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Clinical Pathology > Core Immunology - Immunomodulation and Immunosuppression (13) > Flashcards

Core Immunology - Immunomodulation and Immunosuppression (13) Flashcards

1
Q

Immunomodulation

A

Manipulating the immune system using immunomodulatory drugs

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2
Q

What is the therapeutic effect of immunomodulation?

A
  • Immunopotentiation
  • Immunosuppression
  • Immunological tolerance
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3
Q

Immunopotentiation

A

Enhancing immune response by adding another substance, increasing it’s rate/prolonging duration

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4
Q

Mechanisms of immunomodulation

A

Immunisation, replacement therapy, immune stimulants, immune suppressants, anti-inflammatory agents, allergen immunotherapy/desentisation, adoptive immunotherapy

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5
Q

Biologics - immunomodulators

A

Medicine products produced using molecular biology techniques - recombinant DNA

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6
Q

Classes of biologics immunomodulators

A
  • Substances nearly identical to body’s own key signalling proteins
  • Monoclonal antibodies
  • Fusion proteins
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7
Q

Anti-TNF

A
  • Adalimumab (human IgG)
  • Infliximab (chimeric mouse-human IgG)
  • Etanercept (fusion protein)
  • Cetrolizumab (humanised)
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8
Q

Immunopotentiation

A

Increase immune response by administration of another substance (increasing rate/prolonging duration)

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9
Q

Examples of immunopotentiation

A

Immunisation, replacement therapies, immune stimulants

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10
Q

Passive immunisation

A

Transfer of specific, high-titre antibody from donor to recipient, provides immediate but transient protection

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11
Q

Problems with passive immunisation

A

Risk of transmission of viruses, serum sickness

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12
Q

Types of passive immunisation

A

Pooled specific human Ig, animal sera (antitoxins and antivenins)

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13
Q

Uses of passive immunisation

A

Hep B (prophylaxis and treatment), Botulism, VZV (pregnancy), Diphtheria, Snake bites

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14
Q

Active immunisation

A

To stimulate the development of protective immune response from immunological memory

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15
Q

Active immunisation immunogenic material

A

Weakened forms of pathogens, killed inactivated pathogens, purified materials (proteins, DNA), adjuvants

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16
Q

Active immunisation problems

A

Allergy to any vaccine component, limited usefulness in immunocompromised, delay in achieving protection

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17
Q

Replacement therapies - Pooled human Ig

A

Used in treatment of antibody deficiencies (IV/SC)

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18
Q

Immune stimulation - G-CSF/GM-CSF

A

Act on bone marrow, to increase production of mature neutrophils

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19
Q

Immune stimulation - IL-2

A

Stimulates T cell activation (rarely used)

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20
Q

Immune stimulation a-INF

A

Hep C

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21
Q

Immune stimulation B-INF

A

MS

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22
Q

Immune stimulation y-INF

A

Intracellular infections (atypical mycobacteria), chronic granulomatous disease, IL-12 deficiency

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23
Q

Interferon

A

Increases anti-viral response, occurs naturally, increase protein synthesis > increased resistance (makes you feel flu-like)

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24
Q

Immunosuppression

A
  • Cortiocosteroids
  • Cytotoxic agents
  • Anti-proliferative/activation agents
  • DMARD’s
  • Biologic DMARD’s
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25
Q

Corticosteroids action

A

Decrease neutrophil margination, reduce cytokine production, inhibit phospholipase A2 (reduced arachidonic acid metabolites production), lymphopenia, decreases T cell proliferation and Ig production

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26
Q

Corticosteroid side-effects

A
  • Carb and lipid metabolism (diabetes and hyperlipidaemia)
  • Reduced protein synthesis (poor wound healing)
  • Osteoporosis
  • Glaucoma and cataracts
  • Psychiatric complications
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27
Q

Uses of corticosteroids

A
  • AI (connective tissue disorder, vasculitis, RA)
  • Inflammatory (Crohn’s, sarcoid, GCA/polymyalgia rheumatica)
  • Lymphoma
  • Allograft rejection
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28
Q

Antimetabolites

A

Stop proliferation of T-cells - Azathioprine (AZA), Mycophenolate mofetil (MMF)

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29
Q

Calcineurin inhibitors

A

Ciclosporin A (CyA), Tacrolimus (FK506)

30
Q

CyA

A

Binds to intracellular protein cyclophilin

31
Q

Tacrolimus

A

Binds to intracellular protein FKBP-12

32
Q

Calcineurin mode of actions

A

Prevent activation of NFAT, factors which stimulate cytokines (IL-2 and INFy) gene transcription

