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Immuno > Immunology week 8 > Flashcards

Immunology week 8 Flashcards

1
Q

Week 8 repeats Week 7
Slides 0-6 wk8 are slides 32-36 wk 7
(Cellular Immune Response III)

A
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2
Q

**Week 8 repeats Another week that must be in physical cards as I can’t find it in digitial cards so I am redoing it so you have it Humoral Immune Response

A
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3
Q

Humoral
Immune
Response
Antibodies
What are AB?

A

AB- are important for eliminating AG
○ They are the only defense mechanism against microbes in the lumen of mucosal organs
and in the fetus and newborns

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4
Q

Humoral
Immune
Response

Antibodies
● Why are AB important?
(5)

A

Why are AB important?
○ Neutralization of microbes
○ Opsonization and phagocytosis of microbes
○ AB dependent cellular cytotoxicity
○ Phagocytosis of microbes opsonized with complement fragments
■ Remember C3B and C5B are important for this ;)
○ Complement activation
■ Inflammation
■ Lysis of microbes

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5
Q

Humoral
Immune
Response
Antibodies
What do AB block? How? what is an example?

A

AB against microbes and toxins BLOCK the binding of these microbes to
cellular receptors
○ Ex: tetanus vax= will produce memory antitoxin cells so if the body ever comes in contact
with that toxin it will already have memory cells to induce an IR

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6
Q

Humoral
Immune
Response
Antibodies
What is Primary IR?
What is Secondary IR?
What is DC1?
What is DC2?

A

● Primary IR= the first time that an AG has entered the body
○ Effector(80%) and memory cells(20%) are produced
● Secondary IR= the AG has already entered the body before so memory
cells have already been produced
● DC1- trap AG endogenous cells produce IL12 and stimulate t helper cells
● DC2- IL1 and stimulate type 2 t helper cells

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7
Q

Humoral
Immune
Response
Antibodies
Primary IR
During primary IR, what 2 types of cells are produced, how many? (% of each)

A

○ Effector(80%) and memory cells(20%) are produced

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8
Q

Humoral
Immune
Response
Antibodies
DC1 traps what?
produces what?
stimulates what?

A

DC1- trap AG endogenous cells produce IL12 and stimulate t helper cells

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9
Q

Humoral
Immune
Response
Antibodies
DC2
produces what?
stimulates what?

A

DC2- IL1 and stimulate type 2 t helper cells

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10
Q

Humoral
Immune
Response
Antibodies
what is opsonization?
what are some things that can increase opsonization?

A

● Opsonization
○ Increases phagocytosis by 10 fold
○ What are some things that can increase opsonization?
● FCyRI(CD64) receptor (Ig1 and IG3)- macs, neutrophils, & NK cells
● Fcdelta(IgE)- eosinophils

graphs on slide 12

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11
Q

Complement system
is it innate or adaptive IR?

A

Both innate and adaptive IR

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12
Q

Complement system
what are the 3 pathways?

A

classical
lectin
alternative

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13
Q

compliment system
what is the final result?

A

MAC

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14
Q

complement system
what are important by products that aid in opsonization?

A

C3B and C5B are important by products that aid in opsonization

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15
Q

Week 8 is a repeat of Week 4
slides 14-15 wk 8 are slides 7-11 wk 4
Compliment sytem

A
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16
Q

Antibodies
Anitbodies–when?

A

exogenous Ag–destroyed by anitbodies–produced by B cells

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17
Q

Antibodies
Anitbodies–when?
exogenous Ag–destroyed by anitbodies–produced by B cells

Name the 4 functions and describe:

A

1-Against Bacteria
neutralisation of toxins or enzymes
killing–compliment–classical pathway
ADCC–Fcy receptor(IgG and Fc8 (IgE)
2-Against viruses
virlon–complement or phagosytosis
3-Against parasites
Th2–IgE+epsinophils
4-Against Tumors**
Not is solid ancers
lymphosarcomas-compliment
lymphosarcomas=50%of cells destoyed by compliment**

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18
Q

BCR
How many chains, what types?

A

Contains 4 peptide chains (2 heavy and 2 light)

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19
Q

BCR
how many and what kind of binding sites?

A

● 2 AG binding sites
○ Is this true for TCR too??

