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UCLMS Yr 1 Mod 2: Infection and Defence > Immune System > Flashcards

Immune System Flashcards

1
Q

What are 3 types of granulocytes

A

Neutrophils
Eosinophils
Basophils

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2
Q

What is the major circulating white blood cell

A

Neutrophils

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3
Q

What is the major mechanism of granulocytes

A

Phagocytosis

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4
Q

What is the name of the enzymes which produce bleach

A

Myoperoxidases

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5
Q

What is a method used by Neutrophils to kill pathogens

A

conversion of oxygen into toxic oxygen free radicals

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6
Q

What is special about necleophiles when seen under a microscope

A

Polynucleated, with 1 nucleus in multiple lobes

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7
Q

Where are the granules kept in the granulacytes

A

Cytoplasm

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8
Q

What is the capsule in which the phagocyte engulfed into called

A

Phagosome

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9
Q

Which type of pathogen do Granulocytes focus on

A

bacteria

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10
Q

How do Nucleophiles move from the blood vessel into the non-immunological organs

A

Walls become sticky to slow down the cells

Cells squeeze through the epithelium cells towards the infection (extravasation)

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11
Q

What happens to the nucleophiles in the blood if there is no infection after 24hrs

A

The Cells die

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12
Q

What is the function of macrophages

A

Remove Debris from damaged tissues

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13
Q

How do macrophages perform their function

A

Phagocytosis

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14
Q

What is the name of Liver Specific Macrophages

A

Kuppfer Cells

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15
Q

What si the name of the precursor of the macrophage, and where is it found

A

Monocyte, found in blood

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16
Q

When are the macrophages used in the immunological defence against pathogens

A

2nd Wave, when the granulocytes fail. Have stringer killing mechanisms than granulocytes

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17
Q

What is the major cell of the adaptive immune response

A

Lymphocytes

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18
Q

What are the names of the 2 sub-populations of lymphocytes

A

T and B cells

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19
Q

Where do T Cells develop

A

Thymus

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20
Q

Where do B Cells develop

A

In the Bone Marrow

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21
Q

Which 2 locations do the lymphocytes circulate through

A

the Tissues and Blood

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22
Q

What is a typical feature of the Lymphocyte when seen under a microscope, unactivated

A

Almost No Cytoplasm

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23
Q

How long does it take for the T Cell to become highly activated

A

24hrs

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24
Q

What does a Plasma Cell Differentiate from

A

B Cells

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25
Q

What is typical for Plasma Cells

A

Packed with Endoplasmic Reticulum

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26
Q

How Long Lymphocytes live for

A

20-30 years

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27
Q

Where do Lymphocytes re-circulate through

A

Blood Vessels and lymphatics

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28
Q

Where do Effector T Cells leave to go to the tissues to control infection

A

Blood Stream

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29
Q

What do Naive and Memor cells leave the bloodstream to enter lymphoid tissue to search for

A

Antigens

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30
Q

Where does the primary immune response start

A

Lymph Nodes

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31
Q

What is the role of dendritic cells (2)

A

Sampling Antigens from the environment

Carrying samples to the lymph nodes

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32
Q

What are 3 types of dendritic Cell

A

Langerhan’s Cell
Veiled Cell
Interdigitating Dendritic Cell

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33
Q

Which Type of dendritic cell can be found in the skin

A

Langerhan’s Cells

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34
Q

Which 3 types of cell are in the innate immune system

A

Granulocyte
Macrophage
Dendritic Cells

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35
Q

Which 2 types of cells are in the Adaptive Immune System

A

T cells

B cells

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36
Q

What is the type of interaction in immune recognition

A

Receptor-Ligand Interaction

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37
Q

What is the name of the receptors of innate immunity

A

Patter Recognition Receptors

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38
Q

What is the name given to the ligands which are molecular components of the microbe

A

Pathogen Associated Molecular Patterns (PAMPs)

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39
Q

What does Toll-like Receptor 3 bind to

A

RNA

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40
Q

What does Toll-Like Receptor 4 bind to

A

Gram-negative Bacterial Lipopolysaccharide

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41
Q

What does Toll-Like Receptor 2 Bind to

A

Lipoteichoic Acid

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42
Q

Where are Pattern Recognition Receptors (PRR) Found (4)

