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Haematology and Immunology > Immunology > Flashcards

Immunology Flashcards

1
Q

List functions of the innate immune system.

A 
Inflammation 
Recruitment of immune cells 
Activate complement 
Natural killer cytotoxicity 
Phagocytosis
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2
Q

List cells of the innate immune system.

A 
Erythrocyte
Eosinophil
Monocytes - dendritic cells, macrophages
Basophil
Neutrophil
Megakaryocyte
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3
Q

What innate cells are found in the tissue?

A

Mast cell
Macrophage
Dendritic cells

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4
Q

What is the difference between MHC 1 and MHC 2 presentation?

A

MHC1 = all nucleated cells and platelets have it, present to CD8

MHC 2 = antigen presenting cells, present to CD4+

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5
Q

Where do T cells encounter antigens?

A

Lymph nodes

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6
Q

How do dendritic cells present antigens?

A

Via MHCII

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7
Q

What cells are the key players of the adaptive immune response?

A

B (differentiate to plasma cells) and T lymphocytes

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8
Q

What cytokines are released from Th1 cells?

A

IFN gamma

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9
Q

What cytokines are released from Th2 cells?

A

IL-4, 5, 13

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10
Q

What cytokines are released from Th17 cells?

A

IL-7A, 17F, 22

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11
Q

What helper cells are particularly good at triggering activation of mast cells and eosinophils?

A

Th2

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12
Q

What helper cells are particularly good at triggering activation of macrophages?

A

Th1

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13
Q

What helper cells are particularly good at triggering activation of netrophils?

A

Th17

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14
Q

What is the function of cytokines?

A

Regulate and co-ordinate cells of innate and adaptive immune responses

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15
Q

How to cytotoxic T cells kills cells by inducing apoptosis?

A

IFN and TNFa
FasL
Perforin and granzymes

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16
Q

What kind of cell is a natural killer cell?

A

Innate

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17
Q

What is the function of NK cells?

A

Kill infected cells

Produce cytokines to stimulate macrophages, Th1 and CD8+ cytotoxic

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18
Q

What is the function of B lymphocytes?

A

Neutralization of microbe, phagocytosis, complement activation
Opsonisation
Antibody-dependent cellular toxicity

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19
Q

What antibody is a pentamer?

A

IgM

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20
Q

What antibody is a dimer?

A

IgA

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21
Q

What antibody is for parasitic infections and allergy?

A

IgE

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22
Q

Where is IgA contained?

A

In secretions?

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23
Q

What antibody is best at activating complement?

A

IgM

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24
Q

What antibody is responsible fro memory in a secondary antigen exposure?

A

IgG

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25
Q

List physical and chemical barriers of the immune system.

A 
Intact mucosal membranes 
Lysozymes in tears 
Normal flora
Fluhsing in urinary tract 
Mucociliary escalator 
Acidic pH of stomach 
Intact skin with sebum maintaining pH
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26
Q

What lymphatic tissues are found in membranes?

A

Mucosa-associated (MALT)
Bronchus associated
Gut associated

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27
Q

List cells formed in the myeloid lineage.

A

Megakaryocyte, mast cells, myeloblasts, erythrocytes

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28
Q

What are formed from megakaryocytes?

A

Platelets

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29
Q

What are formed from myeloblasts?

A

Basophil
Eosinophil
Neutrophil
Monocyte

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30
Q

What are the two types of B lymphocytes?

A

Plasma cells and memory B cells

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31
Q

What system removes erythrocytes?

A

Reticuloendothelial system

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32
Q

What are the main targets of mast cells?

A

Parasites and allergens

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33
Q

What cells contain histamine and target parasites?

A

Basophils

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34
Q

What are the first cells that migrate to the site of infection, targeting bacteria and fungi specifically?

A

Neutrophil

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35
Q

What immune cells target parasites to big for phagocytosis?

A

Eosinophils

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36
Q

What 2 types off cells do monocytes become?

A

Macrophages

Dendritic cells

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37
Q

A dendritic cell is a professional APC. How does it present antigens?

A

Present to CD4+ via MHC II, releasing cytokines

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38
Q

How do natural killer cells work?

A

Granules contain proteins such as perforin and proteases

Activated by IFN and macrophage derived cytokines

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39
Q

List three types of T lymphocytes.

A

CD4+
CD8+
CD4+CD25+ (regulatory)

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40
Q

List cells involved in the innate immune system.

