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BDS stage 2 > Immunology and Healthcare theme 1 > Flashcards

Immunology and Healthcare theme 1 Flashcards

1
Q

What are the pathways to inflammation ?

A 
chronic infection with plaque 
autoimmune 
hypersensitivity- allergic rhinitis etc
metabolic disorder 
immunodeficiency
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2
Q

Why is there redness in inflammation ?

A

increased blood flow

increased heat- against microorganisms

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3
Q

What contributes to the inflammatory state in periodontitis ?

A

imparied host defence

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4
Q

What is necrotising ulcerative gingivitis ?

A

ulceration
loss of epithelium due to acute infection
severe stimuli- stress, smoking and HIV, nutritional deficiency

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5
Q

What is sjogren disease ?

A

autoimmune disorder
swelling of salivary gland
xerostomia
WBC accumulation in H and E slides - immune system destroys salivary glands

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6
Q

What do gingival fibroblasts make in collagen turnover ?

A

MMP

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7
Q

How is MMP stimulated ?

A

Macrophages make IL-1

stimulates MMP Production by fibroblasts

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8
Q

What is IL-1 ?

A

pro inflammatory cytokine

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9
Q

What happens in the disease state with MMP ?

A

bacteira in excess over stimulate macrophages to make IL-1 - fibroblasts respond with increased MMP
collagen turnover
increased tissue production

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10
Q

Which over molecules can stimulate gingival fibroblasts to make MMP ?

A

leptin - type 2 diabetes and obesity

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11
Q

How can we target MMP in periodontitis treatment ?

A

inhibit MMP with doxycycline

use as an adjucnt treatmnet with RSI

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12
Q

How can we measure periodontitis improvement ?

A

probing depth

clinical attachment loss

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13
Q

What are the main functions of the immune system ?

A

recognition of non self molecules
effector function- eradicate infection
Regulation to ensure correct response
Memory - allows stronger and quicker response on reinfection

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14
Q

What are the characteristics of the innate immunity ?

A

rapid
fixed- cant adapt
limited number of specificities
constant during response

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15
Q

What are the characteristics of adaptive immunity ?

A

slow response - cell interactions
variable- large or small
numerous selective specifiities- provide targeted response
improves during the response

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16
Q

What does malfunction of the immune system lead to ?

A

chronic inflammation

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17
Q

What are the ways in which skin acts as a barrier ?

A

thickened keratinised epidermis
sebaceous glands- fatty acids that lower pH
sweat glands- lactic acid
antimicrobial peptides
acts as a barrier to opportunistic infection

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18
Q

What is the risk with burns ?

A

moist surface

vascular damage- promotes bacterial growth

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19
Q

What do cuts and surgery promote ?

A

staph aureus infection

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20
Q

What are examples of mucosal surfaces ?

A

urogenital tract
GI tract
respiratory tract

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21
Q

What do mucosal surfaces act as ?

A

entry infection points

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22
Q

What does ciliated epithelium allow ?

A

coagualtion of particles and ejection

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23
Q

How does mucous work ?

A

mucin is a highly glycosylated protein
attracts water
coagulates particles and allows them to be swallowed

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24
Q

Which cells secrete mucus ?

A

goblet cells

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25
Q

What does the saliva do ?

A

lysozyme and lactoferrrin

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26
Q

What does smoking do to epithelium ?

A

removes ciliated epithelium

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27
Q

When is sepsis likely and what can it cause ?

A

after colon surgery

leads to septic shock

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28
Q

How do commensal bacteria have a protective function ?

A

stimulate colonic epithelial cells- in a balanced state of psychologic inflammation
commensal bacteria compete with pathogens for nutrients, attachmnet sites and space
bacteria produce antimicorbila lactic acid and fatty acids

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29
Q

How does a C.dificile infection occur ?

A

colon is colonised by commensal bacteria
antibiotics kill commensal bacteria - leads to dysbiosis
C. dificile produces toxins that cause mucosal imjury
neutrophils and RBCs that leak between epithelial cells
diarrhoea and anemaia

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30
Q

What are soluble mediators of innate immunity ?

A

enzymes- lysozyme and phospholipase- cell membrane and wall
complement system
antimicorbial peptides

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31
Q

What are the fucntions of the complement system ?

A

opsinisation
chemotaxis
lysis

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32
Q

What is the structure of antimicrobial peptides ?

A

amphipathic

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33
Q

What do antimicrobial peptides do ?

A

kill bacteria, fungi and enveloped viruses - disrupt membranes

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34
Q

Which cells make alpha defensins ?

A

neutrophils and paneth cells

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35
Q

Which cells make beta defensins ?

A

epithelial cells

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36
Q

What are paneth cells ?

A

specialised cells of small intestine

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37
Q

What do paneth cells make ?