A

Blood
Cell Surface
Within Cellular Organelles
Cytoplasm

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43
Q

What are 3 Innate Effector Mechanisms

A

Phagocytosis and intracellular Killing
Extracellular Killing
Interferons and Restriction Factors

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44
Q

How does complement act

A

In a proteolytic amplification cascade system

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45
Q

What is the central step of the complement pathway

A

C3 cleaved into C3b and C3a

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46
Q

What are the 3 major functions of complement

A

Opsonisation
Lysis
Inflammation

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47
Q

What is the opsonisation pathway of complement

A

C3b binds onto C3b receptors on phagocytes leading to Phagocytosis

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48
Q

What is the Cell Lysis pathway of complement (3)

A

C3b cleaves C5 in C5b and C5a
C5b, C9, C6, C7 and C8 form membrane attack complex
Attack Complex causes cell lysis

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49
Q

What does C9 Form

A

Pores in the bacterial cell membrane

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50
Q

What is the Inflammation pathway of complement (5)

A

C3a and C5a cause mast cell degranulation
Degranulation leads to increased vascular permeability
Neutrophils chemotaxis
Granulocytes attracted to the area of infection
Inflammation

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51
Q

What are the 3 ways o activate complement

A

Bacterial Surfaces (Directly activate complement)
Acute Phase proteins
Antibody

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52
Q

What are the 3 pathways which lead to the central step in complement

A

Alternative Pathway
Classical Pathway
Lectin Pathway

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53
Q

What do all the complement activation pathways lead to

A

Cleaving of C3 into C3a and C3b

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54
Q

What is the main defence against viruses

A

Interferons

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55
Q

What cells can produce type 1 interferons

A

All Nucleated Cells

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56
Q

What do Interferons induce

A

A potent anti-viral state

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57
Q

How do interferons act

A

Via the up-regulation of many restriction factors

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58
Q

What does the resistant state mean for a cell infected by a virus

A

Unable to perform regular functions as all energy put into viral defence

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59
Q

What is the virus protected from when inside the cell (2)

A

Complement and Phagocytes

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60
Q

What is inflammation

A

Pathologicalequivalent of a normal immune response

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61
Q

What are the cardinal signs of inflammation, aka the symptoms (5)

A 
Heat
Redness
Swelling
Pain
Loss of Function
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62
Q

What is inflammation caused by (2)

A

Cellular recruitment

Activation of neutrophils followed by macrophages

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63
Q

How is redness caused during inflammation (2)

A

Lots of Cells were recruited, resulting in more blood

More blood results in vasodilation and redness

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64
Q

What Causes the swelling in inflammation (2)

A

Lots of Cells are recruited, which increases the leakiness of the vessels
This causes vasopermeability, which results in swelling

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65
Q

What Causes Loss of function

A

Hypoxia

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66
Q

What does Interleukin 6 act on

A

Acts on tissues around the body to activate proteins found in the blood, such as complement compounds

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67
Q

What is the role of Interleukin 8

A

Main Attractor of Neutrophils

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68
Q

What is the function of Tumour Necrosis Factor

A

INcreases the stickiness of the vessel walls to attract neutrophils

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69
Q

Which proteins are up-regulated in the blood during the acute phase response (4)

A

Inflammatory cytokines, especially IL6
Soluble PRRs
Complement compounds
Coagulation factors

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70
Q

What can the proteins present during the acute response phase be a useful indicator of

A

Marker of Inflammation

71
Q

Which common diseases are affected by chronic inflammation (5)

A 
Arthritis
Atherosclerosis
Diabetes
Dementia
Cancer
72
Q

Which immune cell ism mostly responsible for Chronic Inflammation

A

Macrophages

73
Q

What are the sections of the antibody (Chains and Regions)

A

Heavy and Light Chains

Variable and Constant Regions

74
Q

What are the complementary determining regions called (3)

A

CDR2
CDR3
CDR1

75
Q

What are the types of bonds involved in antibodies (1+4)

A

Non-Covalent Interactions

Electrostatic
Van der Waals
Hydrophobic
Hydrogen Bonds

76
Q

What is the name of the region of the antibody which recognises and binds to the antigen

A

Paratrope

77
Q

What is the name of the antigen which binds to the antibody

A

Epitope

78
Q

Where, and during which cells development, is diversity generated in antibodies

A

During B Cell Development in the Bone Marrow

79
Q

What is the name of the random selection of Variable, Diversity and Joining regions which cause diversity in antibody generation

