Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MF2 Immunology > Immunotherapy > Flashcards

Immunotherapy Flashcards

1
Q

Activation of the TCR results in increased intracellular levels of this ion

A

Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

TCR activation without CD28 costimulation results in this

A

Anergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ca2+ dependent phosphatase that dephosphorylates NFATc

A

Calcineurin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Calcineurin dephosphorylates this transcription factor, which is inactive and sequestered in the cytoplasm when phosphorylated

A

NFATc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Calcineurin is activated by this

A

Increased intracellular Ca2+ from TCR activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NFATc is a transcription factor that leads to activation of genes encoding this

A

Cytokines (specifically IL-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

IL-2 binding to its IL-2 receptor on T cells leads to activation of this, which causes cell cycle progression and promotes T cell division and proliferation

A

mTOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

mTOR is activated by this

A

IL-2 binding to its receptor on T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Big 4 adverse effects for monoclonal antibodies

A

Hypersensitivity
Increased risk of infections
Increased risk of heart failure
Increased risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Chimeric monoclonal anti-CD20 Ag on B cells
Depletes B cells, reduces Ab production

A

Rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rituximab is a monoclonal antibody for this

A

Anti-CD20 antigen on B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rituximab depletes these cells

A

B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chimeric monoclonal antibody to the alpha subunit (CD25) of the IL-2 receptor on activated T cells
Inhibits T cell activation and proliferation

A

Basiliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Basiliximab is a chimeric monoclonal antibody to this

A

Alpha subunit (CD25) of the IL-2 receptor on activated T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Basiliximab inhibits activation/proliferation of these cells

A

T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fatal infusion reactions and fatal multifocal leukoencephalopathy are adverse effects of this

A

Rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

GI upset, hypersensitivity, increased risk of infection, heart failure, and cancer are adverse effects for this

A

Basiliximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Polyclonal, recombinant, cytotoxic antibodies to surface T cells antigens
Indicated for induction and to terminate transplant rejection

A

Anti-thymocyte globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Anti-thymocyte globulin is indicated for these 2 things

A

Induction and to terminate transplant rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Immunosuppression, hypersensitivity, fever and chills, hypotension, increased risk of cytomegalovirus infections are adverse effects of this

A

Anti-thymocyte globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Hypotension from anti-thymocyte globulin can be minimized by pretreatment with these

A

Corticosteroids, acetaminophen, or antihistamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pretreatment with corticosteroids before treatment of anti-thymocyte globulin can minimize this adverse effect

A

Hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Corticosteroid pretreatment can minimize hypotension as a result of this drug

A

Anti-thymocyte globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Class of drugs that cause the death and redistribution of lymphocytes by curtailed activation of NF-kB
Inhibit synthesis of pro-inflammatory cytokines

A

Glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Glucocorticoids curtail the activation of this, resulting in increased apoptosis of lymphocytes

A

NF-kB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

NF-kB activation can be curtailed by these drugs

A

Glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 Indications for glucocorticoids

A

Prevent and treat transplant rejection
Auto-immune disorders
Allergic reactions to other immunosuppressive agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Increased risk of infections such as oral candidiasis and adrenal suppression are adverse reactions to this

A

Glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Drug used for induction and to terminate transplant rejection

A

Anti-thymocyte globulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Drug used to prevent and treat transplant rejection, auto-immune disorders, and allergic reactions to other immunosuppressive agents

A

Glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

2 adverse reactions to glucocorticoids

A

Increased risk of infections such as oral candidiasis
Adrenal suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

2 calcineurin inhibitors

A

Tacrolimus and Cyclosporine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Protein that binds tacrolimus

A

FKBP-12 (FK binding protein)
Blocks calcineurin’s phosphatase activity; blocks IL-2 production

34
Q

Protein that binds cyclosporine

A

Cyclophilin
Blocks calcineurin’s phosphatase activity; blocks IL-2 production

35
Q

Both calcineurin inhibitors (Tacrolimus and cyclosporine) binds to this

A

An immunophilin (chaperone protein)
FKBP-12 (FK binding protein) binds tacrolimus
Cyclophilin binds cyclosporine

36
Q

2 drugs that block calcineurin’s phosphatase activity, preventing movement of NFAT, and blocking the production of IL-2

A

Calcineurin inhibitors - Tacrolimus and Cyclosporine

37
Q

4 adverse effects to calcineurin inhibitors (Tacrolimus and Cyclosporine)

A

Renal toxicity
Cardiovascular risk elevated by hyperlipidemia
Hypertension
Hyperglycemia/diabetes (especially when combined with glucocorticoids)

38
Q

Renal toxicity, cardiovascular risk elevated by hyperlipidemia, hypertension, and hyperglycemia are adverse effects to this type of drug

A

Calcineurin inhibitors

39
Q

FKBP-12 is an immunophilin (chaperone) that binds this drug

A

Tacrolimus

40
Q

Cyclophilin is an immunophilin (chaperone) that binds this drug

A

Cyclosporine

41
Q

Tacrolimus and Cyclosporine primarily act on these cells

A

T cells
Are calcineurin inhibitors; Block the production of IL-2

42
Q

Nephrotoxicity, neurotoxicity, elevated cardiovascular risk, and hyperglycemia are adverse effects of this

A

Tacrolimus (calcineurin inhibitor)

43
Q

4 toxicities of Tacrolimus

A

Nephrotoxicity
Neurotoxicity
Cardiovascular risk
Hyperglycemia/diabetes

44
Q

Widely used immunosuppresive drug that can treat dry eye

A

Cyclosporine (calcineurin inhibitor)