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20
Q

BCR
T dependent
explain

A

● T dependent
○ Typically “better”
○ Strong IR and produces memory cells
○ Cells will undergo class switching so IgM-> IgG and IgA

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21
Q

BCR
T independent
explain

A

T independent
○ Really only good for AG with repeating polymers
■ E.coli, salmonella, etc

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22
Q

BCR
BCR has two roles, what are they

A

BCR has two roles:
○ Binding to the AG results in biochem signals-> activation
○ BCR internalized the bound AG (protein) into peptides that may be presented by class 2
MHC on the b cell surface for recognition by t helper cells

**Structure of Tcell and Bcell receptors p. 17

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23
Q

Costimulation of B cells
4 steps

A

● Helper t cells will be presented an AG by an APC
● Next the B cell will receive costimulation from the t cell that was just
activated by that APC
●** B cells can activate T helper cells with 1/1000 of the AG
concentration that is required to activate macrophages**
○ He said this was good to know and it was especially true to secondary IR!! ;)
● Remember the innate IR has to be fast

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24
Q

B cell activation and AB production
3 steps?

A

B cells are activated -> proliferate -> then differentiate (memory and Plasma
cells)

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25
Q

B cell activation and AB production
what is important about Humoral IR

A

Humoral IR must be initiated by specific B cell recognition of AG in secondary
lymphoid organs (remember b cells don’t interact with MHC)

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26
Q

B cell activation and AB production
what occurs with the AG?

A

The AG will bind to the membrane of the immunoglobulin on mature b cells
resulting in proliferation and differentiation into plasma cells
○ What immunoglobulins are found on mature B cells??

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27
Q

B cell activation and AB production
what is relevent about the plasma cell?

A

Remember the plasma cell will be specific for the same AG that the original B
cell that was stimulated was specific for!!!!

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28
Q

B cell activation and AB production
what is required to fight off rapidly dividing microbes?

A

Cell expansion and AB secretion are essential to fight off rapidly dividing
microbes!

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29
Q

B cell activation and AB production
Activation is facilitate by other signals, what are they?

A

Activation is facilitate by: other signals
○ CR2 coreceptor
■ Complement 2 receptor
○ OR the Toll-like receptor (innate IR)
■ Remember PAMPS and DAMPS

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30
Q

B cell activation and AB production
Activation based on AB responses:
what are the 4 steps?

A

Activation based on AB responses:
○ IR is initiated by recognition of AG by B cells and CD4 t cells
○ The lymphocytes will move towards each other and interact at the interface of t and b
cell zones
○ In the extrafollicular area it results in the proliferation and isotype switching and turn into
plasma cells. (early AB response)
○ They then migrate to the germinal center -> Germinal center rxn results in long lived
memory cells

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31
Q

B cell activation and AB production
Activation based on AB responses:
IR is initiated by what?

A

○ IR is initiated by recognition of AG by B cells and CD4 t cells

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32
Q

B cell activation and AB production
Activation based on AB responses:
○ IR is initiated by recognition of AG by B cells and CD4 t cells
what happens withthey lymphocytes?

A

The lymphocytes will move towards each other and interact at the interface of t and b
cell zones

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33
Q

B cell activation and AB production
Activation based on AB responses:
○ IR is initiated by recognition of AG by B cells and CD4 t cells
○ The lymphocytes will move towards each other and interact at the interface of t and b
cell zones
in the extrafollicular area what happens?

A

In the extrafollicular area it results in the proliferation and isotype switching and turn into
plasma cells. (early AB response)

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34
Q

B cell activation and AB production
Activation based on AB responses:
○ IR is initiated by recognition of AG by B cells and CD4 t cells
○ The lymphocytes will move towards each other and interact at the interface of t and b
cell zones
○ In the extrafollicular area it results in the proliferation and isotype switching and turn into
plasma cells. (early AB response)
Where do they migrate and what result?

A

They then migrate to the germinal center -> Germinal center rxn results in long lived
memory cells

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35
Q

Proteins and T dependent AG
Are protein Ag t dependent?

A

Protein Ag are t dependent!!!

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36
Q

Proteins and T dependent AG
● Protein Ag are t dependent!!!
○ Naive CD4 t cells are activated where? How?

A

Proteins and T dependent AG
● Protein Ag are t dependent!!!
○ Naive CD4 t cells are activated in the t cell zones by AG presented by DC cells

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37
Q

Proteins and T dependent AG
● Protein Ag are t dependent!!!
○ Naive CD4 t cells are activated in the t cell zones by AG presented by DC cells
○ The activated CD4 cell and the activated B cells migrate where and what happens? why?