A

alpha defensins
lysozyme
phospholipase

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38
Q

What is the complement system ?

A

innate effector function
family of 30 blood proteins
potent so a re highly regulated and kept inactive

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39
Q

How are complement proteins activated ?

A

blood clotting

apoptosis

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40
Q

Which pathways activate complement system ?

A

lectin
alternative
classical

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41
Q

What happens in activation complementation ?

A

activation of c3 and c5

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42
Q

What ar the actions of the activated complement ?

A

perforation of cell membranes
opsinisation
chemotaxis

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43
Q

How do complement proteins attack membranes ?

A

make a membrane attack complex which disrupts bacterial outer membranes
leads to bacterial cell death

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44
Q

How does opsinisation for phagocytosis work ?

A

bacteria in a capsule cant be engulfed by a neutrophil
antobody bound to bacteria activates complement and allows C3 binding to bactiera
engulfment can now be activated by Fc receptors and complement receptors
granules fuse with phagosommes- release toxic oxygen metbaolites that kill bacteria

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45
Q

What is lymphatic tissue ?

A

rich in lymphocytes

immune response mediation

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46
Q

What is primary lymphoid tissue ?

A

bone marrow and thymus gland
lymphocyte formation and maturation
b cells mature in bone marrow
t cells mature in the thymus gland

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47
Q

What is secondary lymphoid tissue ?

A

filters monitoring the blood and lymph for antigens and APCs
lymphocytes are acitvatedh ere

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48
Q

What are examples of secondary lymphoid tissue ?

A 
lymph nodes
tonsils 
spleen 
peyers patches 
MALT
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49
Q

What is the structure of they thymus gland ?

A

bilobed organ above the heart
lobular
outer fibrous cortex and inner medulla

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50
Q

What is the function of the thymus gland ?

A

T cell maturation

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51
Q

What is the purpose of the spleen ?

A

protects against blood bourne infections especially against encapsualted bacteria

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52
Q

What is the structure of the lymph nodes ?

A 
no lobules 
kidney shaped 
no cortex/medulla 
ring structure- follicle 
afferent lymphatic vessel
lymphatic vessel spreads to the thoracic duct - spread lymphocytes 
germinal center
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53
Q

What is the purpose of the germinal center ?

A

centre and location of the immune response

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54
Q

What is the function of lymph nodes ?

A

activation
expansion
presentation of cells

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55
Q

What is a peyers patch ?

A

mass of lymphatic tissue in the ileum of small intestine

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56
Q

What is the structure of a peyers patch ?

A

follicle structure
no afferent lymphatics
surrounded by villi

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57
Q

What is within the peyers patch ?

A

T cells
germinal centrrs
B lymphocytes
macrophages

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58
Q

What is the unique cell in the peyers patch ?

A

M cell

provides antigen for the dendritic cell in the patch

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59
Q

What is waldayers tonsilar ring ?

A

patches of lymphoid tissue around the pharync and mouth
lingual tonsil
palatine tonsil - between muscles
pharyngeal tonsil

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60
Q

What are the sites of MALT ?

A 
GI tract
nasopharynx 
thyroid 
breast 
lung 
salivary glands 
antibodies and stimulated lymphocytes move between these regions
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61
Q

Which cells encounter antigens in the mucosa ?

A

macrophages
T cells
B cells
plasma cells

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62
Q

What are the innate immune effector cells ?

A 
phagocytes 
macrophages 
granulocytes- neutrophils 
mast cells
dendritic cells
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63
Q

What are monocytes ?

A

circulate in the blood

enter tissues to become macrophages

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64
Q

What is the function of macrophages ?

A

phagocytosis
antigen presentation
scavengers
activation of T cells

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65
Q

What happens in the process of phagocytosis ?

A

bacteria binds to receptors on the neutrophil - its been covered in complement or antibodies
into phagosome
phagosome acidified- kills most
fuses with lysosome
degradation via lysosome by lysozyme and AMPs
NO and ROS also assist

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66
Q

What are neutrophils ?

A

granular
lobed nucleus
large reserves in bone marrow

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67
Q

What is the function of neutrophils ?

A

engulf microorganisms
rapidly mobilised on early staged of infections like gingivities
contribute to inflammation

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68
Q

What happens between macrophages and phagocytes in the inflammatory response ?

A

macrophaes engulf bacteria
induce cytokines and trigger neutrophil release from bone marrow
endothelial cells expand - tissue is red and swells and neutrophils enter
neutrophils phagocytose bacteria
neutrophils themselves are phagocytosied by macrophages

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69
Q

What are mast cells ?

A

release granules that contains histamine
part of defence against parasites
mediates hypersensitivity

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70
Q

What are dendritic cells ?

A

professional APCs
phagocytose
present antigen to initiate the immuen response in secodnary lymphoid tissues

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71
Q

Which cells are APCs ?

A

dendritic cells
macrophages
B cells

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72
Q

Phagocytes activate effector functions like ?

A

chemotaxis of new phagocytes like neutrophils
interferon response
systemic effects
activation of adaptive immunity

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73
Q

What is the interferon response ?

A

the anti viral response

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74
Q

Which type of immunity is inherited specifically in a genome ?

A

innate

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75
Q

Which type of immunity has receptors expressed by all cells of a specific type ?

A

innate

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76
Q

Which type of immunity triggers an imemdiate response ?

A

innate

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77
Q

Which type of immunity interacts with a range of molecules of a specific type ?

A

innate

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78
Q

Which type of immunity is coded for in multiple gene segments ?

A

adaptive

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79
Q

Which type of immunity requires gene arrangement ?

A

adaptive

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80
Q

Which type of immunity has clonal distribution ?

A

adaptive

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81
Q

Which type of immunity is able to discriminate between closely related structures ?

A

adaptive

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82
Q

What do PRRs do ?

A

recognise a wide range of molecular structures- PAMPs

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83
Q

Where are PAMPs found ?

A

on pathogens

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84
Q

What must precede adaptive recognition ?

A

innate recognition

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85
Q

What are adjuvants ?

A

used in vaccines

allow the innate response to occur first and then adaptive response

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86
Q

What is the structure of PRRs ?

A

can be free receptors in the serum - mannose binding lectin

can be membrane bound - on Dendritic cells

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87
Q

What is the mannose receptor and what does it do ?

A

a PRR

recognises carbohydrate structure on pathogens

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88
Q

What are the classes of PRRs ?

A

Toll like receptors

NOD like receptors

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89
Q

How many different types of Toll like receptors in humans and where are they ?

A

10 types in humans

theyre in macrophaes, dendritic cells, B cells and epithelial cells

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90
Q

What do cell surface toll like receptors detect ?

A

extracellular pathogens and their products

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91
Q

What do intracellular TLRs detect ?

A

phagocytosed pathogens

or viruses- theyre intracellular

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92
Q

What does TL4 recognise ?

A

LPS in gram negative

lipoteichoic acid in gram positive

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93
Q

Are Toll like receptors specific ?

A

no they have a broad range

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94
Q

What does double stranded RNA act as ?

A

a non self indicator as humans only have single stranded RNA

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95
Q

What is the conformation of the TLR ?

A

heterodimer
most of it is intracellular
activate an intracellular pathway when ligand binds

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96
Q

What happens when a PAMP binds to TL4 ?

A

IRF and NKB transcription factors are made
IRF induces type 1 interferon leading to the antiviral response
NKB induces cytokines, chemokines and AMP leading to chemotacis, bacterial lysis and inflammation

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97
Q

What do mutations in TLRs lead to ?

A

immunodeficinecies

recurrent bacterial infections

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98
Q

How do immunosupressant drugs work ?

A

interfere with TFs produced from the binding of the PAMP to the TLR

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99
Q

What do NOD like receptors respond to ?

A

intracellular infections

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100
Q

What do NOD like receptors identify ?

A

cell wall peptidoglycan

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101
Q

How do NOD like receptors link to crohns disease ?

A

NOD like receptors are mutated
inappropriate AMP response
commensal bacteria invade colonic epithelium leading to inflammation

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102
Q

What happens when macrophages sense microbial products ?

A

secrete pro-inflammatory cytokines

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103
Q

What are some of the effects of the cytokines produced by macrophages that have sensed PAMPs ?

A

activates vascular endothelium
activate lymphocytes
increases vascular permeabilty
recruits neutrophils

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104
Q

What attracts neutrophils to the site of infection ?

A

chemokines allow chemotaxis

extravasation from blood to tissues

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105
Q

What do dead neutrophils form at wound margins ?

A

pus

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106
Q

What are the type 1 interferons and how are they secreted ?

A

IFN alpha
IFN gamma
secreted by virally infected cells and cells where TL3 and RIG have been activated by nucleic acids
plasmacyoid dendritic cells makes more IFN than any other cell

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107
Q

Describe the IFN response ?

A 
virally infected cells
IFN alpha and gamma 
induce resistance to viral replication 
Increase MHC class I expression
increases antigen presentation in cells
activate dendritic cells and macrophages 
activate NK cells to kill viruses 
induce chemokines to recruiit lymphocytes
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108
Q

What are NK cells ?

A

kill virally infected cells early in the infection
type of innate lymphoid cell
activated by IL12 and type 1 IFN
have activating and inhibitory receptors

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109
Q

How do NK cells recognise infected and non infected cells ?

A

via TLR and Fc receptors and disregulated MHC expression - infected cells
non infected cells- characterisitc MHC expression

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110
Q

How do NK cells activate T cells and macrophages ?

A

secretion of IFN gamma- type II IFN

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111
Q

What is the mechanism of action of NK cells ?

A

contain the infection
activate T cells to provide targeted response and long term response - prevents infection spreading
hence why herpes doesnt spreasd

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112
Q

What type of cell are NK cells ?

A

lymphoid

innate

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113
Q

How are ILCs distinguised from T and B lymphocytes ?

A

lack of antigen receptors

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114
Q

What are the fucntions of NK cells ?

A

amplify signals via cytokine secretion
fucntion as effector cells in response to inante recognition
ampligy interferon response to a viral infection

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115
Q

What is the early induced innate resposne ?

A

PAMPs recognised

effector cells made

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116
Q

What is the adaptive response ?

A

transport antigen to lymphoid organs and recognition by B and T cells - clonal expansion of effector cells

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117
Q

Why do we need the adaptive response ?

A

the innate response is insufficient in removing pathogen

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118
Q

How do B lymphocytes develop ?

A

develop in the bone marrow from common progenitor

mature in bone marrow

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119
Q

How do T lymphocytes develop ?

A

Develop from bone marrow progenitor but mature in the thymus gland

120
Q

What are the 2 classes of T cells ?

A

CD4+

CD8+

121
Q

What are CD4+ cells ?

A

helper T cells- helps CD8+ cells and B cells

122
Q

What are CD8+ Cells ?

A

cytotoxic T cells

kill infected cells

123
Q

What are the characteristics of adaptive immunity ?

A

delayed response

more specific response

124
Q

What is key to the adaptive response ?

A

activation of CD4+ T cells - go on to activate CD8 cells and B cells

125
Q

What is the evidence that CD4 + cells are key for immunity ?

A

HIV- severely reduced CD4+ T cells
SCID- RAG deficiency
susceptible to infection

126
Q

Which cells link the innate and adaptive immune responses ?

A

APCs- dendritic cells

T cells are activated by processed antigen presented on APC

127
Q

What does the interaction between dendritic cells (APCs) and T cells lead to ?

A

immunity to pathogens

tolerance to self antigens

128
Q

Why do we need to develop tolerance to self antigens ?

A

to prevent auto immunity

129
Q

Where do dendritic cells interact with T cells ?

A

in lymph nodes

130
Q

How is migration of the dendritic cells mediated ?

A

Dendritic cells remain in tissues and survey for pathogen
express a chemokine that allows them to remain in tissues- CCR7
pathogen detected and phagocytosed
danger signals like PAMPs activate the dendritic cell
change chemokine receptor- recruit migration to lymph node
T cell and dendritic cell interact

131
Q

What is the signal mechanism of antigen recognition ?

A

signal 1- recognition of antigen, presentation by APC to T cell via MHC
signal 2- co-stimualtion
signal 3- cytokines

132
Q

Which receptors detect PAMPs in the innate system ?

A

PRRs- NOD and TOL

133
Q

Which receptors detect antigens in the adaptive response ?

A

TCRs and BCRs

134
Q

How is the antigen presented by APCs ?

A

the antigen is processed by the APC and presented by MHC molecules

135
Q

What are MHC molecules ?

A

transmembrane glycoproteins expressed on surface of cells

136
Q

What are the classes of the MHC molecules ?

A

Class I- Activates CD8 cells

Class II- activates CD4 Cells

137
Q

Why is MHC difficult for pathogens to evade from ?

A

Polygenic- encoded for by several genes
Polymorphic- SNPs produce differnet alleles in the population- produces different MHC proteins capable of binding a variety of antigens
population is mostly heterozygous

138
Q

How are MHC genes inhertied ?

A

MHC Molecules are inhertied alongside the polymorphisms that increase the variety of the antigen binding site

139
Q

What is significant about MHC alleles ?

A

inherited in haplotypes

selected for by populations in evolutionary terms

140
Q

How can automimmune diseases be linked to MHC ?

A

autoimmune disease might come about from mutations that induce MHC molecules that bind self antigens

141
Q

What does MHC class I present to ?

A

CD8 + T cells

142
Q

Which cells express MHC class I ?

A

most nucleated cells

allows most cells to be killed by CD8

143
Q

What size peptides does MHC class I bind to ?

A

8-10 amino acids long

144
Q

What is the structure of MHC class I ?

A

3 alpha domains- alpha 1,2 and 3
B2 microglobulin unit
peptide binding groove in the alpha subunits

145
Q

How is the single heavy chain class I encoded for ?

A 
6 class I genes
have a lot of allotypes 
increasing number of MHC possibilities
146
Q

What does MHC class II present to ?

A

CD4 t Cells

147
Q

Which cells express MHC class II ?