A

Phagocytes
Dendritic cells
NK cells
Complement

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41
Q

List cells that work by phagocytosis.

A

Basophil
Neutrophil
Monocytes (macrophages and dendritic cells)

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42
Q

List the classic professional antigen presenting cells.

A 
Dendritic cells 
Macrophages 
Dendritic cells 
Langerhans cells 
B cells
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43
Q

What cells are involved in the adaptive immune system?

A

B cells
T cells
APCs

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44
Q

All nucleated cells display set markers via what protein?

A

MHC I aka HLA

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45
Q

What does MHC I present?

A

Self antigens and intracellular foreign antigens

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46
Q

What is the function of MHC II?

A

Present exogenous or extracellular antigens from pathogenic invaders

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47
Q

What cells contain MHCII?

A

Dendritic, macrophages, B lymphocytes

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48
Q

What does MHCI and II complexes bind to?

A

MHC I = CD8+

MHC II = CD4+

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49
Q

Discuss the cause of autoimmunity.

A

CD8+ cells destroy MHCI presenting self antigen i.e destroys healthy cell

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50
Q

How does the body prevent CD8+ cells binding and destroying self antigenic?

A

Immunological tolerance:

  1. Central = in primary lymph nodes
  2. Peripheral = in secondary lymphoid organs
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51
Q

Where do T and B cells develop central tolerance?

A

T - in thymus

B - in bone marrow

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52
Q

What cells are responsible fro peripheral tolerance?

A

Regulatory T lymphocytes

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53
Q

List conditions which would block chemical/physical barriers of immunity.

A 
Mucositis 
Sjogren's syndrome 
Cystic fibrosis 
Toxic megacolon due to C difficile 
Burns
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54
Q

What are the primary lymphoid organs?

A

Bone marrow and thymus

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55
Q

What are secondary lymphoid organs?

A

MALT, Spleen, Peters patches, tonsils, lymph nodes

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56
Q

Name an immune cell responsible for recognising a viral infected host cell.

A

NK cell

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57
Q

List cells capable of phagocytosis.

A

Macrophage
Basophil
Neutrophil
Monocyte

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58
Q

Can eosinophils phagocytose?

A

No

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59
Q

What cell types are responsible for targeting large parasites that are too large for phagocytosis?

A

Mast cells
Basophils
Eosinophils

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60
Q

How are T cells developed in thymus?

A

Alpha and beta chains on T cell receptor (TCR), contains complimentary determining regions (CDR)

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61
Q

What is V(D)J recombination?

A

Occurs in developing T cells - process of genetic changes which create a diverse selection of Ag binding sites

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62
Q

List the steps of T lymphocyte development.

A

Double -ve –> double +ve –> positive selection –> interaction with MHC –> negative selection –> reacts appropriately

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63
Q

What are the 3 mechanisms used by CD8+ T cells?

A

FasL
IFN and TNFa
Perforin and granzymes

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64
Q

What is the function of helper T cells?

A

Activates other immune cells by releasing T cytokines
B lymphocyte antibody class switching
Activation and growth of cytotoxic T cells
Maximise activity of phagocytes

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65
Q

What cytokines are released by Th1 cells?

A

IFN gamma

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66
Q

What cytokines are released by Th2 cells?

A

IL -4, 5 and 13

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67
Q

What cytokines are released by Th17 cells?

A

IL-17,21,22

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68
Q

What Th cells have roles in allergy?

A

Th2

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69
Q

What occurs with increased Th1?

A

Type 4 hypersensitivity e.g MS

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70
Q

What occurs with increased Th2?

A

Type 1 hypersensitivity e.g Asthma

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71
Q

What occurs with increased Th17?

A

Chronic pro-inflammatory state (RA)

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72
Q

What is the function of Treg?

A

Suppress activation. proliferation and cytokine production of CD4 and CD8 lymphocytes
Monitor self tolerance

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73
Q

What cytokines are released by Treg?

A

IL-10 and TGF-beta

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74
Q

What produces antibodies?

A

Plasma

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75
Q

What is the function of the Fc region on the antibody?

A

Communicate with other components of the immune system

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76
Q

What is the only isotope that can cross the placenta?

A

IgG

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77
Q

What antibody is involved in the primary response?

A

IgM

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78
Q

List functions of antibodies.

A

Bind to Ags - immune complexes
Act as opsonins for phagocytosis
Activate complement cascade
Antibody Dependent Cellular Cytotoxicity (ADCC)

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79
Q

During ADCC, what does the Fc region bind to?

