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204 Musculoskeletal & Immune Systems > Theme 1 - The Immune System > Flashcards

Theme 1 - The Immune System Flashcards

1
Q

What is an antigen, usually? 2

A

Something that the immune system responds to. Usually a protein

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2
Q

What is an antigen receptor?

A

What recognises the antigen

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3
Q

What is the difference between innate and adaptive antigen receptors?

A

Innate - Germline-encoded pattern-recognition receptors

Adaptive - Antigen-specific T and B cell receptors

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4
Q

What are the two types of compact cells with reference to immune cell lineage?

A

Myeloid and lymphoid

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5
Q

Appearance and function of neutrophil?

A

globular nucleus

phagocytosis

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6
Q

Appearance and function eosinophil?

A

sunglasses,

fuck knows

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7
Q

Appearance and function monocyte?

A

large mono nucleus cell in blood stream (pre cursor to macrophage)
Phagocytosis
Antigen presentation

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8
Q

Appearance and function dendritic cell?

A

clear cell with dendrites

antigen presentation

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9
Q

Appearance and function basophil?

A

granular nucleus

fuck knows

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10
Q

what 5 immune cells are in the myeloid lineage?

A 
neutrophil
basophil
eosinophil
monocyte
dendritic
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11
Q

What immune cells make up adaptive immunity?

A

B cells

CD4 &CD8 T cells

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12
Q

Characteristics of immune cells in lymphoid lineage?

A

Similar size to RBC

Little cytoplasm with few granules

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13
Q

4 types of intercellular signalling?

A

Endocrine
Paracrine
Autocrine
Juxtacrine

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14
Q

What are cytokines?

A

small proteins released by cells that have an effect on another cell

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15
Q

What is the main role of chemokines?

A

temporal and spatial organisation of cells and tissues

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16
Q

3 key features of innate antigen receptors?

A 
Do not recognise antigen specifically
Pattern recognition receptors’ (PRRs)
Recognise ‘pathogen associated molecular patterns’ (PAMPS)
Genome-encoded
Not clonally distributed
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17
Q

6 features of adaptive antigen receptors?

A

Recognise antigen specifically
T cell receptor, B cell receptor (antibody)
Produced by random somatic recombination events between gene segments
Huge receptor diversity
Clonally distributed
Permit specificity and memory in immunity

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18
Q

What is compliment?

A

serum proteins that mark pathogens with a molecular flag and also recruit effector cells

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19
Q

What do the two components of compliment do?

A

One covalently bonds to pathogen the other attracts the effector cell

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20
Q

outline the process of inflammation addressing calor, dolor, rubor and tumor

A

Cells damaged release cytokines
Cytokines induce local dilation of blood capillaries (calor&rubor)
Vasodialtion causes gaps between cells in endothelium to widen, increasing leakage of plasma into tissue. Odema (tumor)
Swelling puts pressure on nerve endings (dolor)

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21
Q

4 induced barriers to infection?

A

Innate immune cells
Pattern recognition
Receptors (PRRs)
Interferon

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22
Q

The first time an adaptive immune response is made to a given pathogen is known as what?

A

primary immune responce

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23
Q

What is lysozyme and how does it work?

A

An antimicrobial enzyme in blood and tears.

Disrupts bacteria cell wall by cleaving bonds between the sugars that make up peptoglycan.

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24
Q

In terms of antigen recognition, what is the difference between a B and t cell receptor (antibody)?

A

B cell recognises intact antigen

T cell recognises processed antigen

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25
Q

Physical barriers to infection

A

Skin, hair, nails

Mucosa of GI, respiratory, genital tracts

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26
Q

3 soluble barriers to infection?

A

Compliment
Defensins
Collectins

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27
Q

4 induced barriers to infection?

A

Innate immune cells
Pattern recognition
Receptors (PRRs)
Interferon

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28
Q

What are defensins and how do they work?

A

Antimicrobial amphipathic peptides peptide. They have both a hydrophillic and hydrophobic region on their cell surface. Enter the lipid bilayer of the icrobe and form a pore.

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29
Q

What is lysozyme and how does it work?

A

An antimicrobial enzyme in blood and tears.

Disrupts bacteria cell wall by cleaving bonds between that make up peptoglycan.

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30
Q

Which type of bacteria is lysozyme most effective against?

A

Gram positive

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31
Q

3 examples of antimicrobial peptides?

A

Histatins
Defensins
Cathelicidins

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32
Q

5 features of antimicrobial peptides?