A

Proteins and T dependent AG
● Protein Ag are t dependent!!!
○ Naive CD4 t cells are activated in the t cell zones by AG presented by DC cells
○ The activated CD4 cell and the activated B cells migrate towards one another and interact
at the edges of the follicles.
■ This occurs b/c helper cells will express the CD40 L which will bind the the CD40
receptor on the B cell -> proliferation and differentiation of the B cell

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38
Q

Proteins and T dependent AG
● Protein Ag are t dependent!!!
○ Naive CD4 t cells are activated in the t cell zones by AG presented by DC cells
○ The activated CD4 cell and the activated B cells migrate towards one another and interact
at the edges of the follicles.
■ This occurs b/c helper cells will express the CD40 L which will bind the the CD40
receptor on the B cell -> proliferation and differentiation of the B cell
what happens to some? wht do they form? what happens there?

A

Proteins and T dependent AG
● Protein Ag are t dependent!!!
○ Naive CD4 t cells are activated in the t cell zones by AG presented by DC cells
○ The activated CD4 cell and the activated B cells migrate towards one another and interact
at the edges of the follicles.
■ This occurs b/c helper cells will express the CD40 L which will bind the the CD40
receptor on the B cell -> proliferation and differentiation of the B cell

○ Some of them will migrate into follicles to form germinal centers where the more
intense IR will occur

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39
Q

Spleen extrafollicular activation
what is it? where does it happen? what result?

A

● Extrafollicular foci develop in the outer portions of the t cell rich
periarteriolar lymphoid sheath (PALS) OR between the t cell zone and the
red pulp
○ These are known as PALS foci

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40
Q

T follicular helper cells & Germinal Centers
explain T cell activation:

A

● T cell activation
○ 1. Activation by APC dendritic cell
○ 2. Activation by B cell

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41
Q

T follicular helper cells & Germinal Centers
Activated T cells express what?
why is this important?
what is created?
where does it happen?

A

Activated T cells express CXCR5
which is very important for
germinal center formation and
function which are created in
lymphoid follicles in T dependent
rxns

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42
Q

T follicular helper cells & Germinal Centers
Why are Germinal Centers important?

A

Germinal centers are important
for long lived plasma and memory
b cells & continued isotype
switching

**slide 22 is the Germanal Center Reaction Diagram

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43
Q

Isotope switching & Plasmablasts
what signals aid in isotype switching

A

CD40 signals aid in isotype switching

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44
Q

Isotope switching & Plasmablasts
What is the enzyme essential for isotype
switching!

A

AID is the enzyme essential for isotype
switching!

45
Q

Isotope switching & Plasmablasts
IgM->IgG= ?

A

IgM->IgG= T dependent AB

46
Q

Isotope switching & Plasmablasts
IgG=?

A

IgG= phagocytosis

47
Q

Isotope switching & Plasmablasts
IgE=?

A

IgE=parasitic infections

48
Q

Isotope switching & Plasmablasts
IgA=?

A

IgA=epithelia into mucosal secretions

49
Q

Isotope switching & Plasmablasts
short lived vs. long lived
what is the difference?

A

Short lived- t independent
Long lived- t dependent

50
Q

Isotope switching & Plasmablasts
Almost half of the AB in the blood of a
healthy adult comes from what ?

A

Almost half of the AB in the blood of a
healthy adult comes from long lived
plasma cells

51
Q

Isotope switching & Plasmablasts
what relevence is the Golgi body?

A

Golgi body is very prominent
**diagram p.24

52
Q

T dependent vs. t independent
T dependent AG= ?

A

T dependent AG= rxn occurs in the FOLLICLES

53
Q

T dependent vs. t independent
T dependent AG= rxn occurs in the FOLLICLES
4 fascinating facts:

A

T dependent vs. t independent
● T dependent AG= rxn occurs in the FOLLICLES
○ Isotype switching
○ High affinity
○ Memory B cells
○ Long lived plasma cells

54
Q

T dependent vs. t independent
T independent AG+ do not need the help of helper t cells
3 fascinating facts:

A

T independent AG+ do not need the help of helper t cells
○ Mainly IgM
○ Low affinity
○ Short lived plasma cells

55
Q

Primary response
What happens with activated B cells?
Secondary encounter?
what is the main difference between primary and secondary IR?