A

CD16

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80
Q

If Fc region binds to CD16, what happens?

A

Perforin and granzymes released –> apoptosis

Activates macrophages, eosinophils and neutrophils –> release granules and toxic enzymes

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81
Q

What are the 3 mechanisms of B cell activation?

A

Th dependent
Th independent (B cells activated by antigens)
Memory B cells

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82
Q

What is class switching?

A

Change in Ab heavy chain - same antigen specificity but acts with different effector cells

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83
Q

What antibody is found in the highest concentration in secondary infection

A

IgG

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84
Q

What occurs from a change in Ab heavy chain?

A

Change in isotype

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85
Q

Describe the innate immune system.

A

Fast, non-specific initial response

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86
Q

List cells involved in the innate immune system.

A

NK cells
Mast cells
Myeloblast cells

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87
Q

List functions of the innate immune system.

A 
Antigen recognition 
Inflammation 
Recruitment of immune cells 
NK cytotoxicity 
Phagocytosis 
Opsonisation 
Activation of complement cascade
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88
Q

Give 2 examples of pattern recognition receptors.

A

Toll-like

C-type lectin

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89
Q

What do pattern recognition receptor recognise?

A

Pathogen associated molecular patterns (PAMPs) e.g lipopolysaccharide on gram -ve bacteria

OR damage associated molecular patterns (DAMPs)

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90
Q

Discuss the pathophysiology of inflammation.

A

Macrophages recognise PAMPs and DAMPs –> release IL-1 and TNFa
–> increase vascular permeability and neighbouring vessels express CAMS

Chemokine released to recruit/attract immune cells to point of inflammation

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91
Q

What is leukocyte extravasation?

A

Leukocytes move through endothelium to site of infection/inflammation

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92
Q

What loosens junctions between endothelial cells until neutrophils can squeeze through the gap into inflamed tissue?

A

Histamine and bradykinin

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93
Q

What are the cardinal signs of inflammation?

A

Dolar - pain (from histamine and bradykinin)

Calor - heat
Rubor - redness
Tumour - swelling
by vasodilation and increased vascular permeability

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94
Q

List atypical APCs.

A

Mast cells
Basophils
Eosinophils

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95
Q

List professional APCs.

A

Dendritic cells
Macrophages
B lymphocytes

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96
Q

What nucleated cell does not contain MHCI?

A

Platelets

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97
Q

How do NK cells differ from cytotoxic T cells?

A

Rapid response, no memory, don’t require primary antigen

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98
Q

What cells do NK cells target?

A

Pathogens/cells with reduced or absent MHC I signal

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99
Q

What can NK cells release if activated by MHC I expression?

A

IFN gamma
Perforin and granzyme
TNFa

100
Q

What cells are activated by IFN gamma?

A

Macrophages, NK cells

101
Q

What can activate NK cells?

A

IFN gamma
IL-2
Ab-opsonised Ag binding to Fc receptor

102
Q

What is opsonisation?

A

Binding of an opsin (tag) to an invading cell - ‘prepare for eating’

Increase efficiency of phagocytosis
Increase no of binding sites

103
Q

What is the complement cascade?

A

Biochemical cascade of plasma proteins
Trigger recruitment of immune cells
Opsonise pathogens
Aggregate forming membrane attack complex (through C3, C5 converts)

104
Q

What are the 3 complement cascades?

A

Classical (Ag-Ab immune complex)
Lectin (mannose (bacterial polysaccharides)-binding to lectin)
Alternative (direct binding to microbe)

105
Q

What is the difference between C3a and C3b?

A 
C3b = large fragment, opsonin 
C3a = small fragment, pro-inflammatory
106
Q

What forms the membrane attack complex?

A

C5b + C6 + C7 + C8 + C9

107
Q

What is the function of the membrane attack complex?

A

Forms cytolytic pores which punches holes in cell membrane of target pathogens

108
Q

List types of opsonins.

A

Plasma proteins
Ab
Complement

109
Q

What do cytokines released in response to inflammation induce endothelial cells to produce for leukocyte adhesion?

A

Selectin

110
Q

What is mast cell degranulation dependent on?

A

Cross linking of IgE Abs bound to Fc receptors on mast cell

111
Q

What antibodies protect newborns in the first 6 months of life?

A

Maternally transferred IgG

112
Q

How are immunodeficiencies classified?

