Test 4 Flashcards
(190 cards)
1
Q
Immunity
A
Body’s defense system to prevent disease
2
Q
Innate immunity
A
Born with
- Non specific
3
Q
Adaptive immunity
A
Immunity we develop
- specific
Create memory cells
4
Q
What are physical first line of defense
A
Skin, mucus membranes and cleansing agents
5
Q
Skins goal
A
Keep pathogens out of the body
6
Q
How do mucus membranes keep pathogens out of the body
A
They trap microbes by the use of cilia
7
Q
How do saliva and tears keep pathogens out
A
They wash away or dilute microbes
8
Q
What are some chemical methods for 1st line of defense
A
Lysozymes & low ph
9
Q
Lysozymes
A
Break down cell walls
10
Q
Examples of lysozymes
A
Tears, saliva, sweat
11
Q
Low ph
A
Inhibits bacterial growth
12
Q
Examples of low ph
A
Vagina, stomach acid, skin, ear canal, saliva
13
Q
What are the 3 things part of the 1st line of defense for the immune system
A
Physical, chemical,
Microbiome
14
Q
Microbiome
A
Microbes in/ on our body preventing a adding pathogens
15
Q
5 symptoms of inflammation
A
Pain
Redness
Immobility
Swelling
Heat
16
Q
What are the 2 goals of inflammation
A
- Destroy & remove pathogen
- Remove & repair tissue damage
17
Q
1st step (mechanism) of inflammation
A
Alarm is sounded - cytokines activated
18
Q
Cytokines
A
Signaling molecules
- regulate intensity and duration of immune response
19
Q
3 types of cytokines
A
Chemokines
Interfeurons
Interleukins
20
Q
Chemokines
A
Attract immune cells to an area
21
Q
Interfeurons
A
Help with antiviral responses
22
Q
Interleukins
A
Help regulate intensity and direction of immune response
23
Q
The 2nd step (mechanism) of inflammation
A
Histidine released causing vasodilation = increase permeability
- triggering phagocytes to migrate out of blood to infected site
24
Q
Phagocyte migration
A
Phagocytes phagocytes move from the blood stream to infected tissues
- triggered by cytokines
25
Margination
Phagocytes attach/ stick to endothelium
26
Diapedesis
Phagocytes squeeze out of blood vessel b/w epithelial cells
- 1st neutrophils then monocytes
27
Scar tissue
Lot more collagen present
28
Acute inflammation
Develops quickly
- lasts for short period of time
29
Chronic inflammation
Develops slowly
- last for longer period of time (persistent)
30
Fever
Body temperature is above normal - speeding up the bodies reactions
31
Fever mechanism
1. Macrophage ingests a gram negative
2. Endotoxin is released triggering cytokines
3. Release of interleukins
4. Prostaglandin produced in hypothalamus (resetting body thermostat)
5. Fever
32
Complement system is part of what immunity
Innate immunity
- 2nd line of defense
33
Main mechanisms of complement system
Cytolysis
Opsonization
Inflammation
34
Complement
Proteins involved in phagocytosis and lysis of bacteria
35
Opsonization
Improves (promotes) phagocytosis
36
Complement proteins start with a letter C followed by a #
TRUE or FALSE
True
Ex, Cd3
37
Complement activation
Cascade of complement proteins acting during an infection
38
What are the 3 types of complement
Classical
Alternative
Lectin
39
Classical complement
Activates complement system due to antibody binding to antigen
40
Alternative complement
Activates complement system by - complement protein recognizing pathogen
41
Lectin complement
Activates complement system by - lectin recognizing pathogen
42
Outcome of classical complement
C3 activated and inflammation , cytolysis starts
43
Opsonization
Proteins coat a pathogen and promote phagocytosis
( classical)
44
Outcome of alternative complement
C3 activated and inflammation, cytolysis , Opsonization
45
Cytolysis
Damage to cell membrane resulting in cell destruction
- use of Mac
46
Membrane attack complex (MAC)
Forms pores in membrane
- used in lectin complement
47
Siderophores
Iron binding proteins that take up iron from the host
48
What are two examples of iron binding proteins
Ferritin
Lactoferrin
49
Antimicrobial peptides
Short peptides (12-50 amino acids)
- found in neutrophils, sweat and frog skin
50
Antimicrobial peptides mode of action
Inhibiting cell wall synthesis, forming pores, destroying DNA/RNA
51
Acute phase proteins produced
In liver in response of inflammation
52
Vaccine
Suspension of organisms or fractions of organism used to induce immunity
53
History of vaccine - when was the first vaccine seen in history
Chinese doctors picked off smallpox scabs and made people inhale them
54
Edward Jenner
Injected a boy with cowpox to see if he got smallpox
55
Primary response
The initial response to an antigen (pathogen)
56
Secondary response
The 2nd or later response a person gets when exposed to an antigen (pathogen) they already seen
- faster response
57
How does a vaccine effect a persons immune response?