A

Cover epithelial cells, found in saliva
secreted by epithelial cells, neutrophils and paneth cells
Kill bacteria in mins by disrupting membrane
Also attack fungi and viruses
Inhibit DNA and RNA synthesis

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33
Q

What are histatins and where are they found?

A

antimicrobial peptide, found in the mouth. active against fungi.

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34
Q

What are defensins and how do they work?

A

Antimicrobial amphipathic peptides peptide. They have both a hydrophillic and hydrophobic region on their cell surface.

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35
Q

What does collectin do?

A

Binds to surface sugars of bacteria. Targeting them for opsination

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36
Q

How does ficolin work?

A

recognise acylated compounds (COCH3) such as n-acetylglucosamine, a monosaccharide found in bacterial cell walls

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37
Q

name the three compliment pathways

A

classical
lectin
alternative

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38
Q

where is complement made?

A

liver but also produced by monocytes, macrophages and epithelial cells of the intestine and urinary tract

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39
Q

What 4 effects are mediated by compliment?

A

Lysis
Opsonisation
Activation of an inflammatory response
clearance of immune complexes

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40
Q

What complement protein is associated with the classical pathway?

A

C1

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41
Q

What does C1 bind to?

A

Fc region of an antibody usually IgM

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42
Q

How many Fc regions must C1 bind to, what is the significance of this?

A

At least 2

Therefore IgM most effective at activating compliment as it has 5 Fc domains

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43
Q

Why does C1 not bind with serum IgM?

A

Serum IgM cannot bind C1 as it has a planar conformation, the shape changes on binding antigen to reveal binding sites for C1q

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44
Q

Draw the classical pathway

A 
Binding C1q with the Fc domain causes a conformational change in C1r
C1s is cleaved and can activate C2 and C4 splitting into their large and small fragments
C3 convertase (C4b2a) can then activate over 200 C3 molecules producing a massive amplification of the signal
C4b, C2a and C3b fragments form the C5 convertase that activates C5 leading to the membrane attack complex
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45
Q

What is the lectin pathway activated by?

A

Antibody independent, activated by ficolins and mannose binding lectin (MBL)

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46
Q

Draw the lectin pathway

A

Upon binding MBL forms a complex with MASP-1 and MASP-2 (serine proteases)
Active complex cleaves C2 and C4

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47
Q

What is the alternative pathway activated by?

A

Solid surface of bacteria. C3 spontaneous hydrolyses into C3a and C3b

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48
Q

Draw the alterantive pathway in relation to the other pathways.

A

c3 to c3b + c3a

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49
Q

What complement components initiate the membrane attack complex?

A

C5b binds C6 initiating the formation of the MAC

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50
Q

How does the MAC distrupt a cell?

A

MAC forms a pore that inserts into the membrane allowing diffusion of ions and small molecules, water moves into the cell killing it

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51
Q

Why doesn’t the MAC destroy the body’s own cells?

A

Human cells have soluble and cell surface associated proteins that prevent MAC formation

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52
Q

3 examples of compliment inhibitors?

A

C1 inhibitor
membrane bound c3 inhibitors
memebrane bound inhibitirs prevent actibation of MAC

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53
Q

Example of compliment inhibitor deficiency?

A

Heridatory angiodema - C1 inhibitor deficiency

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54
Q

What is the overall conseqience of complement deficiency?

A

recurrent infections

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55
Q

What does defiency in MBL typically cause?

A

serious pyogenic infections in neonates and children

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56
Q

A defiency in which type of complement is the most severe?

A

C3 most severe, leading to successive severe infections

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57
Q

What are patients deficent in compliment component C8 prone to?

A

Neisseria meningitis infections

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58
Q

What do 90% of people with C4 deficency develop?

A

systemic lupus erythematosus

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59
Q

In terms of phagocyte recruitment, what are the 4 stages of rolling and extravasation?

A

Rolling
Activation
Arrest/adhesion
Transendothelial migration

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60
Q

During phagocyte recruitment what molecules assist in the adhesion process?

A

ICAM-1 and ICAM-2 are upregulated on the endothelium

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61
Q

3 examples of opsonins

A

Complement components (C3b)
Collectins (mannose-binding lectin)
Antibodies

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62
Q

4 examples of phagocyte receptors

A

Complement receptors
Fc receptors
mannose receptor
Scavenger receptors

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63
Q

What are the 6 mechanisms of action utilised by phagocytes?

