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MBBS - Year 1 > Intro to immunology > Flashcards

Intro to immunology Flashcards

1
Q

Primary function of immune system

A

Eliminate pathogens

Minimise damage they cause

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2
Q

How are foreign substances recognised by the immune system

A

Antigens are ANTIbody GENerators

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3
Q

Clonal selection

A

Maturation into mature and genetically committed cells in bone marrow
Antigen-dependent proliferation and differentiation into plasma and memory cells in peripheral lymphoid tissue

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4
Q

How is the immune response tailored to viruses and intracellular bacteria

A

Identification and killing of infected cells by cytotoxic T cells

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5
Q

How is the immune response tailored to extracellular fungi, parasites, bacteria

A

Detection of surface structures by antibodies and destruction by phagocytes

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6
Q

How is the immune response tailored to large parasites

A

Deposition of toxic substances or killing by mast cells/eosinophils

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7
Q

How is the immune response tailored to immunoprivilged areas

A

No response as infl would be caused, damaging the tissues

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8
Q

Immunoprivileged areas

A

CNS
Eyes
Placenta
Reproductive organs

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9
Q

Commensal bacteria

A

Bacteria that the body has learnt to tolerate - esp in gut

2 kg in whole body

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10
Q

Levels of defence in immune system

A

External defences
Innate immune system - ‘primitive’
Adaptive immune system - highly spp

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11
Q

Exterior defences of body

A 
Ear
Eyes 
Nasal cavity 
Skin 
Urethra 
Anus 
Vagina 
Stomach 
Trachea and bronchi 
Mouth cavity
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12
Q

Ear as a defence

A

Cerumen inhibits bacterial growth

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13
Q

Eyes as a defence

A

Cleansed by tears which also contain antibacterial chemicals

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14
Q

Nasal cavity as a defence

A

Hairs and mucus traps organisms

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15
Q

Skin as a defence

A

Impervious barrier

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16
Q

Urethra as a defence

A

Urine flow prevents bacterial growth

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17
Q

Anus as a defence

A

Mucous membrane traps microorganisms

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18
Q

Vagina as a defence

A

Acidic secretion inhibits growth of pathogens

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19
Q

Stomach as a defence

A

Acidic juices kill many microorganisms

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20
Q

Trachea and bronchi as a defence

A

Mucous layer traps microorganisms

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21
Q

Mouth cavity as a defence

A

Mucous membrane traps microorganisms and the mouth is cleaned by saliva

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22
Q

Innate vs adaptive immune system

A

Non-spp vs spp
Fast response (mins) vs slow (days)
No memory vs memory

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23
Q

Immune dysregulation

A

Balance between activation and suppression

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24
Q

Types of immune dysregulation

A

Hypersensitivity
Autoimmunity
Immunodeficiency

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25
Q

Hypersensitivity

A

Overaction to benign antigen

Can be presented as anaphylactic shock

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26
Q

Types of hypersensitivity

A

I - IV

Type I is allergy e.g. hay fever, asthma, hives, eczema

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27
Q

What are allergies mediated by

A

Particular immunoglobulin, IgE and mast cells

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28
Q

Anaphylactic shock

A

Severe, life-threatening, allergic response

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29
Q

Tolerance

A

Immune system distinguishing between ‘self’ and ‘non-self’

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30
Q

What typically happens to self-reactive immune cells

A

Eliminated by immune system, either in thymus or bone marrow before it reaches the bloodstream

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31
Q

What is autoimmunity caused by

A

Breakdown of tolerance

Certain genetic and environmental factors can make you predisposed

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32
Q

Examples of autoimmunity

A

Multiple sclerosis - immune system attack against nerve sheaths on brain/CNS leading to neuromuscular dysfunction
Crohn’s disease - attack on microbiota/ gut epithelium –> poor food absorption

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33
Q

Immunodeficiency

A

Component of innate/ adaptive immune system absent or defective

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34
Q

Primary immunodeficiency

A

Inherited

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35
Q

Most common form of primary immunodeficiency

A

Severe Combined Immunodeficiency (SCID) - no functional adaptive immunity, has low life expectancy

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36
Q

Secondary immunodeficiency

A

Caused by damage by external agents

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37
Q

Most common form of secondary immunodeficiency

A

Acquired Immune Deficiency Syndrome (AIDS) - Infection w/ HIV, destruction of Thelper cells –> death by opportunistic infections