A

VDJ Recombination

80
Q

What are the 2 types of Light Chains fromed during recombination

A

Lambda

Kappa

81
Q

What is somatic hypermutation

A

Introduction of addition mutations after antigen recognition

82
Q

What is the equivalent antibody on the T Cells Called

A

T-Cell Receptor (TCR)

83
Q

What is one way in which TCR is different to antibody

A

TCR not secreted, only acts as a receptor

84
Q

During the generation of TCR Diversity, which process is notably absent but present in Antibody Diversity generation

A

Somatic Hypermutation

85
Q

What are the 3 independent sets of antigen receptors

A

Antibody
TCRab (alpha-beta)
TCRyd (gamma delta)

86
Q

What is the name of the enzymes involved in the rearrangement of the VDJ Regions

A

Recombinase Enzymes (RAG)

87
Q

What is the benefit of the large diversity of antibodies

A

Almost any pathogen, including those which can mutate, can be recogised

88
Q

What is the difference between Transmembrane antibody and secreted antibody

A

Secreted antibody does not have the part which anchors the antibody to the cells

89
Q

What are the differences between the primary (PIR) and secondary Immune Response (SIR)

A

More antibodies in SIR (More specific B Cells)
SIR Faster than PIR
the Antibody in SIR have a stronger affinity than those produced in PIR

90
Q

What are the Different Antibody Isotypes and there Heavy Chain specific gene

A 
IgG - y (Gamma)
IgA - a (alpha)
IgM - u (mu)
IgD - d (delta)
IgE - e (epsilon)
91
Q

What is the most common Antibody Isotype

A

IgG

92
Q

Which Antibody is found on mucosal surfaces

A

IgA

93
Q

Which is the main antibody produced during PIR

A

IgM

94
Q

What is the antibody expressed during the start of life in B Cells

A

IgM

95
Q

Which is the Antibody isotype expressed in Naive B Cells

A

IgD

96
Q

What is the main Antibody Isotype expressed in allergy

A

IgE

97
Q

What type of polymer is produced by IgA

A

Dimer (Dimeric Secretory IgA)

98
Q

What type of polymer is produced by IgM

A

Pentamer (Pentameric Circulating IgM)

99
Q

What si the name of the chain which holds together the monomers in the IgA and IgM Polymers

A

J Chain

100
Q

Antibody-antigen reactions are … and as a result are able to reach … (2)

A
  1. Reversible

2. Equilibrium

101
Q

What is Avidity

A

the overall binding strength of the antibody to the antigen

102
Q

During an immune response, which antibody is released at the start of the infection and why

A

IgM, due to its high avidity

103
Q

During an immune response, which antibody is released second and in larger amounts

A

IgG

104
Q

Why is IgM production turned off during an immune response after the release of IgG (2)

A

High Affinity better than Avidity

High Avidity can form large complexes, which could block blood vessels

105
Q

What is the Effector Function of IgM

A

Complement

106
Q

What are the effector functions of IgG (3)

A

Neutralisation (toxins and viruses)
Direct opsonisation
Phagocytosis

107
Q

How is antibody involved in the neutralisation of toxins

A

The Binding of antibodies prevents the toxin from being able to bind to the receptor and create pathology

108
Q

What are 2 examples where toxin neutralisation is required

A

Tetanus

Diptheria

109
Q

How is antibody involved during virus neutralisation

A

Viral Particles bind to the antibody, which prevents it from binding to the receptor and entering the cell, causing disease

110
Q

What is the name of the receptors which allow phagocytes to bind to antibody

A

Fragment C Receptors (Fc Receptors)

111
Q

How is antibody involved during opsonisation and phagocytosis (3)

A

Encapsulated Bacteria (usually resistant to phagocytosis) are coated with antibody (IgG)
IgG has Fragment C (Fc) Receptor, which binds to the Fcy (gamma) on phagocytic neutrophils
Bacteria able to be destroyed by the neutrophils

112
Q

Which complement pathway is activated by antibody

A

Classical Pathway

113
Q

Simply, what are monoclonal Antibodies

A

Antibodies of a single specificity

114
Q

Monoclonal antibodies are used as drugs to treat which diseases (3)