A

APCs and thymus cells

hence only a small number of cells can activate CD4 cells

148
Q

What size peptides does CD4 cells bind ?

A

13-18 amino acids long

149
Q

What is the structure of MHC class II ?

A

2 alpha domains- alpha 1 and 2
2 beta chains- beta 1 and 2
peptide binding groove in alpha 1 and beta 1

150
Q

How is MHC class II encoded for ?

A

3 alpha and 6 beta genes

151
Q

How are class I antigen complexes assembled ?

A

via intracellular cytosolic pathway

for endogensou or intracellular antigens and viruses

152
Q

Describe the intracellular cytosolic pathway ?

A

antigen in cytosol degraded by proteosome into short peptides
peptides transported to ER via TAP protein
peptide binds to class I in the ER- in the peptide binding groove
MHC antigen complex expressed on cell
CD8 recognises antigen- kill infected cells with help of CD4

153
Q

Multiple MHC class I moleule on a single cell does what ?

A

increases chances of presenting different peptides

154
Q

Which cells express MHC class II ?

A

Macrophages - semi professional APC
B cells - semi professional APC
Dendritic- professional APC

Fibroblasts, epithelilial and endothelial cells- Non professional APC- induced to express class II via IFN gamma

155
Q

How are MHC class II antigen complexes made ?

A

via the extracellular exogenous pathway

156
Q

Describe the exogenous extracellular pathway ?

A

Bacteria phagocyosed by APC
proteolysis to break antigen down
Antigen in a phagosome binds to lysosome
MHC class II in golgi and ER binds to antigen via peptide binding groove
expressed on surface
CD4 T cell recognises MHC class II and activates

157
Q

What type of receptors do T cells ahve ?

A

each t cell is covered in TCR of one type - single antigen specificity
creates a large repertire of T cells that have a high diversity of binding sites for antigen.

158
Q

What is the structure of a TCR ?

A

Dimeric- 1 alpha and 1 beta chain
span whole membrane
each TCR has constnat and variable region

159
Q

How many genes encode for individual domains of the TCR ?

A

several

160
Q

Where are TCRs generated ?

A

thymus

161
Q

How do TCR genes recombine ?

A

via random somatic DNA recombination by RAG

162
Q

What does RAG deficiency result in ?

A

no functionally active T cells

163
Q

What is the nature of the TCR ?

A

randomly assembled and different but unique to one antiggen

164
Q

What is MHC restriction ?

A

each TCR recognises parts of the antigen and the MHC

each TCR is specific to a specifc antigen MHC complex

165
Q

What does positive selection ensure ?

A

TCRs recognise specific MHC

166
Q

How does positve selection work ?

A

in the thymus gland
different TCRs interact with specific MHC
if no recognition- die by apoptosis
if there is recognition of MHC by the TCR- t cell survives and moves into the blood- t cells are now MHC restricted

167
Q

What is a co receptor ?

A 
CD8 cells have CD8 protein on surface acts as a co receptor and recognises the specifc MHC class I too 
same for CD4 protein and class II
168
Q

How can CD4 cells be subdivided ?

A

Th1 cells- help CD8 cells via IFN gamma

Th2 cells- help B cells make antibodies via IL4

169
Q

What happens in signal III ?

A

cytokines produces that polarise the effector cells to become a specifc effector T cell

170
Q

What is the vigorous training process that T cells undergo ?

A

positive and negative selection

171
Q

What is the purpose of T cell training ?

A

to ensure that T cells only respond to foreign antgen only and dont recgonise self antigen

172
Q

What happens during positive selection ?

A

make sure TCRs bind to MHC and recognise it
in the thymus cortex
Interaction between the TCR and the MHC antigen complex
if there is no recognition the T cell dies by apoptosis
recognition- T cell survives and is MHC restricted

173
Q

What happens during negative selection ?

A

Ensures the TCR does not have a strong affinity for self antigen - known as central tolerance
takes place in the medulla
T cell interact with MHC antigen complex
binds strongly- dies by apoptosis
recognition at the right level- survives and enter blood and is known as naive T cell

174
Q

What are naive T cells ?

A

antigen inexperienced and first bind to the APC

175
Q

What leads to expression of costimulatory molecules on cell surface ?

A

activation of PRRs by PAMPs

leads to expression of CD80 and CD86 on the cell surface

176
Q

What are the co stimualtory molecules ?

A

CD80 AND CD86

177
Q

What is the purpose of the costimualtory moelcules ?

A

increases the ability of the CD4 T cell to interact with APC

178
Q

What is the interaction between the APC and the CD4 t Cell ?

A

CD4 T cell expressed CD28

interacts with CD80 and CD86 on the APC

179
Q

What does co stimulation lead to ?

A

support ability of CD4 T Cell to proliferate and differentiate into effector form

180
Q

What does accumulation signal 1 and 2 lead to ?