A

● Activated B cells produce low affinity IgM then
high affinity IgG but if there is no AG left the
titers will decrease
● Secondary encounter- long lived plasma cells
○ Faster and better response
● Main difference between primary and
secondary IR
○ The high levels of IgG in secondary IR is basically the
IgM levels in the primary IR (but slightly higher)

diagram on slide 26

56
Q

Where the RXNs occur
Follicular B cells in secondary lymphoid organs-> ?
are they T dependent or independent?

A

Follicular B cells in secondary lymphoid organs-> AB responses to protein
AG and they require the help of t helper cells
○ So t dependent

57
Q

Where the RXNs occur
Marginal zone B cells in the spleen,….
where are tehy found?
Are they t dependent or independent?
what is an example?
what type of pathoden does the spleen filter?

A

Marginal zone B cells in the spleen, B1 cells in the mucosal tissues and in
the peritoneum are t independent (ex: polysaccharides)
○ What type of pathogen does the spleen filter?

58
Q

How are AG captured and delivered to B cells?
4 steps:

A
  1. Transported to lymph nodes via afferent lymphatic vessels which drain
    into the subcapsular sinus of the node. They can reach the B cell zone
    through the subcapsular sinus and underlying follicles
  2. Subcapsular macrophages capture the large microbes which results in
    AG-AB formation and deliver them to the follicles.
  3. When entering the spleen they may bind to the complement receptors on
    the marginal zone and then transfer them to the follicles
  4. Polysaccharide AG can be captures by macs in the marginal zone and
    displayed to b cells
    ***they are always presented undegraded, intact, and not processed by

APCS*****

59
Q

How are AG captured and delivered to B cells?
1. Transported to lymph nodes via ? where do they drain? how do they reach the B cell zone?

A
  1. Transported to lymph nodes via afferent lymphatic vessels which drain
    into the subcapsular sinus of the node. They can reach the B cell zone
    through the subcapsular sinus and underlying follicles
60
Q

How are AG captured and delivered to B cells?
1. Transported to lymph nodes via afferent lymphatic vessels which drain
into the subcapsular sinus of the node. They can reach the B cell zone
through the subcapsular sinus and underlying follicles
2. Subcapsular macrophages capture what? resulting in what?

A
  1. Subcapsular macrophages capture the large microbes which results in
    AG-AB formation and deliver them to the follicles.
61
Q

How are AG captured and delivered to B cells?
1. Transported to lymph nodes via afferent lymphatic vessels which drain
into the subcapsular sinus of the node. They can reach the B cell zone
through the subcapsular sinus and underlying follicles
2. Subcapsular macrophages capture the large microbes which results in
AG-AB formation and deliver them to the follicles.
when intering the spleen they may what?

A
  1. When entering the spleen they may bind to the complement receptors on
    the marginal zone and then transfer them to the follicles
62
Q

How are AG captured and delivered to B cells?
1. Transported to lymph nodes via afferent lymphatic vessels which drain
into the subcapsular sinus of the node. They can reach the B cell zone
through the subcapsular sinus and underlying follicles
2. Subcapsular macrophages capture the large microbes which results in
AG-AB formation and deliver them to the follicles.
3. When entering the spleen they may bind to the complement receptors on
the marginal zone and then transfer them to the follicles
4. polysaccharide AG can what? what result?

A
  1. Polysaccharide AG can be captures by macs in the marginal zone and
    displayed to b cells

***they are always presented undegraded, intact, and not processed by

APCS*****

63
Q

CLINICAL CORRELATION!!!!!!!!
● 80% chinese shar peis develop what?
why?
explain?

A

CLINICAL CORRELATION!!!!!!!!

● 80% chinese shar peis develop recurrent dermatitis and other allergies
associated with body surfaces. (you have the list)
● This is due to selective immunoglobulin deficiencies
○ Normal levels of IgG & IgM but abnormal levels of IgA!!!!
● Deficiency in IgA AB in the skin and mucosal surfaces results in these
allergies.
● Possibly genetics??

64
Q

Development of B lymphocytes
what are the 3 stages?

A

Development of B lymphocytes
● 3 stages
○ Maturation- gen of mature
immunocompetent B cells
○ Activation- contact of B cells with specific
AG
○ Differentiation- activated B cells become
plasma cells that produce AB or become
memory B cells

65
Q

Development of B lymphocytes
where are B cells produced?
what do Plasma cells secrete?
How does activation occur?
relevence of MHC
How are they activated?

