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PMCOL 344 > Immune-6 > Flashcards

Immune-6 Flashcards

1
Q

what are 2 examples of polyclonal antibodies

A
  • intravenous immune globulin

- hyperimmune immunoglobulins

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2
Q

what are intravenous immune globulin

A

polyclonal human immunoglobulins from a pool of thousands of donors with no specific antigen target

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3
Q

what is the point of doing intravenous immune globulin

A

prevents second encounter with antigen - used for people with no immune system

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4
Q

who would get benefit from intravenous immune globulin therapy + disease

A

people with no immune system, X-linked agammaglobulinemia

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5
Q

what is hyperimmune immunoglobulins

A

intravenous immune globulin from a pool of selected donor with specific antibodies against a particular agent

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6
Q

what are some diseases that hyperimmune immunoglobulins are available for

A

hep B, herpes, rabies, tetanus

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7
Q

What do immunomodulatory biologics do generally

A

engage and manipulate cell surface signalling molecules on host immune cells

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8
Q

what kind of things do immunomodulatory biologics target (4)

A

co-stimulatory and co-inhibitory molecules, membrane receptors involved in adhesion and migration

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9
Q

how do immunomodulatory biologics control lymphocyte response generally

A

modulate antigen-specific TCR and BCR signals

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10
Q

what are the 2 groups of immunomodulatory biologics

A

antagonists and agonists

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11
Q

what do antagonist immunomodulatory biologics do

A

block or neutralize the interaction between receptors and ligands

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12
Q

what do agonist immunomodulatory biologics do

A

induce signalling via the receptor by mimicking the ligand

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13
Q

what is CD3 (1)

A

part of the t cell receptor

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14
Q

what is the role of CD3 (3)

A
  • antigen recognition
  • cell signalling
  • proliferation
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15
Q

what is the function of CD4

A

co-receptor of the TCR in T helpers and T reg

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16
Q

when is CD4 active

A

when antigen is presented by MHC class 2

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17
Q

what does CD4 initiate

A

T-cell activation

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18
Q

what does CD4 participate in (what type of infection)

A

HIV

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19
Q

what is CD28

A

most effective co-stimulatory molecule

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20
Q

who expressed CD28

A

naive and activated T cells

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21
Q

what does CD28 interact with + on who

A

CD80/86 expressed by mature APCs

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22
Q

what is CTLA-4

A

inhibitory molecules homologous to CD28

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23
Q

who expresses CTLA-4

A

activated T cells

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24
Q

what does CTLA-4 bind to and how strong

A

the same ligand as CD28 much at a much higher affinity

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25
Q

what are 3 targets of biologics that target T cells

A
  • anti CD3 antibodies
  • anti CD4 antibodies
  • recombinant fusion protein targeting CD28
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26
Q

which drug is anti CD3 antibodies

A

teplizumab

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27
Q

which drug is anti CD4 antibodies

A

ibalizumab

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28
Q

which drug is recombinant fusion protein targeting CD28

A

abatacept

29
Q

what is teplizumab (basic)

A

anti CD3 antibodies

30
Q

what is ibalizumab (basic)

A

anti CD4 antibodies

31
Q

what is abatacept (basic)

A

recombinant fusion protein targeting CD28

32
Q

what class of diseases is antiCD3 used for

A

autoimmune

33
Q

what type of cells does anti CD3 target

A

all activated T cells

34
Q

is anti CD3 antigen specific therapy, explain

A

it is non-antigen specific therapy, it targets all activated T cells

35
Q

what is the rational behind anti CD3

A

during new onset, autoimmune disease activated T cells are present only in the pancreas or CNS (diabetes CNS)

36
Q

what are the expectations of anti CD3

A

that anti CD3 mAbs would cause autoreactive T cell depletion

37
Q

what happen to people using anti CD3 first gen

A

it cause cytokine storm in MS patients (disease axacerbation)

38
Q

what kind of antibody is teplizumab/ anti CD3

A

humanized CD3

39
Q

how was teplizumab mutated

A

it is mutated to prevent binding to FcRs (avoid ADCC, CDC and CDCC)

40
Q

what is teplizumab shown to work for

A

type 1 diabetes

41
Q

what is ibalizumab used for

A

inhibiting HIV-1 infection

42
Q

what kind of antibody is ibalizumab

A

CD4 specific mAb, human monoclonal

43
Q

where does ibalizumab bind

A

extracellular region of CD4 away from MHC class 2 site

44
Q

does ibalizumab do immunosuppression + why

A

no because it binds away from MHC class 2 (not close by)

45
Q

how does ibalizumab inhibit gp120 binding to CD4

A

it doesnt!

46
Q

what is ibalizumab mechanism

A

prevents CD4 bound gp120 from interacting with CCR5 or CXCR4

47
Q

does ibalizumab bind to MHC class 2

A

no it binds away from the site

48
Q

what is CCR5 and CXCR4

A

co-receptors for HIV, needed for viral entrance

49
Q

what is the structure of abatacept

A

soluble fusion protein, extracellular domain of human CTLA4 fused to Fc portion of Ig

50
Q

where does abatacept bind

A

on CD80 and CD86 on APCs

51
Q

what is the mechanism of abatacept

A

prevents binding of CD80/86 to CD28 and to CTLA4 on T cells (blocks co stim signal)

52
Q

what is the result of abatacept

A

inhibits T cell activation, proliferation, production of TNFa, interferon (Gamma) and IL-2

53
Q

what do we use abatacept for

A

RA, a second line DMARD (when methotrexate or other biologics have failed)

54
Q

what is CD20 and where is it

A

antigen on the surface of pre-B cells and mature B lymphocytes

55
Q

what is the function of CD20

A

it remains unclear

56
Q

what are 2 anti CD20 antibody drugs

A

rituximab and ocrelizumab

57
Q

what kind of antibody is rituximab

A

chimeric antibody against CD20

58
Q

what is rituximab used for (3)

A

RA and MS, B cell neoplasms

59
Q

what kind of antibody is ocrelizumab

A

humanized anti-CD20

60
Q

what is the difference between rituximab and ocrelizumab

A

rituximab is chimeric and ocrelizumab is humanized

61
Q

what is ocrelizumab used for

A

PPMS

62
Q

what is 2 similarities between rituximab and ocrelizumab

A

they bind to the same epitope and both against CD20

63
Q

what do rituximab and ocrelizumab do to B cells

A

deplete the majority of B cell subsets

64
Q

what do rituximab and ocrelizumab do to plasma cells

A

nothing (no effect)

65
Q

how do rituximab and ocrelizumab cause B cell depletion

A

by activating their removal by indirect mechanisms (CDC and ADCC)

66
Q

can rituximab and ocrelizumab cause direct cell death

A

yes, but minimal

67
Q

which cell types do rituximab and ocrelizumab effect

A

B cells

68
Q

which cell types do rituximab and ocrelizumab NOT effect

A

plasma cells

69
Q

what 2 mechanisms do rituximab and ocrelizumab use

A

antibody dependent cellular toxicity and complement dependent cytotoxicity (CDC and ADCC)

PMCOL 344 (27 decks)

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