A

IL2 is made and IL2 receptor

IL2 is a survival factor- allows T cell to survive and proliferate into effector cells

181
Q

What is the purpose of signal 3 ?

A

polarises the T cells to become specific effector cells

182
Q

How is signal 3 initiated ?

A

PAMPs bind to PRRs which trigger cytokine production by the APC
different PAMPs produce different cytokines that polarise the T cells
virus - IL-12
Parasite- IL-4

183
Q

What do the cytokines produces in signal III do ?

A

act on receptors on the naive T cell
determines the type of T cell via TFs
allows appropriate cells fro the pathogen to be produced,

184
Q

Describe the process of T cell polarisation ?

A

Cytokines produced by the APC (triggered by PRR)
STAT pathway
TF
cell profile made
cytokines also produced by the newly polarised T cell

185
Q

What are the different T cell profiles ?

A 
Th1
Th2 
Th17
Tfh
iTreg
186
Q

What are the cytokines like that are produced by the newly polarised T cell ?

A

most cytokines and pro-inflammatory mediators

except for TGB IL10 and IL35- made by iTreg which turns of inflamamtion and regualtes the immune response

187
Q

How do newly polarised CD4 T cells contribute to positive feedback loops ?

A

the polarised cells produce cytokines that induce their own polarisation allowing more polarisation from the naive T cell to the effector cell

188
Q

How can CD4 t Cells also contribute to negative feedback loops ?

A

Th1 cells produce IFN gamma that acts on Th2 cells inhibiting their proliferation
Th2 cells produce IL-4 which inhibits differentiation of Th1 cells
negative feedback loops can suppress other T cell responses

189
Q

When an effector T cells detects an antigen which 3 braod classes of activity can they take ?

A

cytotoxic- CD8
Helper- CD4- Th1 and Th2
regulatory- Treg

190
Q

What are cytotoxic T cells ?

A 
CD8 cells 
kill infected cells with intracellular antigens that are expressed by MHC class I
191
Q

What are the killing mechanisms of cytotoxic T cells ?

A

cytotoxins -perforin and granzymes - induce apoptosis
Fas L - Fas L expressed on T cell interacts with Fas on target cell- signal for apoptosis
get help from Th1 CD4 T cells

192
Q

What is the function of regulatory T cells ?

A

some cells escape central toelrance and can respond to self peptides
peripheral tolerance in the periphery is set up to counteract this
maintain immune homeostasis by supressing proliferation of self reactive t CELLS -

193
Q

What are the mechanisms of action of T reg cells ?

A

Produce tolerogenic molecules like adenosine
consuption of IL-2 survuval factor
inhibtion of costimualtion- using ctal4 to block action of CD28 on T cell
granzymes and apoptosis

194
Q

What are memory T cells ?

A

T cells that persist after most have died (most go to site of infection and some stay to activate B cells)
responsible for long lasting protective immunity following reexposure to pathogen

195
Q

Why are memory cells faster ?

A

reactivated in an antigen specific manner
more quickly
lower threshold for activation

196
Q

What happens to B cells ?

A

they take up antigen and present To Tfh cells that are involved in B cell maturation
b cell activates and turns into plasma cell - secrete antibody

197
Q

What do B cells have on their surface ?

A

antibodies

198
Q

What are the cellular features of plasma cells ?

A

eccentric nucleus

excessive ER

199
Q

Which cells stimulate B cell maturation ?

A

Tfh cells

200
Q

What happens to antibodies during the immune response ?

A

undergo affinity maturation

isotype switching from igG to igM

201
Q

What are the fucntions of antibodies ?

A

activate complement
target bound antigen to other immune cells
neutralise toxins
prevent pathogens gaining entry to cells

202
Q

What is the N terminii on an antibody ?

A

amine group that forms antigen binding site

203
Q

What is the c terminii on the antibody ?

A

carboxylic acid group

204
Q

What does the hinge region on the antibody allow ?

A

flexibility

205
Q

What is the variable region of the antibody ?

A

unique to an antigen type

206
Q

What is the most abundant antibody in body fluids ?

A

igG

207
Q

Where is igG made ?

A

lymph nodes
bone marrow
spleen

208
Q

Where can igG get to ?

A

extracellular spaces and across placenta to protect developing embryo

209
Q

Which immunoglobulin has the most effector functions ?

A

igG

210
Q

What does the antibody class determine ?

A

the response

211
Q

How are antibodies divided into class ?

A

on the basis of heavy chain structure

212
Q

What is the first antibody produced in the immune response ?

A

igM

213
Q

Where is igM prodcued ?

A

lymph nodes
spleen
bone marrow

214
Q

What does igM do ?

A

circulates in blood and lymph

stimulates complement activation and phagocytosis

215
Q

What is the structure of igM ?

