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Immunology Flashcards

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1
Q

what are the 3 main functions of the immune system?

A

eliminate danger
without harming the body
remember the threat to respond more efficiently next time

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2
Q

what is the main purpose of the immune system?

A

eliminate a threat to our bodies health

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3
Q

what type of threat is usually eliminated by the immune system?

A

infection by a pathogen

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4
Q

define pathogen

A

a microorganism which causes disease to the host

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5
Q

what are the four main types of infectious microorganism?

A

bacteria
viruses
fungi
parasites

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6
Q

what are commensals?

A

non-harmful bacteria that live within or on the bodies of humans and animals

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7
Q

how do commensals protect us from pathogens?

A

using up lots of nutrients so there are fewer available for the bad bacteria to live off

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8
Q

What effect do products produced by commensal bacteria have on us?

A

good effect or none

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9
Q

does our immune system usually attack commensal microbes?

A

no

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10
Q

what do immune cells defend us from as well as infection?

A

cancer cells

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11
Q

what is the difference between a cancer cell and a normal body cell?

A

a cancer cell is a normal body cell that has accidentally acquired DNA mutations that make it go wrong

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12
Q

how does the immune system know to kill cancer cells if they are formed from self-cells?

A

as it is not functioning normally the immune system is able to recognise mistakes and kill it

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13
Q

what must the immune system do in order to eliminate threats?

A

use defences which could harm our own body

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14
Q

what must the immune system not do?

A

attack normal body tissues

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15
Q

what is immune recognition?

A

the ability of the immune system to distinguish self from non-self

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16
Q

what happens if immune response goes wrong and attacks normal body cells?

A

we get autoimmune disease

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17
Q

why are cancer cells treated as non-self?

A

they are not behaving normally and are dangerous to the body if not destroyed

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18
Q

what is immune effector function?

A

the ability to deal with infection and if possible eliminate it without harming our body in the process

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19
Q

why do we get symptoms of illness when we get an infection?

A

because it takes time for the immune system to recognise, respond and fight off the pathogen

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20
Q

what actually makes us unwell during an infection?

A

the toxic actions of the pathogen

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21
Q

what happens if we see the same immune threat twice?

A

the second time the immune system responds faster so it kills the threat before we get symptoms

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22
Q

define immune memory

A

the ability of the immune system to remember antigens from pathogens and mount and immune response of greater magnitude and with faster kinetics upon re-encounter of the same antigens

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23
Q

what are the 2 arms of the immune system?

A

innate and adaptive

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24
Q

which arm of the immune system is the first line of defence against pathogens?

A

innate immune system

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25
Q

what are the 2 functions of the innate immune system?

A

rapidly respond to slow down pathogenic threats

recruit adaptive immune cells

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26
Q

define innate immune system

A

a mixture of cells and barriers which act within minutes to slow down or limit microbial invasion and disease causing processes

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27
Q

is the innate immune system specific?

A

no

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28
Q

what is the more specific arm of the immune system?

A

adaptive

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29
Q

what is the adaptive immune system made up of?

A

cells and the antibodies produced by B lymphocytes

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30
Q

what are the cells of the adaptive immune system?

A

T cells and B lymphocytes

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31
Q

what are the functions of the adaptive immune system?

A

mount a highly specific defecnce against pathogens

rememeber the threat in case it is encountered again

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32
Q

define adaptive immune system

A

an immune response mediated by T and B lymphocytes which is highly specific to the pathogen that induced it and elimiminates disease-causing processes alongside the innate immune system

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33
Q

what allows lymphocytes to exert specialised functions tailored to specific pathogens?

A

they take longer to respond than innate immune cells but they are more specific

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34
Q

what cells stay in the body for a long time and are able to respond quicker upon re-encounter of the pathogen?

A

memory lymphocytes

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35
Q

do innate immune cells behave like memory lymphocytes?

A

no

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36
Q

what is one of the key differences between innate and adaptive immune responses?

A

their anatomical location

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37
Q

where are all immune cells made?

A

in the bone marrow

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38
Q

what cells are all immune cells formed from?

A

pluripotent haematopoetic stem cells

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39
Q

where do innate immune cells reside?