A

Primary/congenital, secondary/acquired

113
Q

What are patients with immunodeficiencies susceptible?

A

Infection
Cancer
Autoimmunity

114
Q

What can be affected by primary immunodeficiencies?

A

Components of innate immune system
Stages of lymphocyte development
Response of mature lymphocytes to antigenic stimulation

115
Q

List examples of congenital disorders that affect innate immune system.

A

Chronic granulomatous disease, leukocytes adhesion deficiency

116
Q

What causes SCID?

A

Defects in T and B cells

117
Q

If Serum Ig levels reduced, what type of deficiency does this suggest?

A

B cell deficiency

118
Q

What changes are seen in follicles and germinal centres?

A

B cell deficiency - absent

T cell deficiency - normal

119
Q

What does repeated infection with encapsulated bacteria a sign of?

A

Defective antibody production

120
Q

If deficiency in IgG and IgA, what can this lead to?

A

Recurrent respiratory infection by pneumococcal or haemophilus spp.

121
Q

What are infections with staph, gram -ve bacteria and fungi a sign of?

A

Reduced number of phagocytes

122
Q

What defects can predispose to meningitis?

A

Complement defects

123
Q

What do T cell/macrophage defects result in?

A

Predisposition to infection with protozoa, viruses, intracellular bacteria

124
Q

What is reactivation of latent herpes virus?

A

T cell immunodeficiency

125
Q

What does recurrent attacks of cold sores or shingles suggest?

A

Mild immunodeficiency (specifically T cell)

126
Q

Give examples of herpes virus- induced tumours caused by T cell dysfunction.

A

Kaposi’s sarcoma

NHL

127
Q

What pathway is likely to be defected with recurrent candida infections?

A

TH17

128
Q

List causes of primary immunodeficiency.

A 
Mutations 
Polymorphisms (two or more variants of a particular DNA sequence)
Polygenic disorders (more than one gene involved)
129
Q

List genetic causes of SCID?

A

Autosmal inherited

X-linked

130
Q

What is a curative treatment for SCID?

A

Stem cell transplant (soon after birth)

131
Q

What are common variable immunodeficiency (CVID) caused by?

A

Polygenic disorders - IgA deficiency

132
Q

What does CVID cause?

A

Recurrent respiratory tract infections

133
Q

What antibody fights fungal infections?

A

IgE

134
Q

What do patients with APECED have a defect in?

A

Central tolerance

Produce antibodies against IL17

135
Q

What do patients with APECED have an increased risk of?

A

Recurrent candida infections

136
Q

How do you diagnose primary immune deficiency?

A
  • Recurrent infections
  • Unusual infections
  • Family history of neonatal death
  • Lymphocyte count (low)
  • Flow cytometry for antibody count (IgG, IgE, IgM)
137
Q

How do you treat primary immunodeficiency?

A 
Prevent infection by...
Prophylactic antibiotics
If severe --> Immunoglobulin replacement therapy
Stem cell transplant e.g for SCID
Gene therapy
138
Q

What are secondary causes of low antibodies?

A

Kidney or gut disease

139
Q

When can you give gene therapy for primary immunodeficiency?

A

Gene mutation identified
Evidence correcting mutation will improve condition
Transfected gene must confer a d proliferative survival advantage
Must not cause malignancy

140
Q

List 3 types of antigens that can cause hypersensitivity?

A

Infection
Harmless environmental substances
Self-antigen

141
Q

Name a virus that can cause hypersensitivity reactions.

A

Influenza

damage endothelium –> exaggerated immune response –> trigger cytokine storm –> hypotension and coagulation

142
Q

How does IgE get produced in hypersensitivity reactions?

A

Th2 –> IL-4 –> B cells –> IgE

143
Q

List environmental factors that can trigger hypersensitivity.

A

Pollen
Dust
Food
Nickel (contact dermatitis)

144
Q

What is the difference between IgE and IgG mediated hypersensitivities?

A

IgE –> immediate, allergy symptoms

IgG –> farmer’s lung

145
Q

What are haptens?

A

Small molecules that bind to proteins and elicit and immune response.
Can’t bind to antibodies but bind to other small proteins,

146
Q

What is a type 1 hypersensitivity reaction?

A

Allergy

Immediate reaction
IgE mediated
Mast cells and eosinophil degranulation

147
Q

What is a type 2 hypersensitivity reaction?