A

● Where are B cells produced?
● Plasma cells- secrete AB for a SPECIFIC
AG

● Activation- driven by presence of AG->
proliferation-> differentiation into
plasma and mem cells
● REMEMBER: NO MHC!!!
● Activated by thymus dependent TD AG
or thymus independent TI AG

66
Q

B cell responses
what are the 2 responses?

A

B cell responses
TD response
TI response

67
Q

B cell responses
TD response:
what is required?
what are the 3 steps?

A

● TD response:
○ Requires a CD4 cell to be activated
○ DC activated T cell
○ T cell then activates B cell
○ B cell-> plasma cell

68
Q

B cell responses
TI response
how do they activate B cells?

A

TI response:
○ Directly activate B cells

69
Q

B cell responses
TI response:
Tl-1 v Tl-2
explain

A

○ TI-1
■ Polyclonal activators (activate
non-specifically) not good for us :(

○ TI-2
■ Activate B cells by extensively
cross-linking to Ig receptors

70
Q

B cell responses
TI response
Strong? weak?
memory?

A

TI response- usually weak and no
memory is made

71
Q

B cell responses
TI response:
Dominant Ig= ?

A

Dominant Ig= IgM
○ (mom- first to the scene)
diagram slide 32

72
Q

BCR and Humoral response
What 2 Ig molecules must a BCR have???

A

What 2 Ig molecules must a BCR have???

○ They both have short cytoplasmic tails-
can’t transduce a signal

73
Q

BCR and Humoral response
BCR= ?

A

BCR= binds to AG

74
Q

BCR and Humoral response
● Signal transduction= ?
what about tails?

A

Signal transduction= performed by Iga
and Igb chains
○ Longer tails= ITAMS

75
Q

BCR and Humoral response
If it is the first time infected w/ that AG-> ?

A

If it is the first time infected w/ that AG->
primary IR-> AB production(plasma cells)
& memory produced

76
Q

BCR and Humoral response
LAG TIME:
Clonal selection-?
Clonal expansion-?
Differentiation-?
Production of AB-?

A

LAG TIME:
○ Clonal selection- selection of b cells with
specificity for that AG
○ Clonal expansion- inc. in #
○ Differentiation- development of plasma
and memory cells
○ Production of AB- IgM and IgG

77
Q

IMMUNE RESPONSE!!!!!!
● Primary IR?

A

● Primary IR
○ Overall low levels of AB
■ IgM- main
■ IgG- low (gma slow)

78
Q

IMMUNE RESPONSE!!!!!!
● Secondary IR ?

A

● Secondary IR
○ Body has already come in contact with
this AG
○ Dependent on the existence of memory
B and T helper cells
○ Overall high levels of AB
■ IgG- main
■ IgM- low

79
Q

IMMUNE RESPONSE!!!!!!
4 fascinating facts about Secondary IR?

A

● Secondary IR
○ Body has already come in contact with
this AG
○ Dependent on the existence of memory
B and T helper cells
○ Overall high levels of AB
■ IgG- main
■ IgM- low
● Gen rapidly
● Stronger than primary
● Lasts longer
● AB have higher affinity to AG

80
Q

I would know this ;)
Property : Responding B Cells
Primary Response?
Secondary Response?

A

I would know this ;)
Property : Responding B Cells
Primary Response: Naive B cells
Secondary Response: Memory B cells

81
Q

I would know this ;)
Property : lag time after antigen administration
Primary Response
Secondary Response

A

I would know this ;)
Property : lag time after antigen administration
Primary Response Generally 4-7 days
Secondary Response Generally 3-4 days

82
Q

I would know this ;)
Property : peak of response
Primary Response?
Secondary Response?

A

I would know this ;)
Property : peak of response
Primary Response 7-10 days
Secondary Response3-5 days

83
Q

I would know this ;)
Property : Magnitud of response
Primary Response?
Secondary Response?

A

I would know this ;)
Property : Magnitud of response
Primary Response varies depending on the antigen type
Secondary Response100-1000 more than primary response

84
Q

I would know this ;)
Property : Isotype of antibody produced
Primary Response?
Secondary Response?

A

I would know this ;)
Property : Isotype of antibody produced
Primary Response IgM dominates
Secondary Response IgG dominates

85
Q

I would know this ;)
Property : type of antigen inducing response
Primary Response?
Secondary Response?