A

the peripheral tissues

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40
Q

where do adaptive immune cells reside?

A

at the central lymphoid tissues, the spleen and lymph nodes

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41
Q

where do B lymphocytes mature?

A

in the bone marrow

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42
Q

where do B lymphocytes travel to once mature?

A

the spleen and lymph nodes

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43
Q

where do T lymphocytes mature?

A

in the thymus

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44
Q

where do T lymphocytes travel to once mature?

A

the spleen and lymph nodes

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45
Q

what happens to B and T lymphocytes one in the spleen and lymph nodes?

A

they wait to be activated

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46
Q

what happens when infection is encountered in the body?

A

innate immunity kicks in and repsonds straight away, it sends portions of the pathogen to central lymphoid tissues for analysis by adaptive immune cells. It also kills the pathogen (tries!!)

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47
Q

where can immune cells enter the spleen and lymph nodes?

A

via the blood and lymphatic vessels

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48
Q

what happens when the pathogen is shown to the T and B lymphocytes by the innate immune system?

A

they become activated and mobilise to the infected tissue in order to join the immune defence

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49
Q

what is the importance of re-circulation of innate and adaptive immune cells from the infected tissues to the spleen and lymph nodes and back again?

A

makes a bridge between the innate and adaptive immune systems

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50
Q

describe the life of an immune cell

A

haematopoetic stem cell differentiates into immature/naïve immune cell in the bone marrow which then ‘lives’ in home tissue. it is activated if it comes into contact with a pathogen and so preforms effector function. One this has happened it becomes a memory cell, switches off or dies

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51
Q

what happens if an immune cell never meets an antigen?

A

it remains naive

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52
Q

where are immune cells made?

A

in the bone marrow

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53
Q

define haematopoetic precursor cells

A

stem cells which are capable of differentiating into red (oxygen carrying) and white (immune) cells

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54
Q

why do we always need a new supply of new immune cells in the bone marrow?

A

immune cells can be used up or die

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55
Q

why is there always a population of immune cells available?

A

the haematopoetic precursor self renews

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56
Q

when may immune cells be activated?

A

at any point in the person/animals life when they meet their specific pathogen

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57
Q

describe the timeline of an immune response

A

infection, innate immunity, innate and adaptive immunity, elimination of pathogen, healing, immune memory

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58
Q

when does innate immunity occur?

A

0-5 days after meeting the pathogen

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59
Q

when does innate and adaptive immunity occur?

A

5 days- weeks after meeting pathogen depending on the severity ofinfection

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60
Q

within what time frame does elimination of pathogen occur?

A

weeks after meeting pathogen

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61
Q

how long does immune memory last?

A

months-years, potentially entire life

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62
Q

are immune responses to different pathogens the same?

A

no - immune responses to different pathogens are varied and helped by different specialised cell types

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63
Q

what do cytokines do?

A

help immune cells to communicate and tell each other what type of pathogen they are facing and what responses are needed

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64
Q

define cytokines

A

small secreted proteins released by immune cells, which allow them to interact and communicate

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65
Q

what do interferons do?

A

induce cells to resist viral replication

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66
Q

what are interlukins?

A

cytokines produced by WBC which have many different functions

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67
Q

what are chemokines?

A

cytokines that tell immune cells where to go

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68
Q

what must happen to innate and adaptive immune cells before they can start work?

A

they must be activated

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69
Q

what does it mean when innate and adaptive immune cells are activated?

A

they detect the presence of something not self and switch on

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70
Q

what do innate and adaptive immune cells respond to in order to be activated?

A

different receptors

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71
Q

what receptors does the innate immune system respond to?

A

protein recognition receptors (PRRs)

FC receptors

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72
Q

what receptors does the adaptive immune system respond to?

A

T and B cell receptors

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73
Q

what do pattern recognition receptors do?

A

bind PAMPs and DAMPs

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74
Q

what do FC receptors do?

A

bind antibodies

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75
Q

what do T and B cell receptors do?

A

bind antigen epitopes presented on MHC on the surface of antigen presenting cells

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76
Q

What are PRRs?