It is their 1st exposure /but actually 2nd therefore it goes directly into secondary response
- creates those memory antibodies
58
Immunological memory
- remember pathogens
Key result of adaptive immunity
59
What 2 ways can you generate immunological memory
Getting infected
Getting vaccinated
60
Importance or significance of immunological memory
Allows for a stronger and faster response next time person exposed to pathogen
61
What are some vaccine types
Live attenuated
Inactive killed
Subunit
Toxoid
DNA
RNA
62
Live attenuated vaccine
Weaker version of the pathogen
63
Pros of a live attenuated vaccine
- mimics actual infection
- doesn’t need boosters
- stimulates antibodies / T cells
64
Cons of live attenuated vaccines
Could mutate to more pathogens
- different to store/ transport
65
Inactivated killed vaccine
Where pathogen is killed or inactivated
66
Pros of inactivated killed vaccine
Easy to transport
Little risk of infection
67
Cons of inactivated killed vaccines
- often require boosters
- activated mostly antibody response
68
Subunit vaccine
Exposed to key antigen parts of pathogen
69
Pros of subunit vaccine
Only proteins used not pathogen (it’s safer)
70
Cons of subunit vaccine
- require multiple doses
- must really understand pathogen to use this method
71
Toxoids
Inactivated bacterial toxins
72
DNA vaccine
DNA for antigen placed in a vector
73
Pros of a dna vaccine
It is inexpensive and easy to make
74
Cons of a dna vaccine
Finding a safe virus to deliver the dna is difficult
75
RNA vaccine
RNA for antigen is delivered to the body
76
Pros of a RNA vaccine
- safe to produce and easy to make
77
Cons of RNA vaccines
It has to be stored at cold temperatures: due to it being very unstable
78
What type of vaccine is covid?
MRNA
79
Adjuvants
Components included in vaccines to improve their effectiveness
80
When are vaccines especially helpful?
When antivirals do not work
81
Infection
When virus enters body and begins to reproduce
82
Disease
When viral replication causes immune response = symptoms
83
Do vaccines prevent infection or disease?
They prevent disease for occurring
- individuals still likely to get infected with a pathogen
84
Are vaccine preventable disease on the rise?
Yes!!!
