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Immunology Flashcards

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1
Q

What are the four types of innate immunity?

A

Anatomical barriers, physiological barriers, phagocytic barriers and inflammatory barriers

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2
Q

What are examples of anatomical barriers?

A

Skin and mucous membranes

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3
Q

What are examples of physiological barriers?

A

Temperature, acidity, soluble factors

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4
Q

What are examples of phagocytic barriers?

A

Phagocytes

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5
Q

What are the characteristics of the epidermis?

A

Dead outer, impermeable, nutrition by diffusion, sheds every 10-15 days, made up of keratinocytes

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6
Q

What are the characteristics of the dermis?

A

Vascularised, connective tissue, glands, sebum secretion

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7
Q

What is the most common entry point for pathogens?

A

Mucous membranes

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8
Q

What composes the mucous membranes?

A

Outer epithelial and connective tissue layers

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9
Q

What makes up mucus?

A

Mucin (glycoproteins), anti-microbial, proteins, inorganic salts

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10
Q

How does the influenza virus evade the mucous membrane defence?

A

It has specialised adhesion molecules

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11
Q

How does gastric acidity destroy most ingested pathogens?

A

Low pH denatures enzymes, affects transport mechanisms and metabolic activity

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12
Q

What are the soluble factors and how to they defend the body?

A

Lysozyme (cleaves peptidoglycans, weakens cell wall, osmotic lysis), interferon (anti-viral activity, prevents viral replication), opsonins (ficolin, surfactant proteins, mannose binding protein, promotes phagocytosis), complement (lyse target cells, enhance phagocytosis and chemotaxis)

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13
Q

What are cells of the myeloid lineage of the innate immune system?

A

Neutrophils, monocyte/macrophage, eosinophils, basophils, mast cells

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14
Q

What are cells of the lymphoid lineage of the innate immune system?

A

Natural killer cells

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15
Q

What is the difference between endocytosis and phagocytosis?

A

Endocytosis is the ingestion of macromolecules, phagocytosis is the ingestion of particles. All cells are endocytic but only certain cells can phagocytose.

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16
Q

What are the two major mechanisms of endocytosis?

A

Pinocytosis (nonspecific) and receptor-mediated endocytosis (specific)

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17
Q

What is the mechanism of phagocytosis?

A

Plasma membrane expands to form pseudopods. Pseudopod retracts and seals intelf into a phagosome. Phagosome fuses with lysosomes. Processing then similar to endocytosis.

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18
Q

What is the function of opsonins?

A

Tagging microbes to make it more palatable for phagocytes

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19
Q

What are the two functions of complement?

A

Generate reaction products to clear antigens and generate an inflammatory response

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20
Q

How is complement activated in adaptive immunity?

A

Classical pathway - C1 recognises immune complexes formed by the binding of antibodies to antigen

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21
Q

How is complement activated in innate immunity?

A

Alternative pathway - non-specific activation by bacteria, fungi, parasites and viruses, C3b deposits on surfaces of microbes. Lectin pathway - mannose binding lectin attaches to mannose sugar residues on bacteria surface

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22
Q

What is the first important mechanism which occurs following complement activation?

A

Opsonisation - coats surface with C3b proteins to promote phagocytosis

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23
Q

What is the second important mechanism which occurs following complement activation?

A

Initiates an inflammatory response - release anaphylatoxins C3a, C4a and C5a, which bind to immune cells to trigger the inflammatory response. Anaphylatoxins are also chemoattractants to phagocytes

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24
Q

What is the third important mechanism which occurs following complement activation?

A

Punches holes in cell membranes - formation of the membrane attack complex on surface of cells, bacteria and evneloped viruses

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25
Q

Define the inflammatory response

A

A complex sequence of events that occur following tissue damage caused by invasion or wounding

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26
Q

How are leukocytes transported?

A

In the circulatory system

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27
Q

What is the function of precapillary sphincters?

A

Prevent the backflow of blood

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28
Q

What are the three types of capillary?

A

Continuous, fenestrated, sinusoidal

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29
Q

What are the features of continuous capilaries?

A

Least permeable, most common (skin, muscle), don’t let cells pass through in normal homeostatic conditions

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30
Q

What are the features of fenestrated capillaries?

