Immuno 12: Acquired Immune Review Flashcards

1
Q

T/F: The immune system will respond to a minimal amount of antigen (small antigen burden) with full force .

A

False. A minimum threshold of antigen must be met before the immune system will respond. Once the threshold is met, the innate response initiates inflammatory responses that control the pathogen replication while promoting antigen presentation to naive T cells and flow of antigen that can be recognized by B cells in the secondary lymphoid tissues.

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2
Q

Immunological memory take this form:

A

Clonally expanded memory B cells and T cells. The host is left with long lived B cell and T cell-mediated immunity to reinfection with that particular pathogen.

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3
Q

If the _________ immune response is unable to clear the infection by around day 4 of the infection, _______ immune responses are primed and ultimately, these responses will clear the infection from the body. Unless the person has full-blown AIDS.

A

innate; acquired

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4
Q

Describe the barrier functions that inhibit infectious disease from 0-4 hrs (Immediate)

A

Skin, epithelia

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5
Q

Describe the barrier functions that inhibit infectious disease from 4-96 hrs (Early)

A

Local inflammation C5a

Local TNF-alpha

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6
Q

Describe the barrier functions that inhibit infectious disease from 96-100 hrs (Late)

A

IgA in luminal spaces
IgE on mast cells
Local inflammation

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7
Q

Describe the general immune response to extracellular pathogens from 0-4 hrs (Immediate)

A

Phagocytes

Alternative and MBL complement pathways

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8
Q

Describe the general immune response to extracellular pathogens from 4-96 hrs (Early)

A

MBL
C-reactive protein
T-independent B-cell antibody
Complement

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9
Q

Describe the general immune response to extracellular pathogens from 96-100 hrs (Late)

A

IgG antibody and Fc receptor bearing cells

IgG, IgM antibody and classical complement pathway

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10
Q

Describe the general immune response to intracellular bacteria from 0-4 hrs (Immediate)

A

Macrophages

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11
Q

Describe the general immune response to intracellular bacteria from 4-96 hrs (Early)

A

Activated NK-dependent macrophage activation

IL-1, IL-6, TNF-alpha, IL-12

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12
Q

Describe the general immune response to intracellular bacteria from 96-100 hrs (Late)

A

T-cell activation of macrophages by IFN-gamma

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13
Q

Describe the general immune response to virus-infected cells from 0-4 hrs (Immediate)

A

NK cells

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14
Q

Describe the general immune response to virus-infected cells from 4-96 hrs (Early)

A

IFN-alpha & IFN-beta

IL-12 activated NK cells

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15
Q

Describe the general immune response to virus-infected cells from 96-100 hrs (Late)

A

Cytotoxic T cells

IFN-gamma

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16
Q

Recognition of a PAMP by dendritic cells and other APCs, causes them to express this receptor (aka CD80) on their surface that binds to CD28 on T cells for activating T cells and in the case of APC B-cells, serves as their 2nd signal of activation.

A

receptor B7 (aka CD80)

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17
Q

________ cells underlying mucosal surfaces can extend between epithelial cells to sample antigen in the gut lumen. (similarly to M cells)

A

Dendritic cells

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18
Q

Well over 50% of the lymphocytes in our bodies reside in the _______.

A

MALT (mucosa-associated lymphoid tissue)

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19
Q

CD4 T cells recognize their cognate peptides (antigen) bound to MHC class _____ molecules.

A

MHC class II

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20
Q

CD4 effector cells have two primary effector functions:

A

1- supply the second signal of activation to B cells

2- activation of macrophages

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21
Q

MHC class II molecules are only expressed on these 3 immune cells:

A

Macrophages
Dendritic cells
B cells

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22
Q

CD8 T cells must recognize their cognate peptide determinant bound to MHC class _____ molecules.

A

MHC class I

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23
Q

Which cells express MHC class I molecules?

A

ALL NUCLEATED cells in the body EXCEPT RBCs (notable non-nucleated cell) and neurons!

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24
Q

CD8-mediated immune responses are typically most important for clearing intracellular or extracellular infections?

A

Intracellular

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25
Q

Why is it critical that some extracellularly derived antigens be presented on MHC class I molecules and some intracellularly derived antigens be presented on MHC class II molecules? (cross-presentation)

A

If not for cross presentation, there would be no way to produce Th1 type effector CD4 T cells that have specificity for determinants of intracellular pathogens.

It would also be impossible to produce an acquired antibody response to an intracellular pathogen.

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26
Q

Briefly describe the two signals of activation of a naive T cell and why they are needed.