A

pentametric

multivalent - multiple binding sites

216
Q

What are the forms of igA ?

A

monomeric in the blood

dimeric in the tissues

217
Q

Where is igA found ?

A

gut
saliva
sweat
tears
mucosal immunity - protect agaisnt streptococci
can be made by GALT- tonsils and peyers patches

218
Q

What is the function of igE ?

A

binds to Fc receptors on mast cells
already bound
little circulating amounts- bound to Fc receptors

219
Q

What triggers mast cells ?

A

cross linking of antigen (pollen) on IgE on mast cells leads to degranulation and activation of innate immunity
increased blood flow
neutrophil migration
histamine released

220
Q

What does excessive activation of mast cells lead to ?

A

hypersensitivity

originally developed for parasitic protection

221
Q

What is clonal selection ?

A

lymphocytes present antigen to Tfh cell
maturation from B cell to plasma cell
clonal selection- plasma cells produced that make an antibody specific to that antigen

222
Q

How Ig diversity generated ?

A

many immunoglobulin genes in every B cell
3 loci for the heavy chain and 2 loci for the light chain
genes are randomly selected from loci
make different combinations
D and J genes also inserted

223
Q

What happens in the rearrangement of DNA in B cells ?

A

Each B cell has different rearrangement of D and j genes
combined with C genes
continuous sequences in the variable region
happens in heavy and light chains

224
Q

What is somatic recombination of DNA in B cells ?

A

random rearrangments of somatic DNA via VDJ recombinase

225
Q

What is VDJ recombinase ?

A

multi enzme complex evovled from DNA repair enzymes

226
Q

Which cells is RAG gene expressed in ?

A

lymphocytes

227
Q

What are the mechanisms of diverisity in VDJ genes ?

A

combinatroial and jucntional

228
Q

What is combinatorial diversity I ?

A

multiple genes which can be selected and combines together

229
Q

What is junctional diversity I ?

A

Imprecise cutting and pasting of nucletodies by VDJ recombinase

230
Q

What is junctional diversity II ?

A

addition of non germline nucleotides between D and J genes and V segments

231
Q

What is combinatorial diversity II ?

A

Assembly of the Ig molecule by heavy and light chains

232
Q

What is the order of change in immunoglobulin genes ?

A 
recombination of DNA somatically 
generation of junctional diversity
somatic hypermutation 
microevolution of affinity 
isotype switch
233
Q

What does somatic hypermutation allow ?

A

during successive immune responses introduces mutations that alter iG protein structure
allows higher affinity igG to be secreted

234
Q

What is the microevolution of affinity ?

A

increasing affinity for antigen provides better immune response
B cells that express high affinity igG survive
those that express low affinity igG die due to natural selection

235
Q

What is the isotype switch ?

A

from igM to igG

236
Q

What are the changes that occur to antibodies after repeated immunisations ?

A

increased quantity of antibody
increased affinity of antibody due to somatic hypermutation
isotype switch
produces better quality response

237
Q

What are memory cells ?

A

B cell sin lymph nodes develop into plasma cells and memory cells under the influence of cytokines from Tfh cells
memory cells remain in blood- provide more vigorous response next time

238
Q

Why are there variations in the immune system ?

A 
vaccination history 
malnourishment- affects immune system 
lifestlye factors- exercise and smoking 
hormonal status 
gut flora
early life events 
stress
239
Q

What is normal ageing assocaited with ?

A

reduction in functional reserve capacity

240
Q

What is the biological basis of ageing ?

A

random cellular damage
accumualtion of cellualr defects
age related frailty, disability and disease

241
Q

How can ageing be accelerated ?

A

accelerated by stress, poor diet and behaviour

242
Q

How can ageing be delayed ?

A

good diet
lifestyle
good environment

243
Q

Why are there decreased immune responses in the elderly ?

A

poor nutrition

244
Q

What happens in protein energy malnutrition ?

A

lack of dietary protein and macronutrients

seen in 10% of over 65

245
Q

What are some immune measures ?

A 
IL-1
IL-2
IL-6
Antibody production 
gut barrier fucntion 
all decreased in elderly with PEM
246
Q

What is the link between malnutrition and infection ?

A

undernutrition
diminished host defence
infection
bidirectional as infection amkes more malnourished

247
Q

How are nutrients lost in infection ?

A

anorexia
diarrhoea
impaired absorption
diarrhoea

248
Q

What do diarrhoea and intestinal damage cause ?

A

exaggerated inflammatory response

249
Q

What do EPA and DHA improve ?

A

rheumatoid arthrits
decrease prostaglandins
leads to less NSAID usage and improved clincal scrores

250
Q

What is reduced with B6 deficiency ?

A

IL-2 and lymphocytes

251
Q

What does zinc deficiency result in ?