A

Large fenestrations, in areas of high filtration (kidneys, choroid plexus), increased permeability

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31
Q

What are the features of sinusoidal capillaries?

A

Most permeable, only in special locations (spleen, bone marrow), for collecting blood in a network of sinuses

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32
Q

Where are most blood cells being made one month after contraception?

A

Yolk sac

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33
Q

Where are most blood cells being made five months after contraception?

A

Liver and spleen

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34
Q

Where are most blood cells being made at birth?

A

Bones

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35
Q

Which bones quickly stop producing blood cells after birth?

A

Long bones

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36
Q

Which bones slowly stop producing blood cells after birth?

A

Cranium, pelvis, sternum, ribs, vertebra

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37
Q

What are the characteristics of neutrophils?

A

Most numerous of circulating lymphocytes (50-70%), rapidly deployed and expandable, half life about 7 days, lasts 1-2 days, only 5% in circulation

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38
Q

What are the characteristics of eosinophils?

A

1-3% of circulating leukocytes, increased in allergic individuals and upon helminth infections, role in type I hypersensitivity (allergy)

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39
Q

What are the characteristics of basophils?

A

<1% of circulating leukocytes, important role in initiation of inflammation, parasitic infections and allergic reactions

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40
Q

What are the characteristics of monocytes?

A

1-6% of circulating leukocytes, half life around 1 day, circulating precursors of macrophages and dendritic cells, some phagocytic capability

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41
Q

What causes a small, naive B lymphocyte to enter the cell cycle?

A

Antigen activation induces cell cycle entry

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42
Q

What are the T halper cell subsets?

A

Th1, Th2, Th17, iTreg, Th9, Tfh

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43
Q

Which cytokines cause a naive CD4+ T cell to become Th1?

A

IFN-gamma, IL-12

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44
Q

Which cytokines cause a naive CD4+ T cell to become Th2?

A

IL-4

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45
Q

Which cytokines cause a naive CD4+ T cell to become Th17?

A

IL-6, TGF-beta

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46
Q

Which cytokines cause a naive CD4+ T cell to become iTreg?

A

TGF-beta, RA, IL-2

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47
Q

Which cytokines cause a naive CD4+ T cell to become Tfh?

A

IL-21

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48
Q

Which T cells have CD4+ present on their surfaces?

A

T helper cells

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49
Q

Which T cells have CD8+ present on their surfaces?

A

Cytotoxic T cells

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50
Q

What is the major source of inflammatory cytokines?

A

Macrophage

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51
Q

What is the purpose of dendritic cells?

A

Crucial antigen-presenting cells, specialise in presenting antigen to naive T cells, and can be derived from either myeloid lineage or lymphoid lineage

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52
Q

What are tissue-resident dendritic cells called?

A

Migratory

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53
Q

What are lymphoid organ-resident dendritic cells called?

A

Conventional

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54
Q

What do mast cells function as?

A

Sentinal cells of the innate immune system

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55
Q

What are the primary lymphoid organs?

A

Thymus, bone marrow

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56
Q

What are the secondary lymphoid organs?

A

Spleen, adenoids, tonsils, thoracic duct, lymph nodes, tissue lymphatics

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57
Q

What happens in primary lymphoid organs?

A

Sites of antigen receptor rearrangement, release mature antigen-responsive lymphocytes into circulation, sites of positive and negative selection

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58
Q

What happens in secondary lymphoid organs?

A

Sites of engagement of lymphocytes with antigen

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59
Q

What surrounds arterioles as a periarteriolar lymphoid sheath in the spleen?

A

T cell area (containing dendritic cells)

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60
Q

What are in the follicles in the spleen?

A

B cell area

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61
Q

What is in the marginal zone of the spleen?

A

Macrophages, specialised B cells

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62
Q

Which type of capillary does the spleen have?

A

Sinusoidal capillaries

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63
Q

How do naive lymphocytes circulate?

A

Traffic through the blood, peripheral lymhoid tissues and efferent lymphatics, but do not enter non-lymphoid peripheral tissue

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64
Q

How do effector lymphocytes circulate?

A

Can enter non-lymphoid peripheral tissues, but have lost their ability to enter peripheral lymphoid tissues

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65
Q

How do memory lymphocytes circulate?