45
Q

Renal toxicity, cardiovascular risk, hypertension, hyperglycemia/diabetes, and hepatotoxicity are adverse effects to this

A

Cyclosporine

46
Q

5 toxicities to Cyclosporine

A

Renal toxicity (important to monitor renal function through BUN/creatinine, CrCl)
Cardiovascular risk
Hypertension
Hyperglycemia/diabetes
Hepatotoxicity

47
Q

Sirolimus and Everolimus bind this, which complexes with mammalial target of rapamycin (mTOR) to block progression of cell cycle in T cells

48
Q

Drugs that bind FKBP-12 and complexes with mTOR to block progression of cycle cycle in T cells

A

Sirolimus and Everolimus

49
Q

Sirolimus and Everolimus ultimately block this

A

mTOR –> block progression of cell cycle in T cells

50
Q

2 drugs that inhibit the response to IL-2 but do not alter its production
Net effect is blocked cell proliferation

A

Sirolimus and Everolimus

51
Q

Hyperlipidemia, renal failure, hyperglycemia, angioedema, and bone marrow suppression are adverse effects to these

A

Sirolimus and Everolimus

52
Q

5 adverse effects to Sirolimus and Everolimus

A

Hyperlipidemia
Renal failure (especially when combined with cyclosporine)
Hyperglycemia
Angioedema
Bone marrow suppression

53
Q

2 anti-proliferative / anti-metabolic drugs

A

Azathioprine and Mycophenolate mofetil

54
Q

Azathioprine is first converted to this
Then to false/decoy nucleotides that incorporate into RNA to block translation

A

Mercaptopurine (anticancer drug)

55
Q

Drugs that bind FKBP-12, that complexes with mammalian target of rapamycin (mTOR) to block progression of cell cycle in T cells

A

Sirolimus and Everolimus

56
Q

Drug that is converted first to mercaptopurine (anticancer drug) and then to false/decoy nucleotides that incorporates into RNA to block translation
Powerful anti-inflammatory action

A

Azathioprine

57
Q

2 adverse effects of Azathioprine

A

Bone marrow suppression and increased risk of infections

58
Q

Azathioprine ultimately blocks this

A

Translation; inhibits T cell function more than B cell function
(Converted first to mercaptopurine (anticancer drug) and then to false/decoy nucleotides that incorporates into RNA to block translation)

59
Q

Allopurinol inhibits biotransformation of this drug, increasing toxicity

A

Azathioprine

60
Q

Drug that inhibits biotransformation of azathioprine and mercaptopurine, increasing toxicity

A

Allopurinol

61
Q

Drug that is converted to mycophenolic acid, inhibits purine (GMP) synthesis

A

Mycophenolate mofetil

62
Q

Mycophenolate mofetil is converted to this, which inhibits purine (GMP) synthesis

A

Mycophenolic acid

63
Q

Mycophenolate mofetil is converted to mycophenolic acid, which inhibits this

A

Purine synthesis (suppresses both B and T cell activation)

64
Q

2 adverse effects of mycophenolate mofetil

A

Bone marrow suppression
Increased risk of infection

65
Q

Monoclonal antibodies that bind PD-1 on T cells, preventing interaction with PDL1 on tumor cells
Blocks the anti-proliferation signal that activated PD-1 produces in T cells

A

Pembrolizumab

66
Q

Pembrolizumab is monoclonal antibodies that binds this

A

PD-1 on T cells
Blocks the anti-proliferation signal that activated PD-1 produces in T cells

67
Q

Lymphokine that stimulates production of T cells and activates natural killer cells

A

Recombinant interleukin-2 (rIL-2)

68
Q

rIL-2 has this effect

A

Stimulates production of T cells and activates NK cells

69
Q

Fatal multifocal leukoencephalopathy is an adverse effect associated with this

70
Q

Hypotension that is minimized with pretreatment with corticosteroids is an adverse effect associated with this

A

Anti-thymocyte globulin

71
Q

Increased risk of cytomegalovirus infections is an adverse effect associated with this

A

Anti-thymocyte globulin

72
Q

Increased risk of infections such as oral candidiasis is an adverse effect associated with this

A

Glucocorticoids

73
Q

Adrenal suppression is an adverse effect associated with this

A

Glucocorticoids

74
Q

Hyperlipidemia is an adverse effect associated with these

A

Calcineurin inhibitors, Sirolimus and Everolimus

75
Q

Nephrotoxicity is an adverse effect associated with this

A

Tacrolimus

76
Q

Neurotoxicity is an adverse effect associated with this

A

Tacrolimus

77
Q

Renal failure from Sirolimus and Everolimus is more common when combined with this

A

Cyclosporine

78
Q

Angioedema is an adverse effect associated with this

A

Everolimus (also Sirolimus)

79
Q

Bone marrow suppression is an adverse effect associated with these 3 drugs

A

Sirolimus/Everolimus, Azathioprine, and Mycophenolate Mofetil

80
Q

Binds to nuclear receptors to promote T cell death by inhibiting NFkB activation

A

Glucocorticoids

81
Q

Drug class that blocks PD-1 signaling to enhance anti-tumor immunity

A

Immune checkpoint inhibitors

82
Q

Polyclonal antibodies used to induce immune suppression and terminate transplant rejection

A

Anti-thymocyte globulin

MF2 Immunology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions