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MF2 Immunology > Immunotherapy > Flashcards

Immunotherapy Flashcards

1
Q

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

A

Ca2+

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2
Q

TCR activation without CD28 costimulation results in this

A

Anergy

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3
Q

Ca2+ dependent phosphatase that dephosphorylates NFATc

A

Calcineurin

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4
Q

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

A

NFATc

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5
Q

Calcineurin is activated by this

A

Increased intracellular Ca2+ from TCR activation

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6
Q

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

A

Cytokines (specifically IL-2)

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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

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8
Q

mTOR is activated by this

A

IL-2 binding to its receptor on T cells

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9
Q

Big 4 adverse effects for monoclonal antibodies

A

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

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10
Q

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

A

Rituximab

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11
Q

Rituximab is a monoclonal antibody for this

A

Anti-CD20 antigen on B cells

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12
Q

Rituximab depletes these cells

A

B cells

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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

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14
Q

Basiliximab is a chimeric monoclonal antibody to this

A

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

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15
Q

Basiliximab inhibits activation/proliferation of these cells

A

T cells

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16
Q

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

A

Rituximab

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17
Q

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

A

Basiliximab

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18
Q

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

A

Anti-thymocyte globulin

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19
Q

Anti-thymocyte globulin is indicated for these 2 things

A

Induction and to terminate transplant rejection

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20
Q

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

A

Anti-thymocyte globulin

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21
Q

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

A

Corticosteroids, acetaminophen, or antihistamines

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22
Q

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

A

Hypotension

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23
Q

Corticosteroid pretreatment can minimize hypotension as a result of this drug

A

Anti-thymocyte globulin

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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

