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Immunology > Immunosuppression > Flashcards

Immunosuppression Flashcards

1
Q

What are the 6 ways we can suppress the immune response?

A
  • Steroids
  • Anti-proliferative agents
  • Plasmapheresis
  • Inhibit cell signalling
  • Agents directed at cell surface Ag
  • Agents directed at cytokines
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2
Q

What is the MoA of steroids?

A

Inhibit phospholipase A2
Phospholipase A2 converts phospholipids to arachidonic acid
Arachidonic acid is converted to inflammatory prostaglandins by COX

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3
Q

What effect do steroids have on phagocytes + lymphocytes?

A
  • Phagocytes - increased number as suppressed adhesion molecule expression but don’t phagocytose
  • Lymphocytes - reduced numbers (CD4 > CD8 > B) as pass into tissues but don’t function
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4
Q

What are the side effects of steroids?

A

Cushing’s syndrome, osteoporosis, adrenal suppression, avascular necrosis (therefore steroid-sparing agents favoured…)

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5
Q

What are the 3 main anti-proliferative agents?

A

Cyclophosphamide
Azathioprine
Mycophenylate Mofetil

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6
Q

Which cells do the anti-proliferative agents predominantly act upon?

A

Cyclophosphamide B > T

Azathioprine + Mycophenylate Mofetil T > B (more straight lines)

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7
Q

What is the main action of the anti-proliferative agents?

A

Inhibit DNA synthesis to stop replication of adaptive immune cells (T + B cells) by altering structure of DNA monomers. Unfortunately they also suppress replication of any rapidly replicating cell (e.g. in BM)

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8
Q

What are the side effects of anti-proliferative agents?

A

Suppressed replication of any rapidly dividing cells = BM suppression, teratogenic, infection, malignancy

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9
Q

Alkylates guanine
Used in multi-system CT disease with end-organ damage, cancer
Side effects: hair loss, male sterility, haemorrhagic cystitis (metabolite accumulates in urine) + bladder cancer, P jiroveci infections, gum hyperplasia
B>T

A

Cyclophosphamide

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10
Q

Indications for immunosuppression

A

Inflammatory diseases, e.g. CT disease, IBD
Leukaemia
Transplants

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11
Q

Metabolised to 6-mercaptopurine (purine analogue)
Used in transplants, IBD
BM suppression big worry - if TPMT polymorphism can’t inactivate so need to check if patient has it)

A

Azathioprine

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12
Q

Blocks guanine synthesis
Alternative to azathoprine in transplant, cyclo in CT disease
Herpes reactivation > Progressive multifocal encephalopathy (JC virus infection)

A

Mycophenylate Mofetil

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13
Q

What is plasmapheresis?

A

Blood passed through cell separator and Ig removed

Rest of blood replaced

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14
Q

What is the indication for plasmapheresis?

A

Really severe Ab mediated disease - mostly type III like Goodpasture’s, MG, vascular rejection

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15
Q

What is a risk with plasmapheresis?

A

Rebound Ab production

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16
Q

What is the MoA of cell signalling inhibitors?

A

Prevent cytokine PRODUCTION

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17
Q

Name three main types of cell signalling inhibitor

A 
Calcineurin inhibitors (tacrolimus, cyclosporin)
JAK2 inhibitors (e.g. Tofacitinib)
PDE4 inhibitors (e.g. Apremilast)
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18
Q

How do cell signalling inhibitors vary in terms of specificity?

A

Calcineurin inhibitors are specific - inhibits T cell production of IL2 (requires calcineurin)
JAK2 / PDE4 are general cytokine production pathways

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19
Q

Inhibit T cell IL2 production

A

Calcineurin inhibitors e.g. tacrolimus, cyclosporin

Nephrotoxic

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20
Q

JAK2 inhibitor

A

Tofacatinib

Used in RA

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21
Q

PDE4 inhibitor

A

Apremilast

Used in psoriasis and psoriatic arthritis

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22
Q

What are the biologic agents?