A

pattern recognition receptors which bind general bits/building blocks of cells called PAMPs and DAMPs

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77
Q

what are PAMPs?

A

pathogen associated molecular patterns that are fragments of pathogen capable of ligating PRRs on innate immune cells

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78
Q

what are DAMPs?

A

damage associated molecular patterns that are fragments of damaged self-cells capable of ligating PRRs on innate immune cells

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79
Q

give an example of a PAMP

A

bacterial flagella

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80
Q

give an example of a DAMP

A

HMGB-1, attached to DNA but released when cells die

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81
Q

do PAMPs and DAMPs give detailed information about the pathogen?

A

no - the innate immune response is very general

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82
Q

what other receptors do innate immune cells have on their surface?

A

receptors for antibodies

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83
Q

what are Fc receptors?

A

antibody receptors on the surface of immune cells

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84
Q

what is the effect of antibody receptors on the innate immune system?

A

triggers/encourages it to keep working

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85
Q

what are antibodies?

A

proteins secreted by B cells of the adaptive immune system which bind antigens to mediate pathogen destruction and to enhance the innate immune response

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86
Q

through what cells does the adaptive immune system respond?

A

T and B cell receptors

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87
Q

what do T and B cell receptors bind to?

A

epitopes

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88
Q

what are epitopes?

A

a short peptide sequence which is part of an antigenic protein

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89
Q

define antigen

A

a protein which is capable of initiating an immune response

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90
Q

why does the adaptive immune system get much more information than the innate immune system about the nature of an infectious threat?

A

because epitopes are so specific

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91
Q

how many epitopes are located on each lymphocyte?

A

1 they are specific for an epitope

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92
Q

what happens to lymphocytes when pathogens with their specific epitope are delivered by the innate immune system?

A

they begin to replicate

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93
Q

how can the delay between infection and adaptive immune response be explained?

A

massive cell multiplication of the lymphocyte with the specific epitope receptor must take place which takes time

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94
Q

why will multiple lymphocytes respond to a pathogen?

A

there are several antigens on each pathogen

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95
Q

when will T and B cells only recognise antigens and cause lymphocytes to divide?

A

after they have been chopped up into epitopes and presented by ‘antigen presenting cells’ APCs

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96
Q

what do innate immune cells respond to via pattern recognition receptors (PRRs)?

A

pathogen associated molecular patterns (PAMPs) and damage associated molecular proteins (DAMPs)

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97
Q

what do adaptive immune cells respond to via T and B cells?

A

epitopes presented on MHC by antigen presenting cells

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98
Q

where are cells of the innate immune system located?

A

around sites where infections commonly arise (e.g. lungs, GI tract)

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99
Q

why are there limited numbers of PAMPs and DAMPs?

A

they are common to many pathogens so there does not need to be a diverse range of cells

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100
Q

how quickly does the innate immune system respond to infection?

A

rapidly aided by it’s location and speed

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101
Q

what are the main components of the innate immune system?

A

cellular and non cellular

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102
Q

what are the 4 main non cellular components of the innate immune system?

A

physical barriers
chemical substances
microbiological
complement

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103
Q

what are the physical barriers of the innate immune system?

A

epithelial tight junctions

mucous or fluid flow

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104
Q

what are the chemical barriers of the innate immune system?

A

enzymes
acid
microbial peptides

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105
Q

what are the microbiological barriers of the innate immune system?

A

commensals

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106
Q

what are the complement barriers of the innate immune system?

A

a protein cascade which helps the immune system destroy pathogens

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107
Q

what are the cellular barriers of the innate immune system?

A

phagocytes
granulocytes
antigen presenting cells (APC)

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108
Q

how do epithelial cells joined by tight junctions defend against infection?

A

the body needs to be open in order for pathogens to enter. Epithelial cells at susceptible surfaces are joined by tight cell to cell connections that don’t allow pathogens through

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109
Q

how does mucous and fluid flow defend against infection?

A

mucous traps pathogens, cilia wave the mucous out of the body before pathogens can attach and divide. Flow of air, urine or ingesta keep pathogens moving through the body

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110
Q

how does low pH and acids defend against infection?