A

I would know this ;)
Property : type of antigen inducing response
Primary Response T-dependend and T-independedt antigens
Secondary ResponseT dependent antigens

86
Q

I would know this ;)
Property : Antibody Affinity
Primary Response?
Secondary Response?

A

I would know this ;)
Property : Antibody Affinity
Primary Response low
Secondary Response high

Graph on slide 35

87
Q

Humoral induction
AG= ?

A

● AG= concentrate in the lymph nodes unless
they are in the blood then they go to the
spleen

88
Q

Humoral induction
4 steps
IR =?

A

IR= initiated by the recognition of AG by B
and CD4 cells

89
Q

Humoral induction
1. IR= initiated by the recognition of AG by B
and CD4 cells
2. Activated lymphocytes- migrate where? what result?

A
  1. IR= initiated by the recognition of AG by B
    and CD4 cells
  2. Activated lymphocytes- migrate to each
    other and B cells= proliferate &
    differentiate
90
Q

Humoral induction
1. IR= initiated by the recognition of AG by B
and CD4 cells
2. Activated lymphocytes- migrate to each
other and B cells= proliferate &
differentiate
3. Restimulation of B cells by what ? resulting in what?

A
  1. IR= initiated by the recognition of AG by B
    and CD4 cells
  2. Activated lymphocytes- migrate to each
    other and B cells= proliferate &
    differentiate
  3. Restimulation of B cells by CD4 in
    extrafollicular sites-> isotope switching but
    activation of t cells by b cells= follicular
    helper t cells
91
Q

Humoral induction
1. IR= initiated by the recognition of AG by B
and CD4 cells
2. Activated lymphocytes- migrate to each
other and B cells= proliferate &
differentiate
3. Restimulation of B cells by CD4 in
extrafollicular sites-> isotope switching but
activation of t cells by b cells= follicular
helper t cells
4. GERMINAL FREAKIN’ CENTERS!!!!- what result (4)?

A
  1. GERMINAL FREAKIN’ CENTERS!!!!- where the
    late events occur
    a. Somatic mutation
    b. Selection of high affinity cells
    c. Isotope switching
    d. Memory B cells & long lived plasma cells
92
Q

Humoral induction
● Co-stimulation of b cells
○ Signal 1= ?

A

● Co-stimulation of b cells
○ Signal 1= BCR + AG

93
Q

Humoral induction
● Co-stimulation of b cells
○ Signal 2= ?
induces what?

A

● Co-stimulation of b cells
○ Signal 1= BCR + AG
○ Signal 2= CD40 and CD40L on the
activated Th cell
■ Induces the B7 that interacts with
CD28

graph p. 37

94
Q

Don’t sleep on the Germinal center!!!
● GERMINAL FREAKIN’ CENTERS!!!!- where the
late events occur
a. Somatic mutation
b. Selection of high affinity cells
c. Isotope switching
d. Memory B cells & long lived plasma cells
● Within a follicle ? light zone? dark zone?

A

Don’t sleep on the Germinal center!!!
● GERMINAL FREAKIN’ CENTERS!!!!- where the
late events occur
a. Somatic mutation
b. Selection of high affinity cells
c. Isotope switching
d. Memory B cells & long lived plasma cells
● Within a follicle
○ Light zone= DC
○ Dark zone= proliferating B cells (makes sense
bc the N:C ratio)

*diagram p. 37

95
Q

Ig Class Switching
Do to what?

A

Ig Class Switching
● Due to somatic hypermutation that heads to changes in Ig

96
Q

Ig Class Switching
● TD= what happens?

A

● TD= B cells undergo heavy chain isotype switching and can produce AB w/
heavy chains (y,a,e)

97
Q

You are a new baby DOGtor in Romania. While you’re in your clinic, the NUN (from the
conjuring movies) comes in your clinic. She is questioning you about your immunology
background, little does she know that you are a master in immuno. Which of the
following is something you would tell her when she asks which of the following is not a
mechanism of CD8 killing?
A. Apoptosis
B. Perforin
C. Granzyme
D. Fas/FasL
E. All of the above
F. Throw holy water and run

A

E

98
Q

The nun is still trying to trip you up. She tells you naive
CD8 cells can secrete INF-Y and recognize AG from any
cell. Is this true or false??
a. True
b. false