A

Can go everywhere

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66
Q

What is serum?

A

Plasma not containing clotting factors

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67
Q

Where are antibodies found?

A

In the gammaglobulin fraction of serum proteins

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68
Q

What are gammaglobulins?

A

Not very charged proteins in serum

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69
Q

What is one way to transfer passive immunity to someone?

A

Transfer pooled gammaglobulins (doesn’t last long as they have a half-life)

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70
Q

What is the difference between antibody and immunoglobulin?

A

Antibody relates to function, immunoglobulin relates to structure

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71
Q

What is the structure of an immunoglobulin?

A

4 polypeptides held together by disulphide bonds

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72
Q

Where are immunoglobulins made?

A

Made by B cells

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73
Q

What is the mechanism of production of a B cell?

A

Stem cell -> Pro-B cell -> Pre-B cell (with preIg) -> Immature B cell (with IgM) -> Mature B cell (with IgM and IgD) -> released from bone marrow

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74
Q

Which Ig chain is made first?

A

Heavy chains with surrogate light chain (later replaced)

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75
Q

Which antibodies are in highest concentration?

A

IgG

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76
Q

What are the isotypes of Igs?

A

IgM, IgD, IgG(1, 2, 3, 4), IgE, IgA(1 and 2)

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77
Q

Which antibody is made first by B cells?

A

IgM (also first to be secreted in immune response)

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78
Q

Which antibody is protected from enzymatic degradation and how?

A

IgA, by the secretory component (hence it can bind to antigens in the mucosal regions)

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79
Q

Is there Ig allotypic variation within an individual?

A

No (constant regions)

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80
Q

Is there Ig idiotypic variation within an individual?

A

Yes (variable regions in heavy and light chains)

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81
Q

Where does Ig bind on an antigen?

A

On the epitope

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82
Q

How are antibodies generated?

A

B(rest) meets antigen -> activated B cell -> memory and plasma cells -> plasma cell secretes Ig (no hydrophobic region)

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83
Q

What are the three functions of antibodies?

A

Binds to complement protein C1 to initiate the Classical pathway, binds to Fc receptors on phagocytes (neutrophils and macrophages), binds to Banwell receptors on endothelial cells

84
Q

How is antibody diversity achieved?

A

Gene rearrangement within the variable region of the H and L chains (occurs when Pro-B cell becomes Pre-B cell)

85
Q

What is the important antibody in the primary immune response?

A

IgM

86
Q

What is the important antibody in the secondary immune response, and why is it different?

A

IgG. Has higher binding affinity of the antibody for the antigen, production of more memory B cells.

87
Q

What are the different types of vaccine?

A

Live attenuated organisms, killed whole organisms, inactivated components of organisms, recombinant proteins

88
Q

Why do dead vaccines generally result in a poor immune response?

A

Macrophages can come and remove the dead stuf

89
Q

How does an adjuvant work?

A

Enhances the immune response by slowly releasing the antigen or vaccine, so it can persist longer in the body

90
Q

What causes B cells to undergo class switching?

A

The influence of certain cytokines released by helper T cells

91
Q

When class switching, which region is affected?

A

Only the constant region

92
Q

Which cytokine causes a switch to IgG?

A

IFN-gamma

93
Q

Which cytokine causes a switch to IgA?

A

TGF-beta

94
Q

Which cytokine causes a switch to IgE?

A

IL-4

95
Q

What are the characteristics of IgM?

A

Neutralises extracellular bacteria and viruses

96
Q

What are the characteristics of IgG?

A

Can pass through the blood placenta barrier

97
Q

What are the characteristics of IgA?

A

Survive longer in bodily secretions

98
Q

What are the characteristics of IgE?

A

Attaches onto eosinophils (or mast cells/basophils) via its Fc region to help fight against extracellular parasites

99
Q

Why can’t macrophages destroy parasites?

A

They are too small (so IgG is ineffective)

100
Q

What are the factors which affect affinity maturation?

A

Somatic hypermutation and antigen dose

101
Q

What is somatic hypermutation?

A

Random point mutations in the CDR region in the VH and VL regions of the Ig gene. These change the isotype with no guarantee that it will generate higher affinity antibodies.