A

acidic conditions kill pathogens, stomach pH is 3.5 and omega 3 and 6 fatty acids on the skin protect against bacterial infection and enhance killing action of innate immune system

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111
Q

how do enzymes defend against infection?

A

directly kill pathogens or make them susceptible to other forms of killing (low pH)

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112
Q

what are antimicrobial peptides?

A

chemicals which are generally toxic to many different pathogens (bacteria/viruses and parasites)

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113
Q

how do commensals protect against infection?

A

occupy space in the body using nutrients and preventing harmful bacteria from establishing

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114
Q

how does a protein cascade prevent/fight infection?

A

presence of pathogen activates the first protein kicking of the cascade, the end of which leads to proteins which mark pathogens out for destruction and directly destroy pathogens by making a pore in the membrane

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115
Q

define commensals

A

non-harmful bacteria that live within or on the bodies of humans and animals

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116
Q

define competitive exclusion

A

the mechanism by which commensal micro-organisms defend against pathogens by competing for attachment sites and nutrients

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117
Q

what are the 4 main roles of innate immune cells?

A

phagocytosis
degranulation
antigen presentation
antibody dependent cellular cytotoxicity (ADCC)

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118
Q

what process assists phagocytosis and degranulation by dendritic cells?

A

opsonisation

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119
Q

what is phagocytosis?

A

the process of internalisation of large particles by phagocytic cells

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120
Q

what happens during phagocytosis?

A

matter is internalised via formation of membrane pockets called phagosomes. These form with lysosomes to digest pathogenic matter

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121
Q

what do lysosomes contain?

A

toxic acids, reactive organ species, antimicrobial peptide and enzymes

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122
Q

what is degranulation?

A

release of toxic granules to destroy a pathogen

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123
Q

what does the toxic contents of degranulation granules cause?

A

pathogen killing

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124
Q

what do basophils and eosinophils do during degranulation?

A

spit out granules in the immune system in response to pathogens

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125
Q

what do neutrophils do during degranulation?

A

have granules and destroy bacteria or virally infected self cells

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126
Q

what must happen before an innate cell will degenerate?

A

needs to be stimulated by engagement of Fc receptors on innate cell surface by antibody or inflammatory mediators such as histamine in the local environment

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127
Q

what do mast cell granules contain?

A

histamine which activates eosinophils to release own granules

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128
Q

when do allergies occur?

A

when eosinophils, basophils and mast cells mistakenly degranulate in response to an allergen

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129
Q

define allergen

A

a non-pathogenic molecule which should be ignored by the body but initiates an immune response instead

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130
Q

define opsonisation

A

the process by which molecules called opsonins stick to a pathogen and mark it out for degradation

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131
Q

what are the main opsonins?

A

antibodies
Fc receptors on innate cells binding to antibody stuck on the pathogen
complement receptors bind to a complement stuck on the pathogen

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132
Q

what is a complement?

A

a system of inflammatory proteins produced in the presence of a pathogenic threat

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133
Q

what does binding of opsonins to innate immune cells cause?

A

them to degranulate or phagocytose pathogens more effectively

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134
Q

what is antigen presentation?

A

processing and presentation of antigens to activate adaptive immune cells

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135
Q

what are dendritic cells?

A

innate immune cells which take in bits of pathogen, chop it up and present peptides (epitopes) from it to activate T and B cells

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136
Q

what is antibody dependent cellular cytoxicity (ADCC)?

A

specialised killing of virally infected or cancerous self cells by NK-cells, initiated by antibody Fc-receptor binding

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137
Q

how does ADCC differ from opsonisation?

A

self-cell rather than pathogen target

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138
Q

how do antibodies help destruction of virally infected or cancerous self cells?

A

notice self cells have gone wrong so stick to them, which marks the cells out as defective and needing to be destroyed. NK-cells bind via Fc-receptors to antibodies on the surface of the affected cell and activates NK-cells to degranulate and kill them

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139
Q

how is a dendritic cell activated?

A

PRRs bind to PAMPs and DAMPs

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140
Q

what is the function of dendritic cells?

A

combat viruses and bacteria
specialise in antigen presentation to activate T cells
release cytokines to tune the correct type of immune response

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141
Q

how are macrophages activated?