A 
Acidification
Toxic Oxygen derived products
Toxic nitrogen oxides
Antimicrobial peptides
Enzymes
Competetors
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64
Q

What are Neutrophil Extracellular Traps (NETs)? 2

A

When activated some neutrophils undergo a special form of cell death termed ‘NETosis’
nuclear chromatin is released from cells trapping microorganisms

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65
Q

What are pattern recognition receptors and what do they recognise?

A

Receptors able to recognise conserved structures

They recognise patterns termed:
pathogen-associated molecular patterns (PAMPs)

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66
Q

What are DAMPS

A

Damage associated molecular patterns, molecules released from necrotic cells

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67
Q

What are the 4 types of Pattern Recognition Receptors?

A

Toll-like receptors (TLRs)
NOD-like receptors (NLRs)
Rig-I like receptors (RLRs)
Cytosolic DNA sensors (CDS)

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68
Q

What do Toll Like Receptors recognise 4 examples?

A

bacterial prodiucts - Lipopolysaccharide
Flagellin
viral products - ssRNA
DNA

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69
Q

How is an Acute phese response measured?

A

Raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP (a pentraxin)) are characteristic of an acute phase response and are used clinically to detect inflammation

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70
Q

6 Examples of where PRRs could be useful clinical targets, either as agonists or antagonists

A

Infection Autoimmunity
cancer Sepsis
Allergy cancer

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71
Q

A defect in Cytosolic DNA sensors

would result in what condition?

A

(STING)-associated vasculopathy with onset in infancy (SAVI)

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72
Q

Where do T and B lymphocytes develop?

A

B - Bone marrow

T - Thymus

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73
Q

Give 4 examples of inflammatory cytokines?

A

IL-1beta
IL-6
IL-12
TNF-alpha

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74
Q

Give an example of a chemokine and state it’s use?

A

CXCL8 - chemoattractant

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75
Q

What do NOD like receptors recognise?

A

bacterial degradation prodcuts in the cytoplasm

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76
Q

Individuals with defficient Mannose Binding Ligand (MBL) succeptible to what type of infection?

A

Neisseria meningitidis

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77
Q

In terms of immunophenotyping what is expressed by T and B cells?

A

B cells - CD19

T Cells - CD3, 4 and 8

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78
Q

In terms of B and T cell development, what is positive selection?

A

positive selection identifies cells that can bind antigen (in the case of T cells, MHC bound peptide) and signal through their receptor (B cell receptor or T cell receptor)
the signalling promotes their survival.

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79
Q

In terms of B and T cell development, what is negative selection?

A

Negative selection involves the binding of self-

antigen to the B-cell receptor or T-cell receptor, which results in deletion of the cell by apoptosis·

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80
Q

What MHC molecules do the differtn T cells recognise?

A

CD4- MHC II

CD8- MHC I

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81
Q

What is VDJ recombination?

A

the genetic recombination of a variable region with a

diversity region and a joining region.

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82
Q

The key enzymes responsible for VDJ recombination are?

A

Reactivating genes RAG 1 and RAG 2

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83
Q

What is somatic hypermutation?

A

A further refinement of B cell receptor recognition to antigen

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84
Q

What enzyme is critical to somatic hypermutation?

A

activation induced cytidine deaminase (AID)

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85
Q

What is Antibody class switching or class switch recombination?

A

A step in the B cells response to an antigen. Determines what type of antibody is produced.

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86
Q

During B cell class switching, what is NOT affected?

A

The affinity of the B cell receptor for antigen

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87
Q

What occurs during class switching?

A

The constant region of the antibody is replaced so that it can interact with different effector molecules

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88
Q

What 2 alternative isotypes of immunoglobulin are expressed by naive B cells?

A

IgM & IgD

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89
Q

Why are IgM and IgD not produced by class switch recombination in naive B cells?

A

Because the cells have not experienced antigen

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90
Q

How is IgM and IgD produced in naive B cells?

A

By alternative mRNA splicing

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91
Q

Why do T cells need to work with antigen presenting cells?

A

Because their receptors can only recognise the processed components of a pathogen

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92
Q

What are the two alternative pathways for antigen processing?

A

Exogenous

Endogenous

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93
Q

What stops the MAC from destroying own cells? 3

A

enzyme MCP o the surface of the bodies own cells clips to an inactive form.
Decay Accelerating Factor (DAF) accelerated destruction of covertase.
Protectin removes almost completed MACs from cell surface.