102
Q

How does the antigen dose affect affinity maturation?

A

In low antigen dose, high affinity antibodies will predominate and vice versa. They will have to compete for the antigen, so the antibodies with lower affinity will not receive the signal to live and will die by apoptosis

103
Q

Are antibody-antigen reactions reversible?

A

Yes (no covalent bonds)

104
Q

What are haptens?

A

Small foreign molecules that antibodies can bind to but on its own is not immunogenic enough to stimulate antibody production

105
Q

What must happen to raise antibodies to a hapten?

A

Must be conjugated to a carrier (Hapten-Carrier conjugate)

106
Q

What does ELISA stand for?

A

Enzyme-Linked ImmunoSorbent Assay

107
Q

What is the purpose of ELISA?

A

Uses antibodies as a tool to detect and quantify antigens

108
Q

What are the advantages of ELISA?

A

Non-radioactive, cheap, student friendly, fast, wide applications

109
Q

In the absence of antigen, what happens to a resting B cell?

A

No activation so no antibodies produced

110
Q

What happens when antigen presentation goes wrong?

A

Autoimmune disease

111
Q

Where does antigen presentation occur?

A

Regional lymph nodes

112
Q

What does MHC stand for?

A

Major Histocompatibility Class (also called Human Leukocyte Antigen = HLA)

113
Q

What do all nucleated cells express on their surface?

A

MHC I

114
Q

What do antigen presenting cells express on their cell surface?

A

MHC II

115
Q

What is the main function of MHC molecules?

A

Present antigen to T cell receptor of CD4+ or CD8+ T cells

116
Q

Which peptides are presented by MHC I?

A

Those which are small and derived from endogenous presentation

117
Q

Which peptides are presented by MHC II?

A

Those which are larger and derived from exogenous presentation

118
Q

What are immature dendritic cells important for?

A

Immune tolerance

119
Q

How are viral antigens presented?

A

Endogenously via MHC I

120
Q

How are natural killer T cells activated?

A

By Gram-negative bacteria through indirect and direct pathways

121
Q

What is cross presentation?

A

When professional antigen presenting cells (DCs) take up antigen exogenously and present it via MHC I

122
Q

What is cross priming?

A

When CD8+ cells are primed against antigen that has been presented by cross presentation

123
Q

Define a mature lymphocyte

A

Has undergone antigen-independent development in primary lymphoid organs and has entered circulation

124
Q

Define a naive lymphocyte

A

Mature lymphocyte that has not been exposed to cognate antigen in periphery

125
Q

Define an effector lymphocyte

A

Differentiation state that relates to specific function in the immune response, depends on Ag-specific activation

126
Q

Define a memory lymphocyte

A

Ag-activated lymphocyte that has not differentiated sufficiently to become an effector lymphocyte

127
Q

Where do the antigen-independent phases of lymphocyte develoopment occur?

A

For T cells: bone marrow then thymus. For B cells: bone marrow

128
Q

Where do the antigen-dependent phases of lymphocyte development occur?

A

In the peripheral lymphoid tissue

129
Q

What regulates the behaviour of leukocytes?

A

Cytokines

130
Q

How do Th cells regulate other cells?

A

By selective delivery of cytokines and other signals

131
Q

Where does initial T and B cell activation occur?

A

In secondary lymphoid organs

132
Q

Which cells are responsible for priming in secondary lymphoid organs?

A

Dendritic cells

133
Q

Which cytokine is the one driver for lymphocyte proliferation?

A

IL-2 (autocrine)

134
Q

What are the three signals for lymphocyte selection and proliferation?

A

1: Specificity
2: Dendritic cell upregulates B7 for costimulation, which binds to CD28 on the T cell
3: IL-2 is released, and IL-2 receptors are upregulated on the surface (autocrine)

135
Q

What are the signature cytokines of Th1?

A

IFN-gamma, IL-12

136
Q

What are the signature cytokines of Th2?

A

IL-4, IL-5 IL-13

137
Q

What are the signature cytokines of Th17?

A

IL-17, IL-22

138
Q

What are the signature cytokines of Threg?

A

TGF-beta, IL-10

139
Q

What are the signature cytokines of Tfh?