A

PRRs bind to PAMPs and DAMPs

Fc receptors bind antibodies

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142
Q

what is the function of macrophages?

A

combat extracellular bacteria
efficient at phagocytosis
antigen presentation to activate lymphocytes
cytokine release

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143
Q

how are neutrophils activated?

A

Fc receptors bind antibody (IgG)

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144
Q

what is the function of neutrophils?

A

‘first responder’ to site of inflammation
combat virus, parasites and both intra and extra cellular bacteria
phagocytosis
degranulation

145
Q

how are eosinophils activated?

A

Fc receptors to bind antibody (IgE)

146
Q

what responses are eosinophils most involved with?

A

anti-parasite responses
inappropriate responses can cause allergy/asthma
degranulation

147
Q

how are mast cells activated?

A

Fc receptors to bind antibody (IgE)

148
Q

what is the function of mast cells?

A

anti-parasite responses
inappropriate responses can cause allergy/asthma
degranulation containing histamine to enhance the innate response

149
Q

how are basophils activated?

A

Fc receptors to bind antibody (IgE)

150
Q

what is the function of basophils?

A

degranulation

151
Q

how are NK (natural killer) cells activated?

A

NK receptor
Fc receptors (ADCC)
lack of MHC-I (shows that a cell is damaged e.g. cancerous)

152
Q

what is the function of NK cells?

A

anti-viral and anti-tumor responses (responds to self cell gone wrong)
degranulation triggered via ADCC

153
Q

Where do adaptive immune cells reside?

A

in lymphoid tissues so they have to mobilise to the sight of infection

154
Q

what sort of recognition does the adaptive immune system use?

A

sequence specific

155
Q

What does each T and B cell have that is unique?

A

receptor with responds to an epitope (part of the antigen)

156
Q

what is the antigen that a T and B cell receptor binds to called?

A

cognate antigen

157
Q

what are the only lymphocytes that are activated in an immune response?

A

only those with receptors that recognise the pathogenic threat

158
Q

define antigen

A

protein which is capable of initiating an immune response

159
Q

what are the pieces of antigen presented to lymphocytes by?

A

antigen presenting cells

160
Q

define epitope

A

a short peptide sequence making up the processed part of an antigen that can bind to lymphocyte receptors

161
Q

what are B cell and T cell receptors more specific than?

A

pattern recognition generators expressed on innate immune cells

162
Q

when does the adaptive immune response kick in?

A

about 5 days after the innate immune response

163
Q

why is the length of time taken for the adaptive immune system to work needed?

A

because of the location of the cells and specificity of response

164
Q

where must adaptive immune cells travel to the site of infection from?

A

spleen and lymph nodes

165
Q

why do adaptive immune cells take time to multiply?

A

as they are highly specific there is only 1 or 2 that can respond to a specific pathogen, once they are presented with the epitope they then must vastly replicate in order to have enough cells to pass off the infection

166
Q

what cells is the adaptive immune system composed of?

A

B and T lymphocytes

167
Q

what are the 2 main functions of B lymphocytes?

A

produce antibodies during the immune response

memory B cells remain in the body for a long time and will divide and produce antibodies if the pathogen comes back

168
Q

what are plasma cells?

A

activated B cells which produce antibodies

169
Q

define antibodies

A

secreted proteins which facilitate immune neutralisation of pathogens by binding to antigens expressed on the pathogen or it’s products

170
Q

how are antibodies found in the body?

A

secreted by B cells

stuck on the surface of a B cell

171
Q

what is the function of antibodies produced by B cells?

A

neutralisation of pathogens

172
Q

what do antibodies on the surface of B cells do?

A

activate B cells

173
Q

what are antibodies on the surface of B cells known as?

A

the B cell receptor

174
Q

what shape proteins are antibodies?

A

Y

175
Q

what are antibodies made up of?

A

two heavy chains and two light chains stuck together

176
Q

what are antibodies also known as?

A

immunoglobulins

177
Q

what do the ends of the heavy and light chains from?

A

antigen binding region

178
Q

what is the antigen binding region known as?

