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Path guide Immuno > Immune Modulation > Flashcards

Immune Modulation Flashcards

1
Q

Types of Immune Modulation

A

Vaccination
Replacement
Suppression
Sensitisation

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2
Q

Vaccination mechanism

A

Memory lymphocyte production → rapid polyclonal expansion of adaptive immune response

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3
Q

Active vs Passive Vaccination

A

Active - your own body produces response - long-term protection

Passive - pre-formed antibodies given - around 3 weeks

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4
Q

What are Dendritic cell vaccines

A
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5
Q

Summarise Paediatric vaccination schedule

A
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6
Q

Regular adult vaccinations

A
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7
Q

Key travel vaccines

A
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8
Q

2 non-travel vaccines that are given based on risk

A
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9
Q

4 Types of Vaccine

A

Live attenuated
Inactivated/component/toxoid
Conjugate
DNA/RNA

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10
Q

What is a live attenuated vaccine?
Give examples

A

Modified pathogen to limit pathogenesis

E.g. MMR-VBOY

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11
Q

Inactivated vaccine examples

A

Influenza (quadrivalent),
Polio (Salk),
Cholera,
Bubonic plague,
Hep A,
Rabies, Pertussis

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12
Q

Component vaccine examples

A

Hep B [HbS antigen],
HPV [Capsid],
Influenza recombinant quadrivalent) [haemagglutinin, neuraminidase]

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13
Q

Toxoid vaccine examples

A

Diptheria
Tetanus

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14
Q

Conjugate vaccine examples

A

NHS
Tetanus

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15
Q

DNA/RNA vaccine examples

A

SARS-CoV-2

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16
Q

What does an adjuvant do in vaccination?

A

Increases immune response without altering specificity

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17
Q

2 Main types of adjuvant

A

Depot
Stimulatory

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18
Q

How does a depot adjuvant work?

A

Slows antigen release → increased exposure to antigen → promotes immune response

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19
Q

Depot adjuvant example

A

ALUM

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20
Q

How does a stimulatory adjuvant work?

A

Mimics the action of PAMPs on TLR and PRRs → increased receptor activation → boosted immune response

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21
Q

Stimulatory adjuvant example

A

CpG

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22
Q

Types of Immune Replacement

A

Haematopoietic SCT
Ab replacement - specific/unspecific
Adoptive T cell transfer

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23
Q

Types of adoptive T cell transfer

A

Virus specific T cells
TIL T cell therapy
TCR
CAR-T cell therapy

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24
Q

Describe TIL T cell therapy

A

TILs from tumour → expanded with IL2 → infused into lymphoid depleted patient → destroys cancer cells

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25
Q

Describe CAR-T cell therapy

A

Chimeric receptor targets CD19 → greater immune response to tumour than TCR therapy

for ALL, NHL

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26
Q

1/2 life of normal human IVIG

A

18 days

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27
Q

Examples of recombinant cytokines

A

IL-2
IFN-alpha
IFN-beta
IFN-gamma

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28
Q

Recomobinant IL-2 uses

A

Renal cancer
(IL-2 2 kidneys)

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29
Q

IFN-alpha uses

A

Viruses - Hep B & C (ABC)
Cancer

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30
Q

IFN-beta uses

A

Relapsing remitting MS

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31
Q

IFN-gamma uses

A

CGD

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32
Q

Immune Checkpoint blockade drugs

A

Ipilimumab
Pembrolizumab
Nivolumab

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33
Q

Immune checkpoint blockade indications

A

Advanced melanoma
Metastatic renal cancer

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34
Q

Ipilimumab mechanism

A

Normally: CD80 and CD86 (APCs) interact with CTLA4 (inhibitory) and CD28 (stimulatory)

CTLA4 inhibitor → blocks CTLA4, all APC interactions now through CD28 → boosted T cell response

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35
Q

Pembrolizumab/nivolumab mechanism

A

PD-1 (prevent death-1) blocker monoclonal antibody

Normally, cancer cells bind PDL-1 to Treg PD-1 → prevents Treg cell killing of tumour cell

PD-1 blockade prevents binding of PDL-1 to PD-1 → enabling Treg cell killing of tumour cell

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36
Q

3 signals in naive T cell priming

A

Activation: MHC-TCR interaction
Survival: CD86/B7-CD28 interaction
Differentiation: cytokines

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37
Q

What are the adverse effects of immunosuppressive drugs?