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25
Glucocorticoids curtail the activation of this, resulting in increased apoptosis of lymphocytes
NF-kB
26
NF-kB activation can be curtailed by these drugs
Glucocorticoids
27
3 Indications for glucocorticoids
Prevent and treat transplant rejection Auto-immune disorders Allergic reactions to other immunosuppressive agents
28
Increased risk of infections such as oral candidiasis and adrenal suppression are adverse reactions to this
Glucocorticoids
29
Drug used for induction and to terminate transplant rejection
Anti-thymocyte globulin
30
Drug used to prevent and treat transplant rejection, auto-immune disorders, and allergic reactions to other immunosuppressive agents
Glucocorticoids
31
2 adverse reactions to glucocorticoids
Increased risk of infections such as oral candidiasis Adrenal suppression
32
2 calcineurin inhibitors
Tacrolimus and Cyclosporine
33
Protein that binds tacrolimus
FKBP-12 (FK binding protein) Blocks calcineurin's phosphatase activity; blocks IL-2 production
34
Protein that binds cyclosporine
Cyclophilin Blocks calcineurin's phosphatase activity; blocks IL-2 production
35
Both calcineurin inhibitors (Tacrolimus and cyclosporine) binds to this
An immunophilin (chaperone protein) FKBP-12 (FK binding protein) binds tacrolimus Cyclophilin binds cyclosporine
36
2 drugs that block calcineurin's phosphatase activity, preventing movement of NFAT, and blocking the production of IL-2
Calcineurin inhibitors - Tacrolimus and Cyclosporine
37
4 adverse effects to calcineurin inhibitors (Tacrolimus and Cyclosporine)
Renal toxicity Cardiovascular risk elevated by hyperlipidemia Hypertension Hyperglycemia/diabetes (especially when combined with glucocorticoids)
38
Renal toxicity, cardiovascular risk elevated by hyperlipidemia, hypertension, and hyperglycemia are adverse effects to this type of drug
Calcineurin inhibitors
39
FKBP-12 is an immunophilin (chaperone) that binds this drug
Tacrolimus
40
Cyclophilin is an immunophilin (chaperone) that binds this drug
Cyclosporine
41
Tacrolimus and Cyclosporine primarily act on these cells
T cells Are calcineurin inhibitors; Block the production of IL-2
42
Nephrotoxicity, neurotoxicity, elevated cardiovascular risk, and hyperglycemia are adverse effects of this
Tacrolimus (calcineurin inhibitor)
43
4 toxicities of Tacrolimus
Nephrotoxicity Neurotoxicity Cardiovascular risk Hyperglycemia/diabetes
44
Widely used immunosuppresive drug that can treat dry eye
Cyclosporine (calcineurin inhibitor)
45
Renal toxicity, cardiovascular risk, hypertension, hyperglycemia/diabetes, and hepatotoxicity are adverse effects to this
Cyclosporine
46
5 toxicities to Cyclosporine
Renal toxicity (important to monitor renal function through BUN/creatinine, CrCl) Cardiovascular risk Hypertension Hyperglycemia/diabetes Hepatotoxicity
47
Sirolimus and Everolimus bind this, which complexes with mammalial target of rapamycin (mTOR) to block progression of cell cycle in T cells
FKBP-12
48
Drugs that bind FKBP-12 and complexes with mTOR to block progression of cycle cycle in T cells
Sirolimus and Everolimus
49
Sirolimus and Everolimus ultimately block this
mTOR --> block progression of cell cycle in T cells
50
2 drugs that inhibit the response to IL-2 but do not alter its production Net effect is blocked cell proliferation
Sirolimus and Everolimus
51
Hyperlipidemia, renal failure, hyperglycemia, angioedema, and bone marrow suppression are adverse effects to these
Sirolimus and Everolimus
52
5 adverse effects to Sirolimus and Everolimus
Hyperlipidemia Renal failure (especially when combined with cyclosporine) Hyperglycemia Angioedema Bone marrow suppression
53
2 anti-proliferative / anti-metabolic drugs
Azathioprine and Mycophenolate mofetil
54
Azathioprine is first converted to this Then to false/decoy nucleotides that incorporate into RNA to block translation
Mercaptopurine (anticancer drug)
55
Drugs that bind FKBP-12, that complexes with mammalian target of rapamycin (mTOR) to block progression of cell cycle in T cells
Sirolimus and Everolimus
56
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
Azathioprine
57
2 adverse effects of Azathioprine
Bone marrow suppression and increased risk of infections
58
Azathioprine ultimately blocks this
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
Allopurinol inhibits biotransformation of this drug, increasing toxicity
Azathioprine
60
Drug that inhibits biotransformation of azathioprine and mercaptopurine, increasing toxicity
Allopurinol
61
Drug that is converted to mycophenolic acid, inhibits purine (GMP) synthesis
Mycophenolate mofetil
62
Mycophenolate mofetil is converted to this, which inhibits purine (GMP) synthesis
Mycophenolic acid
63
Mycophenolate mofetil is converted to mycophenolic acid, which inhibits this
Purine synthesis (suppresses both B and T cell activation)
64
2 adverse effects of mycophenolate mofetil
Bone marrow suppression Increased risk of infection
65
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
Pembrolizumab
66
Pembrolizumab is monoclonal antibodies that binds this
PD-1 on T cells Blocks the anti-proliferation signal that activated PD-1 produces in T cells
67
Lymphokine that stimulates production of T cells and activates natural killer cells
Recombinant interleukin-2 (rIL-2)
68
rIL-2 has this effect
Stimulates production of T cells and activates NK cells
69
Fatal multifocal leukoencephalopathy is an adverse effect associated with this
Rituximab
70
Hypotension that is minimized with pretreatment with corticosteroids is an adverse effect associated with this
Anti-thymocyte globulin
71
Increased risk of cytomegalovirus infections is an adverse effect associated with this
Anti-thymocyte globulin
72
Increased risk of infections such as oral candidiasis is an adverse effect associated with this
Glucocorticoids
73
Adrenal suppression is an adverse effect associated with this
Glucocorticoids
74
Hyperlipidemia is an adverse effect associated with these
Calcineurin inhibitors, Sirolimus and Everolimus
75
Nephrotoxicity is an adverse effect associated with this
Tacrolimus
76
Neurotoxicity is an adverse effect associated with this
Tacrolimus
77
Renal failure from Sirolimus and Everolimus is more common when combined with this
Cyclosporine
78
Angioedema is an adverse effect associated with this
Everolimus (also Sirolimus)
79
Bone marrow suppression is an adverse effect associated with these 3 drugs
Sirolimus/Everolimus, Azathioprine, and Mycophenolate Mofetil
80
Binds to nuclear receptors to promote T cell death by inhibiting NFkB activation
Glucocorticoids
81
Drug class that blocks PD-1 signaling to enhance anti-tumor immunity
Immune checkpoint inhibitors
82
Polyclonal antibodies used to induce immune suppression and terminate transplant rejection
Anti-thymocyte globulin

MF2 Immunology (21 decks)

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