A

Antibody mediated, on second exposure allergic reaction

148
Q

What is a type 3 hypersensitivity reaction?

A

Immune complexes formed between antibodies and antigens

149
Q

What is a type 4 hypersensitivity reaction?

A

Delayed hypersensitivity

150
Q

What do Th2 cells induce?

A

Production of IgE from B cells via IL-4

151
Q

Define atopy.

A

Immediate hypersensitivity rection to environmental antigens mediated by IgE

Develops within minutes of exposure

152
Q

List signs of atopy.

A 
Anaphylaxis
Angioedema 
Urticaria 
Rhinitis 
Asthma
Dermatitis
153
Q

What is angioedema?

A

Non-specific, non-itchy swelling

154
Q

What is the allergic march?

A

Development of allergic reactions over time

155
Q

Define allergens.

A

Antigens that cause allergic reactions.

156
Q

What is the allergen in penicillin allergies?

A

B-lactam

157
Q

When do B cells produce IgE?

A

Co-stimulation with IL-4 secreted by Th2

158
Q

What causes allergic symptoms?

A

Release of mediators that cause allergic symptoms

159
Q

What cells degranulate causing allergic symptoms?

A

Mast cells
Eosinophils (migrate to tissues)
Basophils (stay in circulation)

160
Q

What receptors are found on mast cells?

A 
For IgE 
(regular and high affinity types)
161
Q

What is a genetic cause of allergies?

A

Polymorphisms in gene encoding filaggrin which is expressed in keratocytes

162
Q

What is the role of fillagrin?

A

Maintains epithelial barriers and moisturising surfaces and controlling pH

163
Q

What are polymorphisms?

A

Slightly different alleles for same gene, present in 1% or more of population

164
Q

List two polymorphism variants that can cause induction of Th2.

A

Filaggrin variant

LPS receptor variant

165
Q

Why is the incidence of allergies increasing globally?

A

Urbanisation

Hygiene hypothesis

166
Q

Discuss the pathophysiology of anaphylaxis.

A

Mast cells produce prostaglandins and leukotrienes through the cyclo-ocygenase and lipoxygenase pathways
–> vasodilation and increased vascular permeability –> shift of fluids from vascular to extra-vascular space –> drop in BP

Histamine in skin –> further increase shift of fluid (oedema)

167
Q

Discuss the pathophysiology of rhinitis.

A

Inhaled allergens stimulates mast cells in nasal mucosa

Leukotrienes increase mucous secretion

168
Q

How do you treat type 1 hypersensitivity reactions?

A

Desensitisation (allergy immunotherapy)

Drugs: B2-adrenergic agonists, adrenaline, antihistamines, leukotriene agionists, corticosteroids

169
Q

What test can be carried out to identify cause of allergies?

A

Skin prick test

170
Q

How does type 2 hypersensitivity reactions occur?

A

Antibody mediated - IgG (through complement) or IgM (through pathogen)

171
Q

What is the most common type of type 2 hypersensitivity?

A

Haemolytic anaemia

172
Q

List examples of immune mediated haemolysis.

A

Alloimmune haemolysis e.g incompatibility with ABO

Autoimmune haemolysis e.g induced by infection or drugs, autoantibodies produced by malignant B cells

Type 2 reactions against solid tissue e.g Goodpastures syndrome

173
Q

Give an example of a condition which release antibodies that affect cell function.

A

Graves disease - Thyroid stimulated with autoantibody that binds into the TSH receptor

174
Q

List examples of hypersensitivity type 2 diseases.

A 
Autoimmune haemolytic anaemia
Autoimmune thrombocytopenia purpura
Pemphigus vulgaris
Vasculitis caused by ANCA
Myaesthenia gravis 
Penicious anaemia
175
Q

What antibody is responsible for type 3 hypersensitivity reaction?

A

IgG
–> form antigen-antibody complex

(large complexes when antibody= antigen, when antibody>antigen = small complex)

176
Q

In type 3 hypersensitivity reactions, what breaks down large complexes?

A

Complement

177
Q

What causes immune complex disease in type 3 hypersensitive reactions?

A

Failure of clearance of complexes by complement

–> activation of innate immune system

178
Q

Give an example of a type 3 hypersensitivity reaction with immune complex disease.

A

Glomerulonephritis
Farmer’s lung
SLE

179
Q

What is the slowest type of hypersensitivity?

A

Type 4 (2-3 days)

180
Q

What initiates type 4 hypersensitivity reactions?