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94
Q

How does the lectin pathway work?

A

Mannose binding lectin in blood has another protein MASP bind to it.
MBL attaches to a pathogen and the MASP then functions like a convertase to cleave C3 in the blood

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95
Q

What is iC3b and what does it do?

A

Inactive C3b.

Binds to surface and marks it for phagocytosis.

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96
Q

To what cells do MHC I and II belong and who do they advertise to?

A

MHC I - Found on most cells. Billboards for killer T cells

MHC II - Antigen presenting cells - Helper T

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97
Q

What 3 PAMPS do the TLR located on the outside of the cell membrane recognise?

A

lipopeptides 1&2, 2&6
flagellin 5
lipopolysaccaride 4

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98
Q

What 3 PAMPS do the TLR located within the cell recognise?

A

dsRNA 3, 10
ssRNA 7, 8
CpG DNA 9

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99
Q

What 6 DAMPs are recognised by TLRs?

A 
HSP70
Fibrinogin
Fibronecctin
dsRNA
ssRNA
DNA
100
Q

What 2 pathways are associated with TLR signalling?

A

MyD88

TRIF

101
Q

Give 2 examples of diseases linked to defects in PRRs or their signalling pathways?

A

Waldenstrom macroglobuleima - MyD88 gain of function

MyD88 deficiency - childhood infections but later compensated for

102
Q

What disease would you typically get if you were deficient in in TLR-3?

A

Herpes Simplex Encephalitis

103
Q

Two examples of NLRs, and where are they found?

A

In the cytoplasm NLRC1 and NLRC2

104
Q

What do NOD1 and NOD2 (NLRC1 and NLRC2) recognise?

A

Components of peptoglycan. iE-DAP and muramyl dipeptide respectively.

105
Q

NOD2 gain of functionwould result in what type of disease?

A

Sarcoidosis

106
Q

NOD2 loss of function results in what disease?

A

Crohns

107
Q

What 2 diseases are a mutation of NLRP3 associated with?

A

Muckle Wells syndrome

Familial cold inflammatory syndrome

108
Q

A mutation of NLRP3 causes an over production of what and how can this be treated?

A

IL-1

IL-1 receptor antagonist - anakinra

109
Q

What activates NLRP3? 3

A

K+ efflux
reactive oxygen species
lysosomal damage

110
Q

What receptor ids linked to inflammasome?

A

NLRP3

111
Q

What does inflammasome activate and ultimately produce?

A

Caspase 1 then IL-1 and IL-18

112
Q

What do RIG-I and MDA5 receptors look out for?

A

Cytoplasmic RNA

113
Q

Give an example of a cytosolic DNA sensor, what does it’s products interact with?

A

cGAS

what it produces interacts with STING on ER

114
Q

What does a STING gain of function result in?

A

SAVI - chronoc inflammation of skin, lungs

115
Q

5 long term side effects of prednisolone?

A 
Diabetes 
Osteoperosis
Cushingoid syptoms/appearnace
Cateracts 
Proximal muscle weakness
116
Q

What is the tiny region on the BCR that actually binds to the antigen?

A

epitope

117
Q

In terms pf lymphocyte development, what type of cells in involved in their development?

A

Stromal cells

118
Q

Where in the body does VDJ recombination take place?

A

Bone marrow

119
Q

Where does the “stimulation by foreign antigen” component of lymphocyte maturation take place?

A

peripheral lymphoid tissue

120
Q

What are the two types of B cell antigen?

A

T dependent

T independent

121
Q

What 2 types of substances are being recognised by B cells when they recognise T independent antigens?

A

Lipids

Polysaccarides

122
Q

T dependent antigens are typically what type of molecule?

A

Proteins, peptides

123
Q

What happens in T independent antigen B cell interaction to become activated?

A

Crosslinking of many epitopes will result in activation.

124
Q

Broadly, what happens regarding T dependent antigens to result in B cell activation? 5 marks

A 
BCR binds to antigen
Antigen processed
Presented as MHC II
Recognised by CD4 T cell
CD4 cell activates B cell
May require additional CD40 signal
125
Q

What proteins are associated with co-stimulation of B cells by a helper T cell?

A

B cell - CD40, CD80, CD86

Th Cell - CD40L, CD28

126
Q

What cytokines are secreted by Th cells during B/Th interaction?

A

IL-4

127
Q

When first activated what is the type of antibody produced by B cells?