A

1st: recognition of cognate peptide:MHC complex on surface of APC thru the TCR.
2nd: Interaction between CD28 on T cell with B7 on APC

2nd signal of activation helps prevent activation of T-cells when there is no infection…if T cells recognize their cognate determinant when there is no infection ongoing, their cognate determinant is most likely a self determinant and the T cell will become anergic and die.
(that is how peripheral tolerance works)

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27
Q

Once the T-cell is activated by the 2nd signal of activation, it produces what cytokine that induces proliferation and differentiation into effector cells?

A

IL-2

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28
Q

Once a T cell becomes activated and begins to proliferate, initially most of the daughter cells will differentiate into short-lived effector cells, while some of the daughter cells will differentiate into ________ cells that represent a clonally expanded population of cells that are specific for a determinant of a pathogen and will live for a very long time in the secondary lymphoid tissues.

A

Memory T cells

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29
Q

Due to the elevated presence (10-100 fold) of these cells after a primary infection or immunization (compared to before), upon subsequent infections, re-exposure to the same pathogen (antigen) will result in much more rapid and effective T cell responses.

A

Memory T cells

30
Q

Do effector T cells require costimulatory (B7) signaling?

A

Nope.

31
Q

What are effector T cells gonna do when they recognize their cognate peptide antigen bound to an MHC molecule?

A

“perform their effector function” aka FUCK SHIT UP

32
Q

How is it that effector T cells access the tissues in which they will “perform their function”, aka raise hell bitches.

A

They have an adhesion molecule array (VLA-4 & LFA-1) on their surface that allows them access. It’s kind of like a battering ram for kicking down doors to FUCK SHIT UP

33
Q

If Effector T cells where a division of local law enforcement, what would they be?

A

The SWAT team. They got the call from the regular police (APCs via MHC and B7), got suited up (IL-2, proliferation, differentiation) and have their battering rams, door breech shotguns, and flash-bangs (adhesion molecule array: VLA-4 & LFA-1) for FUCKING SHIT UP

34
Q

How do naive T cells get into the secondary lymphoid tissues so they can get a taste of what’s going on infection-wise in the rest of the body?

A

They express L-selectin that binds to addressins on high epithelial venules.
Once they enter the 2ndary lymphoid tissues, their ability to express LFA-1 allows them to interact closely enough with APCs to sample their MHC:peptide complexes

35
Q

Let’s say a Cytotoxic T cell aka CD8 aka Badass mofo arrives at a site of intracellular infection. BA mofo diapedeses over to a pissed off looking enterocyte he suspects may be infected with a Salmonella sp. (that the CTL happens to be specific for). What does he need for confirmation before he initiates programmed cell death in the enterocyte aka SHUTS THAT SHIT DOWN.

A
An infected enterocyte would be expressing MHC class I on its surface bearing a peptide that the CTL would recognize, at which point he would initiate apoptosis in the enterocyte aka SHOOT HIM IN THE FACE WITH HIS OWN GUN. 
Note: no secondary activation required
36
Q

Regarding the effector T cell types:

What do CTLs do, basically?

A

Kill infected host cells
Via:
Cytotoxins–> perforin, granzymes, granulysin
Cytokines–> IFN-gamma, LT, Fas ligand

37
Q

Regarding the effector T cell types:

What do Th1 cells do, basically?

A

1- they activate macrophages (primary signal of activation)
2- supply second signals of activation to naive B cells to make antibodies (become a plasma cell)
3- Production of opsonizing antibodies such as IgG1What
Via: Cytokines–> IFN-gamma, expression of CD40 ligand to bind CD40 receptor on macrophages for 2ndary activation, GM-CSF, TNF-alpha

38
Q

Regarding the effector T cell types:

What do Th2 cells do, basically?

A

1- supply second signals of activation to naive B cells to make antibodies (become a plasma cell)
Via:
Cytokines: IL-4, IL-5, IL-10

39
Q

What do CD4 Th17 cells do again?

A

Enhance neutrophil response

40
Q

What do CD4 Treg cells do again?

A

Suppress T-cell responses

41
Q

Let’s say an activated CD4 Th1 cell diapedeses up to a macrophage bearing his cognate antigen on an MHC class I molecule. What’s gonna happen next?

a) they take it to the HOTEL MOTEL HOLIDAY INN
b) Macrophage signaled to get his shit together and start breaking down the intracellular pathogens he’s been hosting in his phagosomes

A

Tehe

42
Q

Let’s say a CD4 Th1 or Th2 cell diapedeses up to a B cell that has his cognate antigen on an MHC class II molecule on it’s surface. What’s gonna happen next?

a) they go on a couple more dates until the B cell realizes the CD4 cell is just using it to get closer to its SISTER.
b) The Th1/2 cell gives the B cell its second signal of activation which stimulates it to differentiate into a plasma cell and start secreting antibodies.

