Module 7 Flashcards

(70 cards)

1
Q

Where do most pathogens enter the body?

A

Through the mucosal tract

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2
Q

What are the three tracts that are made up of mucosal tissue?

A

Respiratory, gastrointestinal and urogenital

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3
Q

What kinds of cells is the mucosal tract lined with?

A

Collated epithelial cells that secrete mucous

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4
Q

What two antibodies are a part of the mucosal secretions?

A

IgA and IgM

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5
Q

What do we provide commensal microorganisms with?

A

Food and warmth

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6
Q

What do commensal bacteria provide us?

A
Competition with pathogens
Digestion aid
Vitamins
Immune system development 
PTreg balance
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7
Q

What part of the gut should commensal bacteria live?

A

The lumen

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8
Q

Where is it dangerous for commensal bacteria to end up?

A

The lamina propria

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9
Q

What does MALT stand for?

A

Mucosal associated lymphoid tissues

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10
Q

What are M cells?

A

Microfold cells, specialized epithelial cells that actively sample antigens from the lumen

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11
Q

What do M cells do with the antigens they sample from the lumen?

A

They don’t degrade them but pass them to APC’s, B cells and T cells

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12
Q

What is the phenomenon of gut homing?

A

When effector cells migrate back to the mucosal tissue where they were initially activated

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13
Q

How long do antibodies usually persist after an infection and protect without the need of a secondary response?

A

A few months

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14
Q

When is a secondary response with the help of memory cells required?

A

After antibodies from the primary response breakdown

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15
Q

When are B and T memory cells created?

A

During the primary response

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16
Q

How can you tell the difference between naive B cells and memory B cells?

A

Naive B cells express IgM while memory B cells have undergone isotype switching

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17
Q

What kind if immune response is associated with the expression of IgM?

A

The primary response

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18
Q

What do naive B cells undergo during proliferation?

A

Hypermutation

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19
Q

How do memory B cells achieve affinity maturation?

A

By selecting for the memory B cells with the highest antigen affinity

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20
Q

Which are easier to activate; memory B and T cells or naive B and T cells?

A

Memory B and T cells

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21
Q

Memory B cells require helper T cells for what?

A

Activation

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22
Q

How can you tell effector and memory T cells from naive T cells?

A

Based on the expression of their surface and intracellular proteins

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23
Q

What two molecules are expressed by effector and memory T cells, but not by naive T cells?

A

Granzymes and Fas ligands for killing target cells

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24
Q

Where do memory T cells circulate?

A

Through the peripheral tissues, not limited to the lymphoid organs

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25
How are memory T cells activated?
Directly by APCs
26
What are the two sub populations of memory T cells?
Effector memory T cells and central memory T cells
27
What kind of memory cell homes directly to peripheral inflamed tissues and quickly differentiate with APCs?
Effector memory cells
28
What kind of memory cells home to secondary lymphoid tissues where they can activated B cells?
Central memory T cells
29
What produces exotoxins?
Extracellular bacteria
30
What is an example of a disease caused by exotoxins?
Tetanus, cholera, anthrax, whooping cough or scarlet fever
31
What is an example of an immune evasion tactic used by pathogens?
``` Antigenic variation Latency Inhibition of humoral immunity Inhibition of inflammation Blocking of antigen presentation and processing pathways General immune suppression ```
32
How does antigenic variation work?
The pathogen makes genetic changes to render itself unrecognizable by antibodies and memory cells
33
Which is more serious, antigenic drift or antigenic drift?
Antigenic shift which creates viral subtypes that can cause pandemics
34
What does HIV stand for?
Human immunodeficiency virus
35
How does latency help a virus?
It can persist in the same host in a dormant form
36
What two viruses use latency in the ganglia of sensory neurons?
Herpes and chicken pox/shingles
37
What can reactivate latent viruses?
Stress and immunosuppression
38
What is unique about HIV’s latency technique?
It forms a pro virus that integrates into the chromosome of an infected cell
39
What is an example of a viral immune evasion technique?
Inhibition of humoral immunity Inhibition of inflammation Blocking antigen processing and presentation Immunosupression of host
40
When did Edward Jenner introduce the vaccine for smallpox using cowpox?
1780’s
41
What are some of the goals around vaccine development?
B and T memory cells Safety High efficacy
42
What is the phenomenon of herd immunity?
The stability of a population established by a pool of relevant memory cells that reduces transmission
43
What are the three main categories of vaccine?
Attenuated live Whole organism killed/inactivated Sub-unit
44
What are some characteristics of a whole organism attenuated live vaccine?
Made with weakened, avirulent pathogen Full antigenic representation Endogenous with CTL memory Risks to those with weakened immune systems
45
What are some characteristics of whole organism inactivated vaccines
No longer infectious Safer than live Exogenous only, no CTL memory Th and B cell memory
46
What are characteristics of a sub-unit vaccine?
Made from purified Ag, not whole pathogen Exogenous only; no CTL memory Adjuvants required; mimics PAMPs to activate PRRs and APCs
47
What are adjuvants?
Nonspecific immunostimulatory agents
48
What are two novel vaccine strategies brought about by recombinant DNA techniques?
Recombinant-live vaccines | DNA vaccines
49
What is a recombinant-live vaccine?
It relies on the Ag from unrelated pathogen and a vaccine “delivery vector” to create endogenous presentation of antigens to create CTL memory
50
What is a DNA vaccine?
An injection of DNA encoding for antigen which creates immune response and then memory cells
51
What is the greatest challenge with vaccinations at this time?
Public distrust
52
What is an immunodeficiency?
A status of impairment within the immune system that decreases the ability to respond to infections or a heightened reaction to infection, both of which cause damage.
53
What are the two types of immunodeficiency?
Primary and secondary
54
What is a primary immunodeficiency?
A genetic defect that results in higher rate of infection or autoimmunity
55
What is a secondary immunodeficiency?
One that has developed due to environmental factors such as immunosuppressive drugs, chemo, or HIV/AIDS
56
When did the CDC first start reporting AIDS infections?
1980’s
57
What is the cause of death with an AIDS infection?
Opportunistic microorganisms
58
Which lymphocyte is depleted as a result of HIV/AIDS?
CD4 T cells
59
What are the two paths of HIV/AIDS infection?
Sexual contact and blood
60
What kind of virus is HIV?
Retrovirus
61
What is the major surface Ag of HIV?
Gp120
62
What is a provirus?
The dormant form taken by HIV while its in its latent stage. Once the infected T cell is activated, the virus will start reproducing.
63
What is seroconversion?
The key clinical diagnostic indicator of exposure due to HIV specific antibodies in the serum
64
What are three ways that AIDS evades immune responses?
Provirus dormancy Error prone reverse transcriptase CD4 Th cell depletion
65
How does the provirus state help AIDS evade the immune system?
Pro viruses are not detectable by antibodies and without replication they are not recognized by CTL
66
How does error prone reverse transcriptase help AIDS avoid immune detection?
By creating thousands of sub-types within a single person that make memory cell identification and vaccine development nearly impossible
67
What does HAART stand for?
Highly active antiretroviral therapy
68
What is HAART?
A combination therapy that target HIV replication enzymes
69
What are the draw backs of HAART?
Toxicities Not a cure Expensive
70
How was one person cured of AIDS?
Through a bone marrow transplant from an donor with a defective CCR5 co-receptor gene