A

IgM

128
Q

What region of the antibody needs to be altered in order for class switching to occur?

A

Fc

129
Q

How many C1 complexes need to come together in orfer to activate the classical complement pathway?

A

2 or more

130
Q

What type of antibody is involved in the classical pathway of complement?

A

IgM

131
Q

What determines the type of antibodies that are produced by B cells?

A

The cytokines released by Th cells can switch B cells from making IgM to another type of antibody.

132
Q

In terms of B cell receptors, what is essential for C cell activation?

A

Crosslinking

133
Q

How does complement influence B cells

A

B cells have a complement receptor.

Which amplifies signal from BCR activating the B cell

134
Q

I cross linking alone enough to activate the B cell?

A

No, it requires a co stimulatory signal

135
Q

What are the proteins involved in Th dependent activation, and what would a deficiency in these proteins mean?

A

CD40L &CD40

Inability to mount a T dependent antibody defence

136
Q

What causes B cells to class switch and change the type of antibody they produce?

A

Cytokines released by Th cells

137
Q

What part of the BCR is affected by somatic hypermutation?

A

Antigen binding region.

138
Q

Why to B cells ununfluenced by Th cells usually not undergo class switching or hyper mutation?

A

These processes require cytokine release from Th cells

139
Q

What is the protein found on antigen presenting cells involved in co stimulation?

A

B7

140
Q

Define immunisation

A

Immunisation is an artificial process by which an individual is rendered immune

141
Q

Define passive immunisation - 2 examples

A

Immunity conferred without an active host response on behalf of recipient
VZV prophylaxis
snake venom anti-serum

142
Q

Define active immunisation

A

Immunity conferred in recipient following the generation of an adaptive immune response

143
Q

What is herd immunity?

A

Vaccination of sufficient numbers impacts the transmission dynamic so that even unimmunised individuals are at low risk

144
Q

Describe a classification system for active vaccines

A

Whole Organism - Live attenuated or Inactivated

Subunit

145
Q

Up to 9 examples of live attenuated vaccines

A 
Measles
Mumps
Rubella
Polio (Sabin)
BCG 
Cholera
Zoster
VZV
Influenza
146
Q

4 Pros of live attenuated vaccines

A

Replication within host, therefore produces highly effective and durable responses
In case of viral vaccine, intracellular infection leads to good CD8 response
Repeated boosting not required
In some diseases, may get secondary protection of unvaccinated individuals, who are infected with the live-attenuated vaccine strain eg polio

147
Q

3 Cons of live attenuated vaccines

A

Storage problems, short shelf-life
May revert to wild type
Immunocompromised recipients may develop clinical disease

148
Q

Difference between Salk and Sabin vaccine

A

Salk - Injected inactivated polio virus

Sabin - Oral live-attenuated virus

149
Q

What is an inactivated vaccine and what does it stimulate?

A

Entire organism used, but physical or chemical methods used to destroy viability (eg formaldehyde)
Stimulates B cells, and taken up by antigen-presenting cells to stimulate antigen-specific CD4 T cells

150
Q

Up to 6 examples of inactivated vaccine

A 
Influenza
Paratyphoid
Typhus
Cholera
Plague
Rabies
Polio - Salk
151
Q

3 pros and 3 cons of killed vaccines

A

No potential for reversion
Safe for immunocompromised
Stable in storage

Mainly CD4/ antibody response
Responses less durable then live vaccines
Generally boosters required
Higher uptake generally required to achieve herd immunity

152
Q

Why are influenza vaccines produced annually?

A

The target antigens are prone to mutation (antigenuc drift)

153
Q

What is antigenic shift?

A

When more major changes in a pathogenic virus occur eg human strain recombines with with animal strain causing a pandemic

154
Q

What are subunit vaccines?

A

Vaccines that use only a critical part of the pathogen in order to generate an immune response

155
Q

What type of immune responses are illicited by a subunit vaccine

A

CD4 and antibody

156
Q

What are subunit toxoid vaccines?

A

Toxins that are typically produced by bacteria are detoxified to become toxoids. These then stimulate ab antibody response.

157
Q

3 examples of toxoid vaccines

A

Corynebacterium diphtheriae
Clostridium tetani
Bordatella pertussis

158
Q

What are subunit polysaccharide vaccines?