A

Inflammatory Disease
Viral Infections
Cancer Treatments

115
Q

What are the 3 subsets of the T Cells

A

CD4 Helper Cells
CD8 Cytotoxic Cells
CD4 Regulatory Cells

116
Q

Which MHC Class do CD8 Cells Recognise

A

Class 1

117
Q

Which MHC Class do CD4 Cells Recognise

A

Class 2

118
Q

What are 2 pathways used by CD8 Cells to kill pathogens

A

Fas/FasL Pathway

Granzyme/perforin Pathway

119
Q

How does the Fas/FasL Pathway work

A

FasL on the CD8 cell binds to the Fas receptor on the pathogen, causing caspase signalling

120
Q

How does the Granzyme/Perforin pathway work (3)

A

Antibody recognises antigen
Perforin makes small holes in the membrane of the pathogen
Granzymes are released into the pathogen, leading to caspase signalling

121
Q

What does Caspase Siganlling cause

A

Apoptosis

122
Q

Why are innate lymphoid cell less precise

A

no TCR (T Cell Receptor)

123
Q

What are the 6 types of cytokines

A 
Interleukins
Chemokines
Interferons
Tumour Necrosis Factor
Colony-Stimulating Factors
Growth Factors
124
Q

What is meant by Cytokine Pleiotropism

A

One cytokine acts on several different types of cells, with different outcomes

125
Q

What is meant by Cytokine redundancy

A

Several cytokines have similar effect on target cells

126
Q

What is meant by Cytokine Synergism

A

Combined effect on two cytokines is greater than additive effect on each

127
Q

What is meant by Cytokine Antagonism

A

Effect of one cytokine inhibits/cancels

128
Q

Which receptors are expressed on the Helper T Cells

A

CD4

129
Q

Which branches are controlled and amplified by the helper T cells (5)

A 
Macrophages and Intracellular pathogens
Eosinophils and mast cells in parasite immunity
Neutrophils and extracellular pathogens
B cells, antibodies and humoral immunity
Cytotoxic T Cells and Viral Immunity
130
Q

What are the important Th subpopulations (4)

A

Tfh (follicular cells)
Th1
Th2
Th17

131
Q

What do Tfh (follicular cells) help with

A

Help B Cells make specific antibody

132
Q

What do Th1 Cells activate (2)

A

Macrophages

Cytotoxic T cells

133
Q

What do Th2 Cells activate (3)

A

Mast Cells
eosinophils
IgE

134
Q

What does Th17 activate (1)

A

Neutrophils

135
Q

How do T-B Interactions work (linked help) (5)

A

Costimulatory molecules B7 (B Cell) bind with CD28 (T Cell)

B cell presents peptide of antigen on MHC Class 2
T Cell Receptor recognise peptide

CD40 on the B Cell binds with CD40L on T Cell

Cytokines released by the T Cell, acting on the the B cell

136
Q

What is Linked Help essential for (3)

A

Class Switching
Somatic Hypermutation
Memory

137
Q

How do Th1 Cells activate macrophages to kill intracellular pathogens (5)

A

Peptides from intracellular pathogens presented on MHC Class 1 on the macrophages
TCR recognises the peptide

CD40 on macrophage binds to CD40L on T Cell

Th1 Cell releases INFy (Interferon-gamma) to mediate macrophage

Macrophage releases TNFa (alpha) and IL-1

138
Q

How do Th1 Cells help activate CTL

A

Th1 cell releases interleukin 2, which activates CTL Cells

139
Q

Th2 helps during parasitic infections. Which interleukins does it release

A

IL3
IL9

IL5

IL13

IL4

140
Q

How do IL3 and IL9 released by Th2 help (1+2)

A

Drive Mast Cell recruitment

Mast Cells:
Release of granules
Recruits Inflammatory Cells

141
Q

how does IL5 released by Th2 help (1+2)

A

IL5 recruits and activates eosinophils

Eosinophils:
Release of Granules
Cause Parasite killing

142
Q

How does IL13 release by Th2 help (1+1)

A

IL13 induces epithelial cell proliferation and stimulates mucus production
Epithelial cells hinder parasite colonisation

143
Q

How does IL4 released by Th2 cells help (1+1)

