
135
antibody structure:
variable vs constant
variable: target binding sites
constant: immune cell binding site
136
the smallest part of an antigen that can be recognized by an immune receptor is?
an EPITOPE!
137
can each antigen have multiple diff epitopes? are these recognized by same or diff immune receptors?
each antigen can have multiple diff epitopes,
each recognized by a diff immune receptor
138
Q: The smallest molecular unit that can be bound to an immune receptor is called a/an…
a) Antigen
b) Ligand
c) Epitope
d) Antibody
e) Immunoglobulin
c) Epitope
139
how can antibodies be used in molecular bio (4)
Immunofluorescence
- Fluorescent tag on antibody that binds to protein
Antigen testing
- Ex covid test
Western blot
- Labelled antibody recognizes protein, run on gel
Affinity chromatography
- Purify protein mixture, gets proteins that bind to antibodies
all related to proteins
140
where are T cells made? how do they have unique receptors?
- made during cell maturation in thymus
- random rearrangements of genes encoding receptors
141
helper T cells:
interact with? what happens when activated?
interact w antigen presenting cells (APCs)
- APCs present peptides from pathogen on MHC II
when activated:
- cytokines are released; some promote growth and activity of T & B cells
- role is NOT to kill cells! helps instead with immune response overall
142
cytotoxic T cells:
interact with? what happens when activated?
interact w antigens on infected host cells on MHC I
- (like opposite of NK that recognize lower MHC I exp)
when activated:
- release of toxic molecules incl perforin and granzymes that trigger apoptosis (like NK!)
143
clonal expansion of activated T cells
clonal expansion & differentiation ->
- effector cells and memory cells
- same T cell receptors as activated T cells
144
T cells: effector vs memory cells
effector
- short-lived and actively fight infection through recognition of antigen
memory
- persist in body for subsequent antigens
145
Q: What is the function of cytotoxic T cells?
a) Stimulation of B-cells for antibody production.
b) Antibody production.
c) The cytotoxic killing of infected cells.
d) Stimulation of macrophages.
e) Stimulation of dendritic cells.
c) The cytotoxic killing of infected cells.
146
unlike T cells, B cells don't need ____ to be presented
antigens;
B cells can recognize antigens still attached to pathogen or free-floating
147
B cells: how do they work?
after engulfing matching antigen,
- display on MHC II -> shows helper T cell
-> activates both the B and T cells
148
activation of helper T/B cells + maturation of B cell
activation of helper T cell:
- makes cytokines
- cytokines make B cells multiply and mature into antibody-producing plasma cells
activation of B cell:
- clonal expansion
maturation of B cell:
- makes antibodies
149
Q: Which of these can activate T cells during the adaptive immune response?
a) Only B cells
b) B cells and macrophages
c) Bacteria
d) B cells, macrophages, and other antigen-presenting cells
d) B cells, macrophages, and other antigen-presenting cells
150
B cells: memory cells vs plasma cells
memory cells - persist for subsequent antigens
plasma cells - make antibodies
151
Q: MHC I molecules are involved in the activation of which type of cell?
a) Helper T cells
b) Cytotoxic T cells
c) B cells
d) Phagocytes
b) Cytotoxic T cells
152
Q: What are two main functions of B cells?
a) Activation of helper T cells
b) Antibody production.
c) Activation of cytotoxic T cells.
d) Activation of phagocytes.
a) Activation of helper T cells
b) Antibody production.
153
what can antibodies do? (3)
1) physically block pathogens from interacting with host cells or molecules
2) recruit complement proteins
3) act as opsonins to promote phagocytosis
BIOL 241
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