A

reduced innate and acquired responses

increased susceptibility to viral and bacterial infections

252
Q

What does zinc deficiency result in ?

A

reduced T cell
reduced NK cells
reduced antibodies

253
Q

What can large amounts of zinc result in ?

A

copper deficiency
interference between copper and zinc uptake
can impair immune function

254
Q

What can zinc be beneficial in ?

A

periodontal health
pocketing
lower plaque and lower pocket depth

255
Q

What can micronutrient deficiencies do ?

A

make individual more susceptible to infection

256
Q

Does ageing have an effect on the immune system ?

A

ageing has less influence on the immune system

environmental factors have more of an effect on the immune system

257
Q

Nam 2 vascular changes responsible for inflammation ?

A

vascular dilation

increased blood flow

258
Q

What histological signs can you see in a tissue with lymphovytic infiltrate ?

A

densely stained cells with no shape or bounday

259
Q

What practical evidence is there that MMP mediated tissue distruction in periodontitis ?

A

Doxycycline and MMP inhibitor is used as an adjucnt treatment in RSI

260
Q

Give 2 examples of emerging human pathogens ?

A

ebola and HIV

261
Q

Give 2 examples of re emerginig human pathogens ?

A

TB and measles

262
Q

Give 2 examples of pathogens that have been eradicated ?

A

polio and small pox

263
Q

Why are there small numbers of effective viral vaccines ?

A

no economic imperative

antigenic variation due to mutation

264
Q

Which pathogen affects lesions due to burns and CF ?

A

pseudomonas aureginosa

265
Q

Which location has the majority of disease due to mucosal infection ?

A

lungs

266
Q

Which molecules stimulate neutrophil chemotaxis ?

A

complement

chemokines

267
Q

How is haematopoieses regulated ?

A

cytokines

bone marrow stromal cells

268
Q

Where does haemoatopoiesis take place ?

A

in bone marrow

269
Q

What are the 3 haemoatopoietic lineages ?

A

myeloid
lymphoid
erythroid

270
Q

Where do lymphatics drian into the blood circulation ?

A

thoracic duct into subclavian veins

271
Q

Which mucosal tissue protects mouth ?

A

salivary glands

272
Q

How do macrophages signalt to T cells ?

A

via cytokines like IFN gamma

273
Q

What is the shape of monocyte ?

A

kidney shaped nucleus

274
Q

What is the shape of lymphocyte ?

A

small and round nucleus

275
Q

Which part of the Ig molecule do phagocytes interact with ?

A

Fc region

276
Q

Which molecules mediate pathgoen destruction through neutrophils ?

A

ROS- NO
AMPs
lysozyme
protease

277
Q

Why dont we know much about basophils and eosinophils ?

A

few in circulation

278
Q

What are the 4 consequences of innate signalling- local and systemic ?

A

neutrophil chemotaxis
activation of adaptive immunity
vascular changes
systemic- acute phase response

279
Q

Which 3 compartments might you fins different PRRs ?

A

membrane bound- TL4
serum- mannose binding lectin
Endosome- TL3

280
Q

Which PRR recognises double stranded RNA and where can you find it ?

A

TLR3

virus

281
Q

Name an important TF activated in response to immune signalling ?

A

NF-kB

282
Q

Give examples of interferons ?

A

type I- IFN alpha and beta- released by virally infected cells

type II- IFN gamma released by NK cells

283
Q

Which cytokines allow Th1 cell development ?

A

IFN gamma and IL12

284
Q

Which cytokines allow Th2 cells to develop ?

A

IL4

285
Q

Which cytokines allow Th17 cells to develop ?

A

TGFB

286
Q

Which cytokines allow Tfh cell to develop ?

A

IL21

287
Q

Which cytokines allow iTreg development ?

A

TGFB

IL10

288
Q

Which transcription factor is needed for Th1 development ?

A

T-bet

289
Q

Which transcription factor is needed for Th2 development ?

A

GATA3

290
Q

Which transcription factor is needed for Th17 development ?

A

RORyt

291
Q

Which transcription factor is needed for Tfh development ?

A

Bcl 6

292
Q

Which transcription factor is needed for Treg cells ?

A

Foxp3

293
Q

What is the job of Th1 cells ?

A

activate macrophages via IFN gamma

target intracellular bacteria like

294
Q

What is the job of Th2 cells ?

A

activate mast cells, eosinophils and basophils
B cell actication
allergy

295
Q

What is the job of Th17 cells ?

A

reinforce innnate immunity with neutrophils

target extracellular bacteria

296
Q

What is the job of Tfh cells ?

A

B cell activation and maturation
help with isotype switching and affinity maturation
IgM to IgG

297
Q

What do Treg cells do ?

A

regulate immune response

lack of T cell activation

BDS stage 2 (28 decks)

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