A

These are agents that act on specific proteins - cytokines + antigens ~ BIND + PREVENT FUNCTION

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23
Q

What are the side effects of biologic agents?

A

Infusion reaction at site of delivery / previous site of delivery
General urticaria, wheeze, headaches after infusion

24
Q

Anti-any T cell antigen

A

Anti-thymocyte globulin (ATG)

T cells, Allograft rejection, Daily IV

25
Q

Anti-IL2R (alpha) (aka CD25)

A

Basiliximab (HP II)

T cells, Allograft rejection

26
Q

Anti-CD80 + CD86

Is a CTLA4-Ig fusion protein

A

Abatacept
(APCs, RA
Prevents CD28 stimulation, promotes CTLA4 proliferation

27
Q

Anti-CD20

A

Rituximab
(naive B cells)
RA, SLE, lymphoma

28
Q

Anti-alpha4 integrin

A

Natalizumab
(endothelial cells - ‘not going through’)
Remitting / relapsing MS

29
Q

Anti-IL6R

A

Tocilizumab
(loads of immune cells)
RA, Castleman’s

30
Q

Tocilizumab

A

Anti-IL6R

31
Q

Natalizumab

A

Anti-alpha4 integrin

32
Q

Abatacept

A

Anti-CD80 + CD86

33
Q

Basiliximab

A

Anti-IL2R (CD25)

34
Q

Rituximab

A

Anti-CD20

35
Q

What are the key biologic agents against cytokines?

A 
Anti-TNFalpha (infliximab, adalizumab, certolizumab, golizumab) 
Anti-TNFalpha + beta (etanercept)
Anti-IL12 + 23 (ustekinumab)
Anti-IL23 (guselkumab)
Anti-IL17 (secukinumab)
Anti-RANKL (denosumab)
36
Q

IL17 + IL23

A

Psoriasis

37
Q

Infliximab, Adalizumab, Certolizumab, Golizumab (IACG)

A

Anti-TNF alpha

38
Q

Etanercept

A

Anti-TNF alpha + beta (not selective)

TAN = TNf

39
Q

Ustekinumab

A

Anti-IL12 + 23

Psoriasis, Crohn’s

40
Q

Guselkumab

A

Anti-IL23

Plaque psoriasis

41
Q

Secukinumab

A

Anti-IL17

Psoriasis

42
Q

Denosumab

A

Anti-RANKL (decreases fracture risk in osteoporosis)

43
Q

Critical for T cell function

A

IL2

44
Q

What are the 4 main side effects of immunosuppression?

A

Infection (acute + chronic)
Malignancy
AI disease

45
Q

Acute infection as a side effect

A

Vaccinate
Avoid contact with infected people
Consider atypical organisms
Prophylactic Abx

46
Q

Chronic infection as a side effect

A

Pt. worry about re-activation (e.g. TB, HepB, HIV, JCV)

JCV polyomavirus - re-activates to destroy oligodendrocytes - PML

47
Q

Malignancy as a side effect

A

Immunosuppression = vulnerable to cancer-causing infections: EBV (lymphoma), HPV (non-melanoma skin cancer)
Melanoma is a key worry in anti-TNFalpha therapy

48
Q

Key side effect of anti-TNFalpha therapy

A

Melanoma

49
Q

Gum hyperplasia (gingivitis)

A

Cyclophosphamide

50
Q

Nephrotoxic (HTN, reduced GFR)

A

Ciclosporin

51
Q

Live vaccines

A

MMR (V) BOY

MMR, varicella, BCG, oral (typhoid, polio sabin), Yellow fever

52
Q

Rheumatoid Arthritis therapy

A

Start on anti-TNF alpha i.e. Etanercept, Adalimumab, infliximab.

Move on to tocilizumab (anti-IL 6)

53
Q

Psoriasis therapy

A

Ustekinemab (anti IL-12 / IL-23)

54
Q

CT with end organ damage

Gingivial hypertrophy

A

Cyclophosphamide

55
Q

JCV virus

A

Progressive multifocal leukoencephalopathy (PML)

Immunology (9 decks)

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