A

Hey, her sister was cuter…

43
Q

CD4 Th17 cells recruit neutrophils with these cytokines:

A

IL-17A
IL-17F
IL-6

44
Q

CD4 Treg cells tell T-cells to CHILL OUT with these suppressive cytokines:

A

IL-10

TGF-beta

45
Q

CD4 Th0 cells activated in the presence of ______ and _______ will become Th1 cells.

A

IL-12 and IFN-gamma

46
Q

CD4 Th0 cells activated in the presence of ____ and ____ will become Th2 cells.

A

IL-4 and IL-6

47
Q

If the infection is caused by an extracellular pathogen, it is likely that a CD4 Th0 cell will be activated to a Th1 or Th2 cell?

A

Th2

48
Q

If the infection is caused by an intracellular pathogen, it is likely that a CD4 Th0 cell will be activated to a Th1 or Th2 cell?

A

Th1

49
Q

CD4 Th1 cells have 3 primary effector functions:

A

1- Macrophage activation
2- Production of IL-2 that can help drive proliferation of activated T cells
3- Production of cytokines and chemokines that promote production of macrophages and neutrophils and migration of those cells to the inflammatory site.

50
Q

In a T-cell activation of a B-cell, what are the reciprocal receptors on their surfaces that bind for activation?

A

1- MHC complex (B cell) with TCR (T cell)

2- CD40 (B cell) with CD40 (T cell)

51
Q

Plasma and memory cells are derived from what immune cell type?

A

Activated B cells

52
Q

What happens during a germinal center reaction?

A

1- B cell proliferation
2- Somatic HYPERMUTATION
3- Affinity maturation
4- Isotype switching

53
Q

In the acute phase serum, higher levels of IgM or IgG will be seen?

A

IgM

54
Q

In the convalescent serum (2 months after first exposure to antigen), higher levels of IgM or IgG will be seen?

A

WAY higher levels of IgG

55
Q

List the Ab isotype(s) most associated with:

Neutralization

A
  • ** IgG1,2,3,4

* ** IgA

56
Q

List the Ab isotype(s) most associated with:

Opsonization:

A
  • **IgG1

* *IgG3

57
Q

List the Ab isotype(s) most associated with:

Sensitization for killing by NK cells

A
  • *IgG1

* *IgG3

58
Q

List the Ab isotype(s) most associated with:

Sensitization of mast cells

A

***IgE

59
Q

List the Ab isotype(s) most associated with:

Activation of complement system

A
  • **IgM
  • **IgG3
  • *IgG1
60
Q

List the Ab isotype(s) most associated with this property:

Transport across epithelium

A

***IgA dimer

61
Q

List the Ab isotype(s) most associated with this property:

Transport across placenta

A
  • **IgG1
  • *IgG3
  • *IgG4
62
Q

List the Ab isotype(s) most associated with this property:

Diffusion into extravascular sites

A
  • **IgG1,2,3,4

* *IgA monomer

63
Q

Which Ab has the highest serum levels?

A

IgG1 (300% higher than 2nd highest)

64
Q

Can all isotypes of Abs that neutralize toxins/pathogens also serve as opsonins?

A

No.

65
Q

List the 3 basic functions of IgA as a neutralizer of toxins or pathogens.

A

1- Export toxins/pathogens from lamina propria, across epithelium (inside cells via Poly-Ig receptor) to lumen of gut. Can also bind toxins/pathogens on its way across epithelium while bound to Poly-Ig receptor.
2- Bind and neutralize toxins/pathogens on mucosal surface in gut.
3- Bind toxin/pathogen on M cell surface and take it to lymphoid tissue/dendritic cell for presentation to T cells.

66
Q

_______ (Ig) and ______ (Ig) can initiate antibody-dependent cell-mediated cytotoxicity (ADCC).

A

IgG1 and IgG3

67
Q

What cell type is the effector cell of Antibody-dependent cell-mediated cytotoxicity (ADCC)?

A

NK cells

68
Q

What are the events of ADCC that lead to the killing of the target cell?

A

1- Ab binds to target cell surface
2- Fc receptors of NK cell recognize/bind Ab on target cell
3- Cross-linking of Fc receptors signals NK cell to kill target cell
4- Target cell dies by apoptosis

69
Q

Mast cells express high-affinity receptors on their surface for this Ab to use as their antigen specific receptors:

A

IgE

70
Q

What cell type’s granules contain the most inflammatory mediators of any immune cell?

A

Mast cell

71
Q

Why do repeated exposures to the same pathogen, several months after Effector T cells have already dropped after the first infection, not yield disease?

A

Antibody levels are still very high (long half-life of plasma cells and IgG) and thus the acquired immune response swiftly aborts the infection before it escalates to disease.