- measles and whooping cough are prevalent now due to people not getting vaccinated
85
What are the 2 types of adaptive immunity
Humoral immunity
Cellular immunity
86
Humoral immunity
Takes place in extracellular fluids
( works outside cell)
87
What cells are part of humoral immunity
B cells - made in the bone marrow
88
Cellular immunity
Focus on fighting viruses and bacteria that are intracellular
( work inside cell)
89
What cells are part of the cellular immunity
T cells - made in the thymus
90
Humoral immunity (b cells) make
Antibodies
91
The cellular immunity have specific receptors called
T cell receptors (TCRs)
92
Each lymphocytes mixes / matches gene segments
True or False
True
93
Antigens
Substances that induces production of antibodies
94
Epitopes
Found on antigens that help antibody’s recognize an antigen
95
Antigen antibody complex
Antigen bound to an antibody
96
Affinity
Strength of bond
97
Constant region of an antibody
Same b/w classes of antibodies
- lower part containing just heavy chains
98
Variable region of an antibody
Binds epitope
- top part containing light and heavy chain
99
Fab is found where on the antibody
Top part of heavy chain
100
Where is fc found on an antibody
Th slower part of heavy chain
101
What are the antibody classes
IgG IgM IgA IgE IgD
(Game d )
102
Can an antigen have more then one epitope
Yes
103
Can an antibody recognize more then one epitope
Yes, since it has different epitopes on its surface
104
Auto immune
Attacks host cells (immune cells)
105
Example of an autoimmune disease
Multiple sclerosis
- myelin sheath on the nerve cell is mistakenly attacked by immune cells
106
Clonal selection
Proliferate lymphocytes bind to foreign antigen forming clones
107
What are clones
Identical b/T cells
108
Clonal deletion
Eliminate lymphocytes that are harmful (attack self cells) during development
109
How is Clonal deletion eliminated
Via apoptosis (cell signals for it to die)
110
MHC1 (major histocompatibility complex)
The id badge !!
- identify self to T cells
- found on ALL nucleated cells
111
MHC2
Present antigen to T cells
Found ONLY one antigen presenting cells (monocytes, B cells, dendritic cells)
112
Once MHC2 presents fragment of peptide on th e outside of the cell what happens
T cell will activate the release of cytokines
113
What are the three phagocytes
Macrophages
Neutrophils
Dendritic cells
114
Antigen presenting cells
Engulf a pathogen (antigen) and present fragments to T cells
115
Initiation of adaptive immune response
Dendritic cells - they link innate and adaptive immune systems
116
What do dendritic cells activate
T helper cells in lymph notes
- they then release cytokines making an immune response occur
117
T cell receptor (TCR)
Bind antigens
118
Cluster of differentiation molecules (CD)
Surface molecules that help TCRs interact with antigens
119
Effector cell
Lymphocytes that has undergone Clonal selection and is capable of mediating an adaptive immune response
120
What does cytokines stimulate during an immune response
Proliferation & different T cells
121
Superantigens
Activates lots of different T cells resulting in a large immune response
122
Why are superantigens bad
- it releases a lot of cytokines = induce fever / nausea
But also wastes immune system resources
123
Example, of superantigen
Streptococcus group A
124
What where the 2 ways CHRISPR was used for
Knocking out a gene of interest
Correcting a mutation
125
Genetic editing
Scientist would purposely make mutation to examine effects
126
CRISPR purpose
To edit a genome quickly and efficiently
127
What are the two ways a gene would try to fix host cell that has cut dna
Non homologous end joining
Homologous recombination
128
Non homologous end joining
Shoves broken pieces of dna back together
- leads to deletion
129
Homologous recombination
Uses available template to fill in the missing nucleotides
( fixes protein)
130
Correct mutation
Gene that has correct sequence
131
What are the 2 ways cRISPR cas9 is used
Gene editing and Germaine editing
132
Gene editing
Fixing problematic mutation in a person
133
Germline editing fixes problematic mutation in an individuals germline
( passed down to next generation)
134
Cytotoxic T lymphocytes bind to antigens on _____
MHC1 receptors
- viral infected cells
135
When CTLs attach to target cell what is released
Perforin protein and granzymes
136
Natural killer cells
Kill cells that doesn’t show MHC1
137
How do NK cells kill cells
With perforin and granzymes causing the cell to lysis
138
What are the two B cell activation types
T independent antigen
T- dependent antigen
139
T independent antigen