A

Thick polysaccharide coats of Streptococcus pneumoniae and Neisseria meningitidis make them resistant to phagocytosis
Vaccines for these organisms formed of purified polysaccharide coats
Vaccines formed of purified polysaccharide coats; aim to induce IgG antibodies that improve opsonisation

159
Q

Whats is the drawback of subunit polysaccharied vaccines, what can be done to counter this?

A

Polysaccharide is weakly immunogenic. So protein conjugates are added

160
Q

What is vaccine conjugation?

A

Protein conjugate is added to polysaccharide
Antibody recognises polysaccharide and both are internalised
conjugate processed by MHC class II pathway
CD4 cell recognises peptides
CD4 cell activates B cell to produce antibodies

161
Q

What is a recombinant protein subunit vaccination? 2 examples

A

HPV

Hep B

162
Q

3 pros and 3 cons of subunit vaccines

A

Extremely safe
Work well where primary infection may be prevented by an antibody response
Works when the virus cannot easily be cultured eg HPV and Hep B

Development requires detailed knowledge of virology, pathogenesis and immunology
Specialised and expensive production
Weaker immune responses – boosting often needed and response rate varies

163
Q

What are adjuvants and what do they do?

A

Helpers that boost immune response to vaccine.
Work by binding to pattern-recognition receptors on antigen presenting cells
This enhances co-stimulation and cytokine secretion, which ensures a robust T/ B cell response

164
Q

What are the 3 main components of a vaccine?

A

Antigen
Adjuvants
Excipients

165
Q

Two examples of novel vaccines

A

DNA vaccines

Viral vector vaccines

166
Q

Describe the steps of TB infection

A

MTB enters lungs
establishes infection in macrophage phagolysosome
antigen presented on MHC II
TH cells relaease IFgamma
more magrophages attracted to from granuloma
Secondary infection is reactivation of this

167
Q

What is the vaccination against TB

A

BCG
M.bovis
Aims to increase IFgamma release from Th1 cells

168
Q

Limitations of BCG?

A

Only really effective in children against disseminated TB or TB meningitis
Works less well in adults
No protection against pulmonary TB

169
Q

give 2 examples of a subunit vaccine utilising polysaccharide capsules

A

Streptococcus pneumoniae

Neisseria meningitidis

170
Q

What’s the principle behind DNA vaccination?

A

Don’t give the antigen but instead the DNA plasmid that encodes the antigen

171
Q

What is Di-George syndrome and what is the consequence of this?

A

Children born without thymus

No T cell responce

172
Q

What is MHC restriction?

A

Positive selection
Epithelial cells in cortical region of thymus check that T cells recognise self MHC molecules
If not they apoptose

173
Q

In terms of T cell maturation, what is meant by double positive and double negative?

A

Immature T cells arriving at thymus express neither CD4 nor CD8.
As they mature in cortex of thymus they then expree both CD4 and CD8

174
Q

Why is MHC restriction important?

A

Ensures that T cells recognise antigen presented by antigen presenting cells. Otherwise antigen presentation won’t work.

175
Q

Where in the thymus does the T cell “tolerance of self” take place?

A

Medulla

176
Q

At what point do maturing T cells become single positive?

A

During or soon after positive selection

177
Q

What 2 cells are involved in negative selection of T cells?

A

Thymic dendritic cells

Thymic medullary epithelial cells

178
Q

What is tolerance of self also known as?

A

Negative selection

179
Q

During negative selection what is tested by the thymic dendritic cells?

A

Does the T cells recognise any of the self antigens presented on my MHC molecules? Anwer should be no

180
Q

How does strength of interaction between TCRs and MHC relate to positive and negative selection?

A

During positive selection weak interaction signal survival

During negative selection a strong interaction signal apoptosis

181
Q

How does the “traffic pattern” of naive T cells aid tolerance of self antigens?

A

naive T cells remain in secondary lymphoid tissue so the will ahve been exposed to same abundant self antigens in the thymus.
Other self antigens too rare to trigger activation here

182
Q

What gene expression is associated with Tregs

A

Foxp3

183
Q

How do natural Tregs aid tolerance induction?

A

provide protection against the T cells that have the potential to react against self antigens

184
Q

How are inductible Tregs cells different from natural Tregs?

A

Inductible Tregs prevent overeaction to foreign antigens and use cytokines rather than cell to cell interaction.

185
Q

What is peripheral immunity?

A

T cells that recognise antigen on self tissue
Do not receive co-stimulation
T cell anergized and can no longer function

186
Q

What checks are in place to ensure T cell tolerance?