A

Macrophages recognise ANTIGEN –> dendritic cells migrate to lymph nodes and present antigen to T cells –> exaggerated response against self antigen

181
Q

What stimulates most of the damage in type 4 hypersensitivity?

A

TNF secreted by macrophages and T cells

182
Q

Give examples of type 4 hypersensitivity reactions.

A 
Rheumatoid arthritis 
Multiple sclerosis
T1DM
IBD
Psoriasis
183
Q

What helper T cells are associated with type 4 hypersensitivity reactions?

A

Th1 and 17

184
Q

How do you treat delayed hypersensitivity?

A

Prevent through avoidance of antigens

Anti-inflammatories: NSAIDs, corticosteroids, drugs that block TNF and IL-6, Abs against B cells

Immunosuppressive drugs

185
Q

Define immunological tolerance.

A

Unresponsiveness to an antigen that is induced by previous exposure to that antigen

186
Q

What are tolerogens?

A

antigens that induce tolerance

187
Q

What occurs from failure of self tolerance?

A

Autoimmunity

188
Q

What are the two types of immunological tolerance?

A

Central - thymus, eliminate T cells with high affinity to self. Bone marrow for B cell tolerance

Peripheral - mature lymphocytes that recognise self in peripheral tissues become incapable of activation or die by apoptosis

189
Q

List mechanisms of peripheral tolerance.

A 
Anergy
Antigen recognition with co-stimulation 
Treg suppression 
Deletion 
Some self antigens sequestered from immune system by anatomic barriers
190
Q

Define autoimmunity.

A

Adaptive immune response to self antigens

191
Q

Define autoantigens.

A

Antibodies directed at normal cellular components

192
Q

autoimmune disease occurs when auto reactive T cells or autoantibodies cause tissue damage through what types of hypersensitivity?

A

2, 3, 4

193
Q

What is the major source of autoantibodies?

A

B1 cells

–> cross-react with inherited A and B antigens of red cells, make IgM anti-A and anti-B even if not exposed

194
Q

What causes breakdown of T cell tolerance?

A

Genetic predisposition (familial clustering, MHC alleles, polymorphisms, rare genetic diseases, AIRE gene)

Environmental factors (infections, drugs, UV radiation )

195
Q

What gene can be mutated to prevent central tolerance from not taking place?

A

AIRE gene (transcription factor expressed by medullary epithelial cells in thymus)

196
Q

What is molecular mimicry?

A

Structural similarity between self-proteins and microbial antigens may trigger an autoimmune response –> caused by infection, drugs

197
Q

Most autoimmune diseases present age 15-65. Give an exception to this.

A

T1DM

198
Q

What are the two different types of autoimmune disease.

A

Non-organ specific

Organ specific (endocrine gland)

199
Q

Give examples of autoimmune diseases.

A

SLE
T1DM
Coeliac disease

200
Q

How is autoimmune diseases treated?

A

suppress damage of immune response (immunosuppressives)

Replace function of organ damaged

e.g Treg cell therapies

201
Q

What gender is autoimmune diseases most common in?

A

Females mostly

202
Q

Define autograft.

A

Transfer of tissue between different sites within same organism.

203
Q

Define isograft.

A

Transfer between genetically identical individuals

204
Q

Define allograft.

A

Transfer between genetically non-identical individuals of same species

205
Q

Define xenograft.

A

Transfer between species

206
Q

What is the most common type of transplant?

A

Allograph

207
Q

List two things to do to prevent transplant rejection.

A 
Tissue match (ABO, HLA-A, B, DR)
Prophylactic immunosuppressive therapy
208
Q

Describe an instance when no tissue matching or immunosuppressive therapy is required.

A

Corneal transplant

209
Q

Define privileged sites.

A

When no tissue typing or immunosuppression required

Can tolerate new antigens without inducing an immune response

210
Q

List 7 complications of transplantation.

A 
Graft rejection 
GVHD 
Infection 
Neoplasm 
Recurrence of original disease 
Drug side effects 
Ethical, surgical problems
211
Q

List two mechanisms of graft rejection.

A

Direct alloantigen recognition or indirect presentation

*Mostly due to incomplete HLA matching

212
Q

Define hyperacute rejection.

A

Minutes, from pre-formed Abs

213
Q

Define accelerated rejection.

A

2-5 days, from T cells pre-sensitised

214
Q

Define acute rejection.

A

7-21 days, from T cells newly sensitised

215
Q

Define chronic rejection.