33
Q

M-TOR inhibitors

A

Sirolimus/rapamycin (structurally related to tacromilus)

34
Q

M-TOR mode of action

A

Inhibits target of rapamycin (Macrolide antibiotic), inhibits response to IL-2

35
Q

M-TOR effects on T cels

A

Can’t proliferate, cell cycle arrests at GI-S phase

36
Q

Calcineurin/M-TOR side effects

A

Increased bp, nephrotoxicity, lymphomas, neurotoxicity, hirsutism (hair growth), hepatotoxicity, opportunistic infections, multiple drug interactions

37
Q

Antimetabolites

A

Inhibit nucleotide/purine synthesis

38
Q

AZA mechanism

A

Guanine anti-metabolite, rapidly converts > 6-mercaptopurine

39
Q

MMF mechanism

A

Non-competitive inhibitor of IMPDH, prevents production of guanosine triphosphate

40
Q

Antimetabolites effects on B and T cells

A

Impaired DNA production, prevents early stages of activated cell proliferation

41
Q

Antimetabolite uses

A

Allograft rejetion, SLE, vasculitis, IBD

42
Q

Cytotoxic antimetabolites

A

MTX and cyclophospamide

43
Q

Methotrexate mechanism

A

Folate antagonist

44
Q

Uses of methotrexate

A

RA, PsA, GvHD in BMT, RA, Polymyositis, Vasculitis

45
Q

Cyclophospamide mechanism

A

Cross-link DNA

46
Q

Cyclophospamide uses

A

SLE, vasculitis, Wagner’s, CSS

47
Q

Side effects of MTX and Cyclophospamide

A

Bone marrow suppression, gastric upset, hepatitis, susceptibility to infections (MTX - pneumonitis, C-cystitis)

48
Q

Biological DMARD’s

A

Biological Disease-Modifying Anti Rheumatic Drugs

49
Q

Types of biological DMARD’s

A

Anti-cytokines (TNF, IL-6, IL-1), anti B-cell, anti- T cell activation, anti-adhesion molecules, complement inhibitors

50
Q

Anti-cytokines

A
  • Anti-TNF (activate macrophages)
  • Anti IL-6
  • Anti IL-1
51
Q

Anti-TNF

A

Used: RA, Crohn’s, Psoriasis, Ankylosing Spondylitis

52
Q

Anti IL-6

A

Tocilizumab, RA and adult onset still’s disease

53
Q

Anti-TNF problems

A

Increased risk of TB

54
Q

Anti IL-6 problems

A

Control of serum lipids

55
Q

Anti IL-1 examples

A

Anakinra, Rilonacept, Canakinumab

56
Q

Anti IL-1 uses

A

AOSD and auto inflammatory syndromes

57
Q

Rituximab

A

Part mouse and part human chimeric mAB against CD20-B cell

58
Q

Rituximab uses

A

Lymphoma (B-cell origin), leukaemia, transplant rejection, autoimmune disorder (chemotherapy resistant diffuse large B-cell lymphoma)

59
Q

Adoptive immunotherapy

A

Bone marrow transplant or stem cell transplant

60
Q

Adoptive immunotherapy uses

A

SCID, lymphomas, leukaemias, inherited metabolic disorders (osteoporosis), AI

61
Q

Immunomodulators - allergy

A

Immune suppressants, allergen specific immunotherapy, anti-IgE monoclonal therapy, anti IL-5 monoclonal treatment

62
Q

Indications of allergy immunomodulators

A
  • Allergic rhinoconjuctivitis not controlled
  • Anaphylaxis to insect venom
  • Steroids low response
63
Q

Mechanisms of allergy immunomodulators

A

Switching of immune response Th2 (allergic) > Th1 (non-allergic), development of T reg cells and tolerance

64
Q

Routes of allergy immunomodulators

A

SC/sublingual

65
Q

Side effects of allergy immunomodulators

A

Localised/systemic allergic reactions

66
Q

Monoclonal antibodies against allergies

A

Omalizumab and Mepolizumab

67
Q

Omalizumab

A

Against IgE

68
Q

Omalizumab uses

A

Asthma, chronic urticaria and angio-oedema

69
Q

Side effects of omalizumab

A

Severe systemic anaphylaxis

70
Q

Mepolizumab

A

Against IL-5, prevents eosinophil recruitment and activation

Clinical Pathology (60 decks)

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