A

variable region

179
Q

why are there a vast number of different variable regions?

A

to bind to all the different possible epitopes

180
Q

what happens if the epitope shape doesn’t match the antibody binding site (variable region)?

A

it wont fit

181
Q

what part of the heavy and light chains of the antibodies forms the constant region?

A

backbone

182
Q

what does the constant region of an antibody provide to the variable regions?

A

scaffold for the variable regions to sit on

183
Q

how many constant region chains of antibodies are there?

A

5

184
Q

what does each different constant region chain of antibodies determine?

A

how the immune system responds to the pathogen

185
Q

what is the constant region chain named by?

A

the greek letter which matches the antibody isotype

186
Q

what are the 5 different antibody isotypes?

A 
IgM
IgG
IgA
IgE
IgD
187
Q

what is the IgM constant chain formed from?

A

Mu

188
Q

what is the function of IgM?

A

first antibody produced after antigen invasion

general, transient defence until B cell switches to a more appropriate antibody for the pathogen

189
Q

what is the structure of IgM?

A

forms a pentamer (5 IgM joined together)

190
Q

what is the IgG constant chain formed from?

A

gamma

191
Q

what is the function of IgG?

A

the best antibody for opsinisation and neutralisation

attacks pathogens such as viruses and intracellular bacteria

192
Q

what is the structure of IgG?

A

monomer

193
Q

what is the IgA constant chain formed from?

A

alpha

194
Q

what is the function of IgA?

A

immunity at mucosal surfaces (e.g resp or GI tract)

195
Q

what is the structure of IgA?

A 
a monomer in tissue fluid and blood
a dimer (2 IgA joined) in mucosal secretions
196
Q

what is the constant chain of IgE formed from?

A

eta

197
Q

what is the function of IgE?

A

induces mast cell and basophil degranulation in response to parasites

involved in allergy response

198
Q

what is the structure of IgE?

A

monomer

199
Q

what is the IgD constant chain formed from?

A

delta

200
Q

what is the function of IgD?

A

unknown

201
Q

where is IgD found?

A

naive B cells before activation

202
Q

what structure is IgD?

A

monomer

203
Q

where are B cells activated?

A

lymph nodes

spleen

204
Q

where are lymph nodes found?

A

junctions between lymphatic vessels

205
Q

what do lymphatic vessels do?

A

collect fluid and cells from tissues and deliver to the lymph nodes

206
Q

what are the 2 main parts of the lymph node?

A

cortex and medulla

207
Q

where do B cells go in the spleen once they meet their specific antigen?

A

areas of the cortex known as germinal centres

208
Q

what happens to B cells in germinal centres?

A

under go intense proliferation to generate clone B cells which respond to the same antigen

209
Q

what do CD4+T helper cells do to aid B cell proliferation?

A

localise to paracortical areas where they produce chemicals which assist proliferation

210
Q

what is found in the white pulp of the spleen?

A

lymphocytes, germinal centres and nearby areas for CD4+T helper cells

211
Q

how is the spleen supplied with innate immune cells bearing antigens?

A

blood supply rather than lymphatic vessels

212
Q

what is the role of the red pulp of the spleen?

A

collection and disposal of old RBC

213
Q

what happens when an epitope is shown to a B cell by an antigen presenting cell?

A

ligates the IgM B cell receptor binding site and triggers B cell activation

214
Q

What happens to B cells after activation?

A

divide at germinal centres and the become either antibody producing cells or memory B cells

215
Q

what is a plasma cell?

A

antibody excreting effector B cell

216
Q

What isotype is found in the blood during early immune response?

A

IgM

217
Q

when does isotype switching occur?

A

after the B cell is stimulated by an antigen

218
Q

define isotype switching

A

the rearrangement of genes which code for antibody proteins, to achieve the production of a different class of antibody

219
Q

how does the B cell undergo isotype switching?

A

after studying the protein the cell decides to make a different antibody for the pathogen
it rearranges the isotype DNA template to produce a different constant protein region

220
Q

where do T cells originate from?

A

like B cells, the bone marrow from the common haematopoetic precursor

221
Q

where do T cells mature?