A

months-years, multifactorial

216
Q

List 4 types of graft rejection.

A

Hyperacute, accelerated, acute, chronic

217
Q

What is the most common cause of GVHD?

A

Bone marrow transplant

218
Q

What circumstance need to be present to cause GVHD?

A

Presence of functioning immunocompetent donor T cells in graft
Defective immunity in recipient
HLA differences

219
Q

Where is GVHD most commonly seen?

A

Skin, gut, liver and immune cells

220
Q

How can GVHD by prevented?

A

Careful/v close tissue matching

Deplete donor marrow of T cells in vitro prior to grafting

221
Q

Before bone marrow transplant, what should be done?

A

Conditioning - High dose chemo and radiotherapy (to destroy recipients SCs and allow engraftment of donor cells)

222
Q

Give an example of an xenograft.

A

Porcine tisse

223
Q

What is a problem with the use of porcine tissue?

A

Humans have naturally acquired IgM against pig Ags and galactose residues

224
Q

Give examples of immunosuppressive drugs.

A 
Cyclosporin 
Tacrolimus 
Basiliximab
Rapamycin
Azathioprine
Methotrexate
225
Q

List side effects of cyclosporin.

A

Nephrotoxic
Infections
DM
HTN

226
Q

List side effects of the monoclonal antibody treatment Rapamycin.

A

Hyperlipidaemia/cholesterolaemia, HTN, Anaemia, Thrombocytopenia, acne

227
Q

What is acute graft rejection associated with?

A

T cell responses that mediate immune cell infiltration into graft

228
Q

What is IV immunoglobulin used for?

A
  1. Replacement therapy - primary and secondary immunodeficiencies
  2. Modulatory therapy - inflammatory and autoimmune disorders
229
Q

What are potential problems with IVIg?

A

ADRs during infusions

Infection transmission e.g Hep C

230
Q

List the two types of immunotherapy and give examples.

A

Direct (targeted) - Monoclonal Abs, CARs, Bi-specific Ab

Indirect - Tumour vaccines, dendritic cell therapies, cytokine therapies, checkpoint inhibitor therapies, stimulatory Abs

231
Q

List established immunosuppressive/modulatory drugs.

A

Corticosteroids
Azathioprine
Cyclophosphamide

232
Q

How do corticosteroids work?

A

affect B and T cells, cytokine network, inflammation, monocytes, transit and circulation of immunologically active cells

233
Q

How does azathipoprine work?

A

inhibits DNA synthesis, T cells and NK cells, anti-inflammatory

234
Q

How does cyclophosphamide

A

Suppress B cells and Ab production

235
Q

List newer immunosuppressives.

A

Cyclosporin, Tacrolimus
Rapamycin
Mycophenolic acid

236
Q

How do monoclonal antibody therapies work?

A

Target specific antigens e.g T cell receptors (CD3, 4 and 52, HLA, Cytokines)

Use mouse/rat derived AB, cleave Fc and replace with human Fc

237
Q

Give 3 examples of monoclonal antibody therapies.

A
  1. Rituximab - NHL
  2. Inflixumab - RA, AS, IBD
  3. Trastuzumab/Herceptin - Breast cancer
238
Q

How do cytokine therapies work?

A

Exert autocrine effects on cells or paracrine effects on cells around them

Involves production of factors that will interfere with cytokines or produce/administer recombinant cytokines

239
Q

What is the purpose of cytokine therapy.

A

Inhibit harmful cytokines or enhance beneficial cytokines

240
Q

Give examples of cytokine therapies.

A

IL-1/TNF - decrease activity in RA

IL-2 - Decrease activity in transplant rejection or increase in tumour therapy

241
Q

What is the purpose of checkpoint inhibitors?

A

Unlock gateway to adoptive immune system - powerful anti-tumour response

242
Q

What is a potential side effect of checkpoint inhibitors?

A

Immune related ADRs

243
Q

Give an example of a checkpoint inhibitor for metastatic melanoma.

A

Ipilimumab

244
Q

Discuss PD1/PDL-1 as targets for inhibitors.

A

In a cancer state, PD1 on T cell binds with PD-L1 on tumour cell causing reduced T cell function and therefore preventing immune system from attacking tumour.

If inhibit these checkpoints, then immune system can attack.

245
Q

Give an example of an adoptive cell therapy.

A

CAR-T

Haematology and Immunology (2 decks)

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