A

Infusion reaction (IgE)
Injection reaction
Acute infection
Chronic infection
Malignancy
Autoimmunity

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38
Q

How do you manage acute infection due to immunosuppression?

A

Prevention: non-live vaccination

Mx: stop immunosuppression,
ABx - cover for atypicals

39
Q

What chronic infections can be seen with immunosuppression?

A

TB
HIV
Hep B, C
JCV

40
Q

TB during immunosuppression Mx

A

Ix: check exposure + CXR
Mx: prophylaxis/treat as needed

41
Q

HIV and immunosuppression

A

Check for HIV before treatment

42
Q

How to manage viral hep during immunosuppression?

A

HBcAb and HCAb before treatment
If positive → further Ix

43
Q

What is John Cunningham virus?

A

Polyoma virus that can reactivate → infecting and destroying oligodendrocytes → Progressive Multifocal Leukoencephalopathy (PML)

44
Q

Prednisolone mechanism of immunosuppression

A
  1. Phospholipase A2 inhibition → reduced prostaglanding synthesis → reduced inflammation
  2. Inhibits phagocyte tracking, phagocytosis and release of proteolytic enzymes → decreased phagocyte activity
  3. Promotes lymphocyte apoptosis, splenic sequestration (CD4>8>B), ↓ antibody productions and blocks cytokine gene expression → lymphopenia
45
Q

Corticosteroid SEs

A

Metabolic: Cushing’s, diabetes, osteoporosis, adrenal suppression

Infection

Eyes: cataracts, glaucoma

GI: peptic ulcers, pancreatitis

Avascular necrosis

46
Q

Antiproliferative agents

A

Cyclophosphamide
Mycophenylate mofetil
Azathioprine
Methotrexate

47
Q

Antiproliferative agents SE

A

Bone marrow suppression

48
Q

Cyclophosphamide mechanism of action

A

Alkylates guanine in DNA → DNA damage → no cell replication
B>T cells

49
Q

Cyclophosphamide key SE

A

Haemorrhagic cystitis

50
Q

Mycophenylate Mofetil mechanism

A

Anti-metabolite
Blocks I-5’-MPHDH → prevents de novo guanine synthesis → stops replication
T>B cell

51
Q

Mycophenylate Mofetil key SE

A

Progressive Multifocal Leukoencephalopathy (JC virus)

52
Q

Azathioprine mechanism of action

A

Anti-metabolite
Pro-drug
Metabolised in liver to 6-metacarptopurine → prevents de novo purine synthesis → prevents DNA replication

53
Q

What to check for before giving azathioprine and why?

A

TPMT mutation - can lead to bone marrow suppression with azathioprine

54
Q

Methotrexate Mechanism of action

A

Anti-folate
Inhibits DHFR → inhibits DNA synthesis

55
Q

Methotrexate SEs

A

F2oL2ate

Foetus - teratogenic
Folate deficiency
Lung - pneumonitis, pulmonary fibrosis
Liver - hepatotoxic

56
Q

Plasmapharesis what is it and indications

A

Removal of pathological antibody

Indicated in severe Type II HS disease e.g. Goodpasture’s

57
Q

Key SEs of plasma pharesis

A

Rebound antibody production
Anaphylaxis

58
Q

Inhibitors of Cell Signalling

A

Calcineurin inhibitors - Tacrolimus, Cyclosporin
mTor (IL-2 pathway) inhibitors - Sirolimus, Rapamycin
Tofacitinib - JAK1/3 inhibitor
Apremilast - PDE4 inhibitor