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38
Q

Challenges w/ immune system

A

Transplantation

Cancer

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39
Q

Why does cancer present as a challenge for the immune system

A

Cancer cells display self-antigen (tolerated) as they are derived from own body and tumour-spp antigens (recognised)
Cancer cells evade immune response by rapid change (mutations) and active inhibition
Immunotherapies against cancer boost body’s natural defences

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40
Q

Primary tissues and organs of the immune system

A 
Development and maturation of adaptive immune cells (lymphocytes)
Bone marrow (B cells) and thymus gland (T cells)
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41
Q

Secondary tissues and organs of the immune system

A

Mature lymphocytes meet pathogens

Spleen, adenoids, tonsils, appendix, lymph nodes, Peyer’s patches, MALT

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42
Q

MALT

A

Mucosa Associated lymphoid tissue

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43
Q

How are lymph nodes placed

A

Strategically around the body as they act as ‘meeting place’ for immune cells

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44
Q

What happens at lymph nodes

A

Pathogens from infected tissue sites are picked up by dendritic cells and arrive at closest lymph node
Circulating T and B cells enter and congregate at spp regions in lymphoid follicles
If they encounter a ‘matching’ dendritic cells, they’re activated and proliferate

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45
Q

Where do B cells congregate in the lymphoid follicle

A

Cortex

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46
Q

Where to T cells congregate in the lymphoid follicle

A

Paracortex

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47
Q

What changes occur to the lymph node after activation of lymphocytes

A

Architecture

Size of the node

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48
Q

What other tissues/organs contain organised lymphoid tissues

A

Spleen and MALT

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49
Q

Haemotopoiesis

A

‘Making of blood’
How immune cells are generated
Takes place in the bone marrow after birth

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50
Q

What determines what multipotent stem cells in the blood differentiate into

A

The growth factors received by the myeloid or lymphoid progenitors

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51
Q

Where do monocytes differentiate into macrophages

A

Circulate in blood before migrating to tissues

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52
Q

Why do the names of macrophages change

A

Depending on where they’re found

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53
Q

Alveolar macrophages

A

Found in lung

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54
Q

Histocytes

A

Macrophages found in connective tissues

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55
Q

Mesangial cells

A

Macrophages found in the kidneys

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56
Q

MIcroglial cells

A

Macrophages found in the brain

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57
Q

Kupffer cells

A

Macrophages found in the liver

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58
Q

Function of macrophages

A

Phagocytosis

Antigen presentation

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59
Q

Process of phagocytosis

A

Bacterium becomes attached to pseudopodia
Bacterium is ingested, forming phagosome
Phagosome fuses w/ lysosome
Lysosomal enzymes digest captured material
Digestion products are released from the cell

60
Q

Pseudopodia

A

Membrane invaginations

61
Q

Endogenous pathway of antigen presenting

A 
Ag presentation to cytotoxic T cells via MHC class I 
CD8
62
Q

Exogenous pathways of antigen presenting

A 
Ag presentation to helper T cells via MHC class II 
CD4
63
Q

Why do dendritic cells have lower degradation potential

A

Better APC’s than macrophages

Leads to antigen preservation

64
Q

Immature dendritic cells

A

Antigen uptake in peripheral tissues

65
Q

Mature dendritic cells

A

Migration to lymph nodes and Ag presentation

66
Q

What do dendritic cells activate

A

Adaptive immune response after finding matching T or B cell

67
Q

Granulocytes

A

Contain granules and have multi-lobed nucleus

Neutrophils, basophils, eosinophils

68
Q

Stained eosinophils colour

A

Appear pink

69
Q

Stained basophils colour

A

Appear blue

70
Q

Stained neutrophils colour

A

Appear purple

71
Q

PMN

A

Polymorphonuclear neutrophils

72
Q

What % of circulating granulocytes is made up by neutrophils

A

95%

73
Q

How are macrophages similar to neutrophils

A

Both phagocytose bacteria but much shorter lived (few days - die after phagocytosis)

74
Q

Chemotaxis of neutrophils

A

Attracted by IL-8

Follows to site of infection

75
Q

How do neutrophils kill and digest bacteria

A

Netosis
Release nuclear elastase from granules (antimicrobial)
NE goes to nucleus, chromatin expands and is relegated from the cell to capture bacteria