A 
MHC restriction - positive selection
Tolerance induction - negative selection
Tolerance by ignorance - doesn't see rare self antigens 
Treg cells - natural and inducible 
Peripheral tolerance 
Inactivation from chronic re-stimulation
187
Q

Give 3 examples of cytokines that interfere with viral replication

A

IFN-alpha (made by lymphocytes)
IFN-beta (made by fibroblasts)
IFN-gamma (made by lymphocytes & NK cells)

188
Q

Examples of cytokines involved in haematopoiesis of myeloid cells

A

EPO - erythrocytes
GM-CSF - neutrophils
G-CSF - neutrophils
IL-6 - mast cells

189
Q

Example of cytokine involved in haematopoiesis of lymphoid cells

A

IL-2

190
Q

Two examples of TNF mediated diseases

A

Rheumatiod arthritis

IBD

191
Q

What are the three strategies in which cytokines can be inhibited?

A

Receptor antibodies - anti TNF, IL-1R
Cytokine antibodies - Anti IL-6
Soluble receptors - soluble TNFR

192
Q

The cytokines responsible for imflamation are usually produced by what type of Th cell?

A

Th1

193
Q

Give an example of the type of cytokine produced by each type of T cell

A

Th1 - TNF, IF gamma

Th2 - IL-4

194
Q

2 cytokines released by Treg cells?

A

IL-10

TGF beta

195
Q

What effect does the interaction of B7 with CTLA-4 have when compared to CD28?

A

Makes it harder for the R cell to be activated

196
Q

In terms of the STRENGTH of interaction between TCRs and MHC, what results in positive and negative selection?

A

Survival of positive selection - weak interaction

Survival of negative selection - strong interaction

197
Q

What cells within the thymus are involved in positive and negative selection and where are these located?

A

Cortical Thymic epithelial cell
Thymic dentritic cell
Medullary Thymic epithelial cell

198
Q

What “question” is posed during positive selection?

A

Do you recognise these MHC molecules?

Answer better be yes

199
Q

What “question” is posed during negative selection

A

Do you recognise any of the self peptides displayed on my MHC molecules?
Answer better be no

200
Q

What is MALT, BALT and GALT?

A

Associated lymphoid tissue

Mucosal, Bronchial, Gut

201
Q

3 main defence strategies in mucosa of intestine and oropharaynx?

A

Commensual flora
Epithelium and mucus
Regionalised immune system

202
Q

What’s specialised about the epithelial cells of the intestines with regard to inflammation?

A

They provide defence without inflammation

203
Q

hat specific structures exist in the intestine to aid the immune system?

A

Peyers patches
Goblet cells
Epithelial cells
Paneth cells

204
Q

What do the following cells do?
Goblet cells
Epithelial cells
Paneth cells

A

Goblet cells - mucus production
Epithelial cells - express TLRs
Paneth cells - produce defensins

205
Q

What do Peyers patches do?

A

Sample antigens from the intestine by transporting those antigens through the M cell

206
Q

What tissue collects lymph and antigens from the intestinal mucosa and is the main site for oral tolerance induction?

A

Mesenteric lymph nodes

207
Q

What are the homing receptors associated with Peyers patches and mesenteric lymph nodes?

A

a4b7

CCR9

208
Q

What are the 2 effector sites of immune responce in the gut?

A

epithelium

lamina propria

209
Q

What is the Gell and Coombes system of classification?

A

mechanism based approach of classifying immunocologicaly mediated disease

210
Q

What are the 4 different Gell and Coombes classifications?

A

1 - IgE vs anitgen (allergy)
2- Pathogenic antibody directly causes disease
3 - Antibody/antigen complex disease
4 - Inflammation directly mediated by T cells

211
Q

What is given to others to prevent Haemolytic disease of the newborn?

A

Anti-D IgG antibodies binds to foetal RBC in mothers circulation preventing sensitisation.

212
Q

Examples of type 1, 2, 3 & 4 hypersensitivity

A

1 - allergy
2 - Haemolytic disease of the newborn
3 - Serum sickness, lupus
4 - Delayed type hypersensitivity - contact dematitis

213
Q

Draw a picture of an indirect immunofluorescence system and a solid-phase immunoassay system for the detection of antibodies in blood

A

Antigen
Pt serum
Marker antibody
check for flourescence

214
Q

Draw a picture of a direct immunofluorescence system for the detection of antibodies bound to tissue

A

Sample of tissue
Marker antibody
check for flourescence

215
Q

describe the steps of an ELISA experiment

A

Direct and indirect

216
Q

What are the two classifications of autoimmune disease?