A

IL-21

140
Q

What do Th1 cells act on?

A

Macrophages, NK cells, CD8+ T cells, B cells -> IgG2

141
Q

What do Th2 cells act on?

A

Eosinophils, mast cells, B cells -> IgE, IgG4

142
Q

What do Th17 cells act on?

A

Neutrophils, epithelial cells

143
Q

What do Treg cells act on?

A

Other lymphocytes

144
Q

What do Tfh cells act on?

A

B lymphocytes

145
Q

What are the major effector functions of Th1 cells?

A

CMI: killing of virus or bacteria-infected host cells

146
Q

What are the major effector functions of Th2 cells?

A

Responses to worms and allergens

147
Q

What are the major effector functions of Th17 cells?

A

Pro-inflammatory: responses to fungiand extracellular bacteria

148
Q

What are the major effector functions of Treg cells?

A

Inhibits function of other sets of T and non-T cells

149
Q

What are the major effector functions of Tfh cells?

A

Promotes high affinity antibody production

150
Q

Which signals cause a CD4+ T cell to become a Th1?

A

IL-12

151
Q

Which signals cause a CD4+ T cell to become a Th2?

A

IL-4

152
Q

Which signals cause a CD4+ T cell to become a Th17?

A

TGF-beta, IL-6

153
Q

Which signals cause a CD4+ T cell to become a Treg?

A

TGF-beta

154
Q

Which signals cause a CD4+ T cell to become a Tfh?

A

IL-21

155
Q

What does effective T and B cell interactions require?

A

Cell-cell contact

156
Q

What are the three important interactions between T cells and B cells?

A

1: MHC2-T cell receptor (with CD4+)
2: CD40-CD40L
3: Cytokines flow from T cell to B cell

157
Q

What is the purpose of cell mediated immunity?

A

To protect from intracellular pathogens (intracellular bacteria, viruses, some tlarge parasites) and controlled by Th1 cells (antigen-specific response)

158
Q

What is the key cytokine in CMI?

A

IFN-gamma

159
Q

How do Th1 cells help macrophages?

A

Macrophage presents epitope on MHC II, leadds to cytokine secretion and macrophage activation, killing the ingested microbes

160
Q

What are the three stages of CTL generation?

A

Stimulation of naive T cell, proliferating T cell, active effector T cells kill virus-infected target cells

161
Q

How does immunological memory occur?

A

Activation of T cells leads to clonal expansion of cells reactive to specific Ags, leads to generation of effector T cells and memory T cells

162
Q

Which cells provide immunological memory in CMI?

A

T cells

163
Q

How do memory T cells enter lymph nodes?

A

Through inflamed tissues

164
Q

How do naive T cells enter lymph nodes?

A

Through specialised blood vessels

165
Q

Where does T cell education occur?

A

Thymus

166
Q

Which T cells develop in the thymus?

A

alpha and beta TCR

167
Q

Which T cells develop in epithelial tissue in the skin and gut?

A

gamma and delta TCR

168
Q

T cell development in the thymus is antigen independent or dependent?

A

Independent

169
Q

What is the difference between T cell precursors and T cells?

A

Precursors are CD4/8 negative and TCR negative

170
Q

What is the purpose of positive selection?

A

Determine functional TCRs

171
Q

What is the purpose of negative selection?

A

Eliminate self-reactive TCRs

172
Q

Where does positive selection occur?

A

Cortical epithelial cells

173
Q

Where does negative selection occur?

A

Dendritic cells and medullary thymic epithelial cells

174
Q

What are the key stages of thymocyte development?

A

Rearrangement of the TCR (beta chain first), pre Talpha (DN cells that have successfully rearranged their beta chains), cells become DP (CD4 and CD8), positive selection (life or death decision, transition to SP stage), negative selection (life or death deciosn), maturing circulating T lymphocytes

175
Q

How is a diversity of TCR achieved?

A

Rearrangement and expression of TCR genes

176
Q

Positive selection

A

DP cells interact with MHC I or II, interaction is with TEC in cortex affinity of outcome is important, interaction leads to survival (B cells don’t have positive selection because B cells never see MHC I or II)

177
Q

What is central tolerance?