A

the thymus

222
Q

what cells are deleted during thymic development of T cells?

A

those T cells which have receptors specific for antigens expressed on normal body self-cells

223
Q

what is a positive effect of having no self-reactive cells within the body?

A

T cells cannot attack the body

224
Q

define immune tolerance

A

the process by which immune cells prevent attack of self tissues

225
Q

what is tolerance during T cell development known as?

A

central tolerance

226
Q

why is tolerance during T cell development known as central tolerance?

A

happens in the thymus

227
Q

where do mature T cells go once leaving the thymus?

A

to spleen and lymph nodes to be activated by engagement of their T cell receptor

228
Q

what family do T cell receptors belong to?

A

immunoglobulins

229
Q

how many chains do T cell receptors have?

A

2

230
Q

what are the names of the two T cell receptor chains?

A

alpha and beta

231
Q

what are the main sections found on a T cell receptor?

A

variable binding region and a constant backbone (similar to antibodies)

232
Q

how many constant regions are found in T cell receptors?

A

one

233
Q

what must happen in order for the T cell to become activated?

A

the T cell receptor must bind to the cognate antigen presented by the antigen presenting cells (e.g. dendritic cells)

234
Q

what are the names of the co-receptors expressed by mature T cells?

A

CD4 and CD8

235
Q

what is expressed alongside T cell receptor on the T cell to help it bind strongly to the antigen?

A

either CD4 or CD8 (never together)

236
Q

do CD4+T cells and CD8+T cells have different functions?

A

yes

237
Q

where does T cell activation occur?

A

at the spleen and lymph nodes

238
Q

what does T cell activation require?

A

3 signals

239
Q

what are the 3 signals required for T cell activation?

A

binding of T cell receptors to epitopes of antigens presented on the surface of antigen presenting cells
co-stimulation through CD80/86 and CD28
cytokines which tell the T cell about the most appropriate response

240
Q

how are epitopes of antigens presented on antigen presenting cells?

A

by MHC (major histocompatibility complex) molecules on the surface of antigen presenting cells

241
Q

what are MHC (major histocompatibility complex) molecules?

A

glycoproteins that are expressed on the surface of cells and which display peptide antigens

242
Q

what are the types of MHC that can be expressed by antigen presenting cells?

A 
MHC class 1 (MHC-1)
MHC class 2 (MHC-2)
243
Q

where is antigen presented on MHC-1 from?

A

within the cell

244
Q

how are antigens presented on MHC-1 receptors on the outside of the cell?

A

antigen sticks to MHC-1 in the endoplasmic reticulum and is then taken to the surface

245
Q

where is antigen presented on MHC-2 from?

A

outside the cell

246
Q

how are antigens presented on MHC-2 receptors from outside the cell?

A

antigen sticks to MHC-2 in endocytotic vesicles and is taken to the surface

247
Q

what are the most efficient antigen presenting cells?

A

dendritic cells

248
Q

what other cells can act as antigen presenting cells?

A

B cells and macrophages

249
Q

what MHC do CD4+T cells recognise?

A

antigen on MHC-2

250
Q

what type of pathogen are CD4+T activated to combat?

A

extracellular pathogens

251
Q

how do CD4+T combat extracellular proteins?

A

offering helpful signals and cytokines to innate cells and B cells

252
Q

what do CD8+T cells recognise?

A

antigen on MHC-1

253
Q

what are CD8+T activated to do?

A

combat intracellular pathogens such as viruses and cancer

254
Q

how do CD8+T combat intracellular pathogens?

A

finding affected self-cells and killing them

255
Q

what is the key point of co-stimulation through CD80/86?

A

helps the T cell to ensure the antigen presented by dendritic cells is definitely dangerous

256
Q

what could T cell activation without a genuine pathogenic threat lead to?

A

destruction of normal body cells and autoimmunity

257
Q

what do PAMPs and DAMPs in the environment cause when there is pathogen present?

A

activation of dendritic cells which upregulate co-stimulatory receptors (CD80/86)

258
Q

what is the name of the co-stimulatory receptors that are upregulated by dendritic cells?

A

CD80/86

259
Q

what does CD80/86 bind to?