76
Q

What do eosinophils, basophils and mast cells kill

A

Larger parasites e.g worms
These are coated by IgE and this allows target recognition - corresponding receptor
Attach to parasite and starts degranulation and release of toxic contents (histamines, proteases)

77
Q

Eosinophils, basophils and mast cells association w/ allergies

A

IgE
Overreaction to harmless antigens e.g dust mites’ compounds
Release cytotoxic compounds, histamine –> infl

78
Q

Abundance of NK cells in the blood lymphocytes

A

5-10%

79
Q

How do certain viruses and cancer stop Ag presentation

A 
Down regulation of MHC class I 
Infected cell has lack of MHC class I molecules 
NK cell receives only +ve signals --> becomes activated
80
Q

Generative lymphoid organs

A

Bone marrow

Brain

81
Q

Peripheral lymphoid organs

A

Lymph nodes
Spleen
Mucosal and cutaneous lymphoid tissues

82
Q

Types of T helper cells

A

Th1 cells help macrophages digest pathogens
Th2 cells help B cells to produce antibodies
CD4 involved in Class II MHC pathway

83
Q

Class I MHC pathways

A

CD8 (cytotoxic T cells) kill virus-infected cells

84
Q

Innate barriers to infections

A

Mucosal surfaces

85
Q

Features of mucosal surfaces

A

Tight junctions in epithelial layers

Goblet cells, Paneth cells secrete antimicrobial peptides and enzymes and mucus

86
Q

Cells involved in innate immune system

A 
Dendritic cells 
Macrophages 
Mast cels
NK cells 
Granulocytes
87
Q

Cells involved in adaptive immune system

A

B cells
T cells
CD4+ T cell and CD8+ T cell

88
Q

Steps in innate immunity

A

Recognition
Disposal
Communication

89
Q

Recognition in innate immunity

A

PAMPs and DAMPs

90
Q

PAMPs

A

Pathogen Associated Molecular Pathways

Signal production of cytokines to stimulate immune cells

91
Q

What are PAMPs recognised by

A

Toll-like receptors on macrophages, neutrophils, epithelial cells of gut and lung

92
Q

Where are PAMPs found

A

Plasma membrane

In endosomes/ phagosomes

93
Q

How do we recognise microbes despite their rapid evolution

A

Using highly conserved and essential features that are different to us e.g cell walls (peptidoglycan), nucleic acids (CpG DNA), sugars (lipopolysaccharides, mannam), flagella

94
Q

DAMP

A

Damage Associated Molecular Pattern

95
Q

Disposal in innate immune system

A

Microbes killed by phagocytic cells

Broken up into common units presented to immune system

96
Q

Recognition by complements

A

Uses 30 diff proteins
3 main pathways: lectin, classical and alternative
Leads to infl, phagocytosis and MAC (membrane attack complex)

97
Q

Activation of lectin pathways

A

Microbial sugars (yeasts and bacteria)

98
Q

Activation of classical pathways

A

Antibodies

99
Q

Acute phase proteins

A

Produced in liver in response to infl

Liver is stimulated by IL1, IL6 and TNF

100
Q

Adjuvant

A

Parts of a pathogen used to activate innate cells in immune systems (macrophages, dendritic cells)

101
Q

Role of IgG

A

Antibodies bind Fc receptors to activate immune defence
IgG is secreted into blood and removed pathogens from blood and tissues
IgG binds pathogen w/ variable region, leaving Fc domains exposed. Fc domains cluster to generate a recruitment signal

102
Q

What do Fc domains recruit

A

Complement –> lysis of pathogens (MAC)

103
Q

What does Fc binding to Fc receptors lead to

A

Binding to Fc receptors on macrophages leads to phagocytosis and killing in lysosomes
Can be helped by complement

104
Q

Opsoninisation and Fc

A

Phagocytic cells carry Fc receptors and also receptors for complement
Fc domains exposed by antibody on pathogen allows recognition by phagocytic cells
Fc receptors interactions trigger phagocytosis by releasing proteosomes or ROS