A

Self-reactive T and B cells undergo apoptosis in the primary lymphoid organs (negative selection)

178
Q

What is peripheral tolerance?

A

Self-reactive T and B cells that evade negative selection can be made tolerant by other mechanisms operating outside the primary lymphoid organs

179
Q

What are the three major mechanisms of lymphocyte tolerance?

A

CLonal deletion (central tolerance), clonal ignorance (peripheral tolerance), clonal anergy (peripheral tolerance), suppression (peripheral tolerance)

180
Q

Negative selection

A

Selection based on TCR, T cells that bind self-antigens with higher affinity are deleted earlier and more completely than those that bind with low affinity, population remaining consists of CD4+ and CD8+ T cells that have selectivity for foreign antigens and self-MHC molecules

181
Q

Clonal ignorance

A

T cell doesn’t see antigen, antigen too low to reach stimulation threshold

182
Q

Clonal anergy

A

Prolonged, antigen-specific suppression of a T cell clone. Becomes anergic, clone has been deleted but not killed

183
Q

Suppression

A

Lymphocyte subsets may act as suppressors of T and B cell activation

184
Q

How do regulatory T cells suppress reactions to self antigens?

A

In the thymus, if the thymocyte has high affinity for the self antigen it will be destroyed

185
Q

How are B cells protected against self antigen?

A

Require T cel help (no autoreactive T cells, no T cell help)

186
Q

What is the definition of a hypersensitivity reaction?

A

Inappropriate or exaggerated immune response to antiglobbulin

187
Q

Type I hypersensitivity

A

Allergic, IgE

188
Q

Type II hypersensitivity

A

Cytotoxic, IgM/IgG

189
Q

Type III hypersensitivity

A

Immune complex (C3b+Ag+IgG)

190
Q

Type IV hypersensitivity

A

Delayed type (Th1+Macro+Cytokines)

191
Q

What will allergens preferentially induce?

A

Th2 responses, leading to IL-4 production and hence B cells produce IgE so mast cells are sensitised and then degranulate

192
Q

Where are IgE receptors?

A

On mast cells and basophils

193
Q

How can type I hypersensitivity be controlled?

A

Avoid allergens, desensitisation, monoclonal anti-IgE antibody treatment

194
Q

How can type II hypersensitivity be induced?

A

Blood transfusion, haemolytic disease of the newborn, drug-induced haemolytic anaemia

195
Q

How does type II hypersensitivity occur?

A

Ab binds to Ag on cell surface, mediated by complement od ADCC

196
Q

How does type III hypersensitivity occur?

A

Ab bind to soluble Ag -> Ab-Ag complexes, phagocytosis and clearance ensue. Changes location and degranulates, causing tissue damage

197
Q

How does type IV hypersensitivity occur?

A

Cell mediated. On first exposure, haptens sensitise Th1 cells. On second exposure, sensitised Th1 cells make IFN-gamma and chemokines

198
Q

Which cells are involved in surveilence?

A

Monocytes, macrophages and dendritic cells

199
Q

How is tissue compatibility for transplation determined?

A

By the response of T and B lymphocytes of the host against the transplantation antigens of the donor. Histocompatibility Locus Antigen, chromosome 6, CLass I, Class II

200
Q

What are the three things that should be matched in organ transplantation?

A

HLA A, HLA B, HLA DR

201
Q

How does detection of the antibody work?

A

Previous exposure of the immune system to foreign HLA results in the formation of antibodies against HLA (pregnancy, blood transfusion, previous organ transplant, infection)

202
Q

What are the damage associated molecular patterns?

A

ROS, HSP, heparin sulphate, fibrinogen, high mobility group box-1 proteins

203
Q

What are responsible for the recognition of the pathogen-associated molecular patterns

A

Members of the Toll-like receptor family

204
Q

How is the immune system sensitised to foreign HLA?

A

Infection, previous transplantation, blood transfusions

205
Q

What are two important pathways that cytotoxic T cells kill infected cells?

A

Secretory and non-secretory

206
Q

What are the two opsonin families?

A

Collectins and pentraxins

207
Q

What are the principles of ELISA?

A

Antigen coating, blocking, primary antibody, secondary antibody, detection/colour development, stop and measurement

Medical Microbiology and Immunology (1 decks)

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