A

IL4 favours IgE production

IgE arms mast cells and eosinophils

144
Q

How do Th17 Cells work in bacterial and fungal infections (2)

A

IL17 activates myeloid (immune) and stromal (non-immune) cells to produce GCSF and IL8
This recruits and activates neutrophils, which release granules that kill

145
Q

What determines the Th type

A

the microenvironment around the antigen-presenting cells at the time the T cell is activated

146
Q

On Th1 Cells … (2) causes … (1) to be presented during activation

A
  1. IFNy (gamma) and IL12

2. IFNy (gamma)

147
Q

On Th2 Cells … (1) causes … (3) to be presented during activation

A
  1. IL4

2. IL4, IL5 and IL13

148
Q

On Th17 Cells … (3) causes … (2) to be presented during activation

A
  1. TGFb (beta), IL6 and IL23

2. IL17 and IL22

149
Q

On Th21 Cells … (1) causes … (1) to be presented during activation

A
  1. IL6

2. IL21

150
Q

What is the qualitative regulation of the T Cell

A

Co-Stimulation via cytokines

151
Q

What is the gatekeeper of the T cell

A

Antigens/MHC

152
Q

What is the Quantitative regulation of the T Cell

A

Co-Stimulation via cell-to-cell contact

Increased co-stimulation = increased response

153
Q

What is Excessive T Cell help associated with

A

the underlining of many pathologies

154
Q

What holds the peptide onto TCR

A

Major Histocompatibility complex

155
Q

Where is the peptide held in TCR

A

the peptide binding groove

156
Q

How is CD3 involved in the T cell antigen receptor

A

CD3 transducer signal and aids in the decision of what happens to the binded cell

157
Q

What is involved in T cell activation, other than the antigen (5)

A

Co-stimulation CD28 and CD80/86 (positive signals)
Negative signals CD28/CTLA4; PD1/PDL1
Professional and non-professional presenting cells
Dendritic Cells
The innate adaptive interface

158
Q

What are the names of the 2 pathways peptides are loaded onto MHC, and which class are they specific to

A

Endogenous - Class 1

Exogenous - Class 2

159
Q

What is Endogenous Processing (4)

A 
Protein (usually viral) is broken into peptides by a proteasome
Peptides enter the endoplasmic reticulum via the TAP gene and transporters
Peptide join MHC class 1 and enter Trans-Golgi vesicle
MHC class 1 and peptide expressed on the cell surface
160
Q

What is Exogenous processing

A

Protein broken into peptides by protease enzyme-containing endoscope
MHC Class 2 and peptide join in MHC Class 2 loading compartment
MHC 2 expressed on the cell surface

161
Q

What is the target for MHC class 2

A

CD4

162
Q

What are the purposes of specialised lymphoid tissue (3)

A

Reticular meshwork to trap antigens
Facilitates cellular communication by slowing cells down
Separate T and B Cell areas for specialised differentiation pathways

163
Q

What is the scaffolding built around lymphoid tissue built of

A

Collagen fibres laid down by fibroblasts

164
Q

What binds naive T and B cells from the blood into the lymphoid tissue

A

High Endothelial Venules (HEV)

165
Q

Where are B Cells differentiated

A

Germinal Centre

166
Q

Where is the germinal centre located

A

Within the outer cortex of the kidney

167
Q

What are the steps in B cell Differentiation (3)

A

Antigen-Specific B Cell undergoes Clonal amplification
Follicular dendritic cells carry antigen in original conformation
Competition exists between B Cells to produce cells with the highest affinity

168
Q

What happens in the Dark Zone (2)

A

Proliferation

Somatic Cell Hypermutation

169
Q

What Happens in the light zone

A

B Cell Selection

170
Q

What are 2 examples of specialised Mucosa-associated lymphoid tissue (MALT)

A

Gut-associated lymphoid tissue (GALT)

Bronchus-associated lymphoid tissue (BALT)

171
Q

What is the receptor which transports secretory IgA across the mucosal barrier

A

Poly Ig receptor

172
Q

How does IgA work in the mucosal surfaces

A

IgA prevents the adhesion of microbes to surfaces

If microbe enters coated in IgA, then it will be rapidly destroyed by granulocytes

173
Q

Which organ is the main producer of the acute phase and complement proteins

A

Liver

UCLMS Yr 1 Mod 2: Infection and Defence (7 decks)

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