105
Q

ROS

A

Reactive oxygen species

106
Q

What is IgA made and secreted by

A

B cells in response to infection of mucosal surfaces but doesn’t stay in blood

107
Q

Role of IgA

A

IgA binds an IgA receptor and is secreted across epithelial cells (protects mucosal surfaces)
Tail of IgA binds to an IgA receptor and this complex is then able to bind to pathogens that haven’t entered body

108
Q

IgE receptors

A

Found on mast cells, eosinophils and basophils

109
Q

What does IgE define

A

The Ag spp of mast cells, eosinophils and basophils, allowing them to recognise Ag

110
Q

Joining chain

A

Protein linking two IgA molecules

111
Q

Why do mast cells release histamine

A

To open up the sites of parasite infections to the rest of the immune system

112
Q

What do eosinophils release

A 
Peroxidase 
Ribonucleases
Deoxyribonuclease
Lipase
Plasminogen
113
Q

What is the same for each subtype of antibody

A

‘Variable’ region

114
Q

Why do the Fc domains differ

A

Differences in coding sequences but lies in same Ig gene

115
Q

Which molecules have variable and constant regions

A

Antibodies

T-cell receptors

116
Q

What does the constant region bind

A

Fc receptors

117
Q

T cell receptors

A

Stay attached to the surface of the T cells

118
Q

Granules in cytotoxic T cells

A

Contain enzymes e.g perforins are released into the space between the T-cell and infected cells

119
Q

Repeated sequences in Ig genes

A

Variable region
Diversity region
Joining region

120
Q

What does gene rearrangement allow

A

One of the duplicated sequences in each region to be used to make the protein

121
Q

1st gene rearrangements

A 
Select diversity and joining regions 
Constant region (Fc) is constant
122
Q

2nd gene rearrangements

A

Selects the variable region and the constant regions (Fc) is constant

123
Q

VDJ recombination

A

Brings one of the remaining variable sequences next to the DJ combi, genes within the loop are removed by RAG proteins

124
Q

What does VDJ recombination provide

A

Antibody and T-cell diversity

125
Q

Rearrangement of T-cell receptors

A

Creates diversity

Only rearranges once and only on one chromosome

126
Q

Rearrangement of T and B cells

A

Rearrange genes at random and each cell can only rearrange genes once

127
Q

What happens to the T-cells that have rearranged the right genes segments

A

Bind Ag —> triggers cell division (clonal expansion)

128
Q

What happens to the T-cells that don’t rearrange the right gene segments

A

Can’t bind antigen so they die

129
Q

How do B-cells get T-cells help

A

By becoming APC’s

130
Q

What happens when T-cells and B-cells agree on the antigen

A

The T-cell is activated by the T-cell receptor
The T-cells then express ligands that can bind to B-cells
Co-stimulation

131
Q

What does co-stimulation induce

A

Cytokine secretion from the T-cell

132
Q

Plasma cells and memory cells

A

Plasma B cells proliferate to make antibodies secreted into bloodstream – remove the membrane anchor and secrete immunoglobulin
Memory B cells retain the membrane bound receptor and can keep communicating w/ T-cells
Diff cytokines released by T helper cells drives diff types of B-cells

133
Q

What does IL4 drive

A

Memory B cells

134
Q

What does IL10 drive

A

Plasma cells

135
Q

When does antibody class switching occur

A

Once VDJ recombination is complete

136
Q

Features of IgM

A

Seen in primary immune response

Low affinity, broad specificity

137
Q

How is IgM produced

A

Signals for the B-cell receptor and cytokine trigger the removal of the membrane anchor
The mu region is added

138
Q

2nd antibody class switch

A

Replaces membrane anchor w/ gamma sequence to make IgG

139
Q

Features of IgG

A

Seen in secondary immune repose

High affinity, narrow specificity

140
Q

Antibody classes

A

Mu - IgM
Gamma - IgG
Alpha - IgA
Epsilon - IgE

Followed by membrane anchor

141
Q

How are isotopes generated

A

Switching of constant domains during recombination

Uses same variable regions

142
Q

What is isotype switching controlled by

A

Cytokine secretion from Thelper cells

143
Q

Which interleukins control isotype switching for IgG

A

IL4

IL6

144
Q

Which cytokines control isotype switching for IgA

A

IL5

TGF beta

145
Q

Which interleukin controls isotype switching for IgE

A

IL4

MBBS - Year 1 (93 decks)

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