59
Q

Mechanism of Tacrolimus and Cyclosporin

A

Inhibit calcineurin → decreased IL-2 expression → reduced T-cell proliferation

60
Q

Side effects of calcineurin inhibitors

A

Nephrotoxic, neurotoxic, hypertension
Tacrolimus - diabetogenic
Cyclosporin - Gingival hyperplasia

61
Q

Sirolimus (Rapamycin) mechanism of action

A

mToR inhibition → T cell proliferation inhibition via IL-2 pathway

62
Q

Sirolimus indication

A

Transplantation

63
Q

Sirolimus SEs

A

Hypertension, less nephrotoxic than calcineurin inhibitors

64
Q

Tofacitinib mechanism

A

Inhibits JAK-STAT signalling → inhibits production of inflammatory molecules by influencing gene transcription

65
Q

Apremilast mechanism

A

PDE4 inhibitor → increases cAMP through protien kinase A pathway → modulates cytokine production

66
Q

Apremilast indication

A

Psoriasis, psoriatic arthritis

67
Q

Main agents against cell surface antigens

A

Rabbit anti-thymocyte globulin
Basiliximab
Abatacept
Rituximab
Vedolizumab

68
Q

Anti-thymocyte globulin actions

A

Lymphocyte depletion
Inhibition of T cell migration and activation

69
Q

Anti-thymocyte globulin uses

A

Allograft rejection

70
Q

Anti-thymocyte globulin SEs

A

Infusion reactions, leukopenia

71
Q

Basiliximab mechanism of action

A

Blocks IL-2 induced signalling and T cell proliferation

72
Q

Basiliximab Indication

A

Allograft rejection (prophylaxis)

73
Q

Abatacept mechanism of action

A

Blocks CD80 and CD86 → reduced co-stimulation of T cells by CD28

74
Q

Abatacept indication

A

Rheumatoid arthritis

75
Q

Abatacept main caution

A

Malignancy

76
Q

Rituximab mechanism of action

A

anti-CD20 → depletes mature B cells

77
Q

Rituximab indication

A

lymphoma, rheumatoid arthritis, SLE

78
Q

Rituximab SEs

A

Infusion reactions, infections (PML), exacerbation CV disease

79
Q

Vedolizumab mechanism of action

A

Anti-alpha-4-beta-7 integrin → inhibits binding to MadCAM1 → stops leukocyte binding to endothelium and extravasation to tissue

80
Q

Natalizumab antibody and indication

A

anti-alph-4-beta-1 integrin
MS and Crohn’s

81
Q

Cytokines and receptor targets for immunomodulatory agents

82
Q

Anti-TNF alpha drugs

A

CAIG
Certolizumab
Adalimumab
Infliximab
Golimumab

83
Q

Anti-TNF-alpha indications

A

PAIR
Psoriasis/psoriatic arthritis
Ankylosing spondylitis
Inflammatory bowel disease
Rheumatoid arthritis

84
Q

TNF-alpha antagonist mechanism and example

A

Inhibits TNF alpha and beta
Etanercept - PAR not PAIR

85
Q

What conditions can IL-1 blockade be used for?

A

FMF
Gout
Adult Stills

86
Q

What disorder does IL-6 play an important role in?

A

Rheumatoid arthritis

87
Q

How do Tocilizumab and Sarilumab work?

A

Anti-IL-6 receptor
→ reduced macrophage, neutrophil, T cell, B cell activation

88
Q

What disorders are IL-23 and IL-17 important for?

A

Axial spondyloarthropathies
Psoriasis/psoriatic arthritis
IBD (IL-23 only)

89
Q

Give an example of an anti-IL-23 drug?

A

Guselkumab
anti-p19(alpha) subunit of IL23

91
Q

What ILs can be targeted for Asthma and Eczema?

A

IL4, 5 and 13

92
Q

How does Denosumab work?

A

It inhibits RANK-mediated osteoclast differentiation and function → decreased bone resorption

93
Q

Allergic desensitisation procedure

A

Start small
Escalate dose every weeek until max dose reached
Maintenance dose given monthly for 3-5 years

Path guide Immuno (12 decks)

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