A

B

99
Q

You’re starting to get real annoyed with the Nun taking up all of your appointment
time. You tell her you are a bomb a** immuno master and that she can ask you one
from question before she leaves but you have other appointments to get to. She
wants to know what PD1: PD ligand is important for.
a. Initiating responses by activating naive t cells
b. Inhibiting the activation of t cells in secondary lymphoid organs
c. Inhibiting the activation of effector cells in peripheral tissues
d. It is important for helper t cell dependent AB responses

A

C

100
Q

You finally are able to get out of the exam room with the nun but your next
appointment has already been waiting for approx. 7 mins and they are very
annoyed. You walk in an apologize then you realize that your next client is edward
scissorhands. While you are conducting a PE on his pet blowfish he asks you what
is clonal expansion. Which is the most correct answer?

A. It results in an increase in the number of AG non-specific
clones
B. It results in an decreased in the number of AG specific clones
C. It results in no change in the number of AG specific clones
D. It results in an increase in the number of AG specific clones

A

D

101
Q

You are still conducting a PE on Mr. scissorhands
blowfish. He now wants to know what is the divergent
pathway that memory cells go undergo?
A. The divergent pathway is a way for effector cells to mature
into memory cells
B. It is how memory cells can go from naive cells to memory cells
C. It is how effector cells can go from naive to effector
D. It is how memory cells can go from naive to effector to
memory cells

A

B

102
Q

Mr. scissorhands is now asking about the different T cell
subsets. Which of the following is true?

A. CD4 cell function is mediated by cytokines
B. The Th1 subset is the central rxn of a cell mediated immunity and its
effector function is mediated by IFNy
C. The TH2 subset is important for helminthic infections and is central to the
development of allergic dz
D. The Th17 subset is important for recruiting leukocytes.
E. All of the above

A

E

103
Q

You are finished with the wellness exam but Edward has
one more question. What is the function of CD69?
A. Retention in the lymph node
B. Retention in the placenta
C. Aids in keeping the cellular IR in check
D. Prevents AG from entering the lymph node

A

A

104
Q

Jack the skeleton brings zero into the vet clinic. While
you are conducting a PE on zero he asks what is t cell
exhaustion. What do you tell him?

A. Response increases due to reduced production of IFNy or increase
expression of multiple inhibitory receptors.
B. Response decreases due to increase production of IFNy or increase
expression of multiple inhibitory receptors.
C. Response decreases due to reduced production of IFNy or increase
expression of multiple inhibitory receptors.
D. Response increases due to reduced production of IFNy or decrease
expression of multiple inhibitory receptors.

A

C

105
Q

Now Jack is asking about the process of how CD8 cells
operate. Put them in the correct order (first to last).

  1. Activation of CTLs
  2. Release of CTLs
  3. Delivery of the letal compounds to kill target cells
  4. AG recognition
A

4,1,2,3

106
Q

You are at monkey bar trying to enjoy your halloween.
When your immuno TA and Prof show up!!! What do say
whenever they ask you about the 2 killing pathways of
CD8 cells?????

Short answer :)

A

You are at monkey bar trying to enjoy your halloween.
When your immuno TA and PRof show up!!! What do say
whenever they ask you about the 2 killing pathways of
CD8 cells?????

● Cytotoxic proteins
○ Granzyme B and perfornin
● FasL and Fas death receptors

107
Q

Your immuno TA and Dr. toka aren’t going to let you get
off that easy. They are asking you why chinese shar
peis= commonly have skin allergies. What do you tell
them?
A. IgE def
B. IgG def
C. Too much IgE
D. IgM
E. IgA def

A

E

108
Q

Your immuno Ta decides to leave but now Dr. toka is still
asking you questions. He wants to know how B cells are
activated. Which of the following is something you
would say?
A. MHC 2 activates all B cells
B. MHC 1 and co-stimulation
C. B cells do not have co-stimulation
D. BCR and AG / CD40 CD40 L

A

D

109
Q

Now Dr. toka tells you that he will let you enjoy the rest
of your night if you will answer 1 last question
correctly.Explain the difference between primary and
secondary IR. (Ig levels and types)

Short answer :)

A

Now Dr. toka tells you that he will let you enjoy the rest
of your night if you will answer 1 last question
correctly.Explain the difference between primary and
secondary IR. (Ig levels and types)
primary - low Ig levels IgM- main
Secondary- high Ig levels IgG- main

Immuno (13 decks)

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