Molecules with repeating units
140
T dependent antigen
Proteins
141
T dependent activation helps prevent the activation of B cells if they are not needed
TRUE or FALSE
True
B cells produce a lot of antibodies
142
B cells are able to recognize both bcr and TCR
True
143
What happens when a T helper cell is activated
It releases cytokines
144
What happens when a B cell is activated
It will release plasma cells (antibidies) and make memory cells
145
Clonal expansion (proliferation)
B. Cells proliferate (turn in to) plasma cells and memory cells
146
Where is the heavy chain located in an antibody
The inner part
147
Where is the light chain of an antibody located on an antibody
The outer part
148
Antigen presenting cells are usually ______ cells
Dendritic
149
What two things can antigen presenting cells do
Phagocytosis
Present antigen on MHC2
150
Activation of T helper cells can do what 3 things
1, activate macrophages
2. Activate B cells to show antigen on MHC2
3. Activate cytotoxic T cells ( destroy cells w/ weird MHC1)
151
What’s re the different antibody classes
IgG
IgA
IgM
IgE
IgD
152
IgG
Can cross tissues / placenta
- long lived during infections
153
IgA
Lots in body secretion
(Breast milk, saliva)
- prevent pathogen from attaching to mucus membranes
154
IgM
Early responder to infection
- monomer found on B cells as BCR
155
What a re the 4 antibody actions
1. Neutralization
2. Agglutination
3. Opsonization
4. Activate complement system (classical)
156
Neutralization
Pathogen can not bind to cell due to it being blocked from entering
157
What class of antibody does neutralization
IgG
158
Agglutination
Clump pathogens to make it easier to phagocytosis
159
What antibody class can do agglutination
IgM
160
Opsonization
Coats antigen w/ antibody’s to enhance phagocytosis
( make them better/ tastier to eat)
161
What antibody class does Opsonization
IgG
162
Activation of complement system (classical)
Results in cell lysis
- antibody binds to pathogen ➡️ c3 ➡️ broken down into C3a & C3b ➡️ increased inflammation, Opsonization & cytolysis
163
Vaccines are supposed to mimic the 1st exposure
TRUE or FALSE
True :
164
What are the 2 classifications of adaptive immunity
Passive & active
165
Passive adaptive immunity
Transfer of adaptive immune defenses from another individual or animal
166
Active adaptive immunity
Activation of an individuals own adaptive immune defenses
167
passive immunity subunits
Naturally- breast milk
Artificially- given antibodies
168
Active immunity subunits
Naturally- exposed to a pathogen in environment
Artificially- vaccine
169
Herd immunity
Immunity is found in most of the population
- many people are vaccinated
170
Vaccines decrease the number of incidence
TRUE or FALSE
True : number of new cases - it helps stop or decrease the spread of disease therefore less new cases or individuals getting sick
171
Microbiome
All the organisms in an environment
172
Symbiosis
Living together of two different organisms or populations
173
How do we identify who (microbes) are there?
Culture bacteria
174
What limitations are there about cultering bacteria?
Not all microbes present on body can be cultured
- selecting the correct environment
- selecting correct media
- living in a community or by self
175
What is the solution to culturing problem?
Gene sequencing
176
What part of a microbe is sequenced since it is highly conserved?
16s subunit on ribosome
177
Organisms that are similar to each other will have similar 16s sequence
TRUE or FALSE
True
178
Where are microbes?
Everywhere!!
179
What impacts who is in our microbiome
- diet
- environmental conditions (temperature, ph, oxygen)
- Genetics
180
Probiotics
Food with live bacteria cultures
181
Identical Twins (monozygotic)
Share 100% of genome
- come from same egg
182
Fraternal twins (dizygotic)
Share 50% of genome
- come from 2 different eggs
183
Nitrogen Fixation
Nitrogen in the air being converted to a useful nitrogen compound
184
What type of bacteria preforms nitrogen fixation
Cyanobacteria
185
What happens if there is too much nitrogen in the environment
Causes an increase of cytobacteria/ alga ➡️ increase of bacteria ➡️ decrease in oxygen ➡️ fish dying
186
Eutrophication
Too much organic matter (nitrogen/ phosphorus) causing the removal of oxygen from a body of water
187
Mycorrhizae
Network of fungi w/ plant roots
- increases surface area of roots
188
Neutrophils can do what 2 things
Phagocytosis
Extracellular traps (nets)
- trap microbes by throwing dna coated in Antimicrobial proteins
189
Macrophages
Remove old cells and pathogens via phagocytosis
190
Dendritic cells
Agranular leukocytes
- phagocytosis