A

Organ specific - insulin dependent diabetes

Non-organ specific - Lupus

217
Q

With regard to autoimmunity what do mutations in IRE genes result in?

A

Failure of negative selection

Strongly associated with autoimmune disease

218
Q

With regard to immune cell numbers what will DI George syndrome result in?

A

No/v low T cells due to thymic aplasia

219
Q

What is molecular mimicry?

A

epitopes relevant to the pathogen (following an infection) are shared with host antigens

220
Q

2 examples of molecular mimicry

A

Autoimmune haemolysis after Mycoplasma pneumoniae

Rheumatic fever: inflammatory disease occurring after streptococcal infection affecting heart, joints, skin and brain

221
Q

2 examples of molecular mimicry

A

Autoimmune haemolysis after Mycoplasma pneumoniae

Rheumatic fever: inflammatory disease occurring after streptococcal infection affecting heart, joints, skin and brain

222
Q

2 examples of molecular mimicry

A

Autoimmune haemolysis after Mycoplasma pneumoniae

Rheumatic fever: inflammatory disease occurring after streptococcal infection affecting heart, joints, skin and brain

223
Q

A deficiency in CD40/CD40L is likely to result in what? 2

A

Unable to mount T cells responce

B cells secrete mainly IgM

224
Q

People suffering from SCIDS lack what type of immune cell?

A

T and B

225
Q

People suffering from SCIDS lack what type of immune cell?

A

T and B

226
Q

What are the main classifications for immunodeficiency?

A

Primary Immunodeficiency syndrome - immune defect is intrinsic to the immune system itself
Secondary Immunodeficiency - secondary to anither disease process

227
Q

4 characteristics of infections due to immunodeficiency

A

Opportunistic
Unusual
Severe
frequent

228
Q

Causes of secondary immunodeficiency

A 
Extremes of age
malignancy (myeloma and lymphoma)
Iatrogenic - steriods, chemotherapy
Diabetes
Infection - HIV
229
Q

What are the 3 IMMUNOLOGICAL classifications of immunodeficiency?

A

Innate
“Antibody/humoral” - B cells eg bacterial infections of resp tract
“Cellular” - T cells eg HIV, viral, fungal

230
Q

What are the immunideficincy syndromes called when they affect both the antibody and cellular component?

A

Combined immunodeficiency

231
Q

What is immune dysregulation?

A

Uncontrolled inflamation in immunodeficiency

232
Q

In antibody deficiency what type of antibody is significant?

A

IgG

233
Q

Two Secondary causes of antibody deficiency

A

IgG loss through burns and nephrotic syndrome

Impaired production via immunosuppressive drugs

234
Q

Two primary causes of antibody deficiency?

A

X linked agammaglobulinemia

X linked hyper IgM syndrome

235
Q

What is Transient hypogammaglobulinemia of infancy?

A

Physiological antibody deficiency

Period when the portenction afforded to them by mother IgG drops as the pordcution of their own antibodies catches up

236
Q

At ahat age would infants with antibody deficiency present and why?

A

after 3-6 months as up unitl this point they are portected by their mother IgG

237
Q

What is X linked agammaglobulinemia?

A

A primary cause of antibody deficiency
Deficiency of Bruton’s tyrosine kinase. so no downstream signalling so B cells undergo apoptosis.
No B cells

238
Q

What is X linked hyper IgM syndrome?

A

failure of B call maturation
Normal or high IgM
No IgA or IgG
No CD40 ligand

239
Q

What is cellular immunodeficiency?

A

CD4 T cell deficiency

240
Q

What is severe combined immunodeficiency?

A

rare life threatening primary immunideficiency
No T cell or B cell function
graft vs host rash

241
Q

3 causes of SCID

A

Common gamma chain deficiency
JAK3 deficiency
RAG1/2 deficiency

242
Q

What are patients with Terminal complement deficiency succeptible to?

A

Neissera infections

243
Q

What are the indications for Azathioprine and Ciclosporin?

A

Immunosuppression for
Crohns
SLE
RA

244
Q

What type of drug is methotrexate and what are its indications?

A

antimetabolite
Crohns
RA

245
Q

What are the indications for rituximab and infliximab?

A

Crohns - infliximab only

RA

246
Q

Example of an antihistamine

A

Chlorphenamine

204 Musculoskeletal & Immune Systems (2 decks)

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