A

CD28 on T cells

260
Q

what does the binding of CD80/86 to CD28 on T cells do?

A

Tells T cell that there is a genuine threat and it should be activated

261
Q

what will activation of a T cell without CD80/86 cause?

A

no ligation of CD28 which will cause T cells to switch off and become tolerant

262
Q

what is tolerance due to lack of signals (CD80/86) at activation a form of?

A

peripheral tolerance

263
Q

define peripheral immune tolerance

A

immune tolerance that develops outside the thymus

264
Q

when do antigen presenting cells produce cytokines?

A

during T cell activation

265
Q

what is the cytokine required for the T cell to start dividing and making clones.

A

IL-2

266
Q

what are the broad roles of cytokines?

A

tell the T cell which kind of pathogen it is responding to

267
Q

if a strong signal 1, 2 and 3 is present what will happen?

A

the T cell will be successfully activated

268
Q

what is the function of CD8T cells?

A

kill compromised self cells

269
Q

what cells is MHC-2 expressed on?

A

professional antigen presenting immune cells

270
Q

what cells is MHC-1 expressed on?

A

all body cells (e.g. epithelium and stroma)

271
Q

what type of molecule is presented on all cell surfaces by MHC-1?

A

peptide

272
Q

what do the peptides presented on cell surfaces by MHC-1 show?

A

that they are either functioning normally or that cells are infected and have become cancerous

273
Q

what will a healthy self cell present on MHC-1?

A

self-antigens and so be ignored by the immune system

274
Q

where does CD8+ T cell activation occur?

A

the lymph node

275
Q

what is CD8+ T cell activation also known as?

A

priming

276
Q

how many times will CD8+ T cells encounter MHC-1 in their life?

A

twice

277
Q

what is happening during the first exposure of CD8+ T cells to MHC-1?

A

activation

278
Q

what happens during priming of CD8+ T cells in the lymph node?

A

a naive CD8+ T cell sees epitopes of viral peptides presented on MHC-1 by dendritic cells

279
Q

what does interaction of a naive CD8+ T cell with its antigen for the first time trigger?

A

activation and proliferation of CD8+ T cell

280
Q

what happens if the CD8+ T cell receptor is specific for the epitope presented?

A

will bind and receive signal 1

281
Q

what happens with CD8+ T cells to cause killing at the tissues?

A

an activated CD8+ T cell sees epitopes of viral peptides presented on MHC-1 by infected target cells

282
Q

describe how an activated CD8+ T cell performs it’s effector function

A

activated CD8+ T cell binds to epitope MHC on the target cell
T cell only requires signal 1 (T cell receptor engagement by epitope) to activate as it is not naive
CD8+ T cells kill by releasing toxic granules at the target cell
once one cell is hit the CD8+ T cells leave to go onto the next

283
Q

what does engagement of T cell receptor of a previously activated T cell trigger?

A

killing rather than activation and proliferation

284
Q

what do the toxic granules released by CD8+ T cells contain?

A

perforin and granzyme

285
Q

what is the function of perforin?

A

pore forming - makes holes in target cell membrane

286
Q

what is the function of granzyme?

A

protein which causes apoptosis when it enters the cell through the pore created by perforin

287
Q

what is the function of CD4+ T cells?

A

coordinate the immune response

288
Q

what are CD4+ T cells often known as?

A

T helper cells

289
Q

when are cytokines released?

A

by innate immune cells at the beginning of the immune response, dendritic cells then carry on producing cytokines when they travel to the lymph node and present pathogenic epitopes

290
Q

when does CD4+ T cell priming occur?

A

when their T cell receptor sees it’s specific epitope presented on MHC-2 by dendritic cells at the lymph node

291
Q

what are CD4+ cells known as before they are activated?

A

Th0 cells

292
Q

what signals do CD4+ T cells receive during activation?

A

signal 1,2 and 3 from dendritic cells

293
Q

what do signals 1, 2 and 3 involve during activation of T cells?

A

1 - TCR engagement
2 - co-stimulation through CD80/86
3 - cytokines

294
Q

what do signal 3 cytokines tell the Th0 cell?

A

about the type of immune response required by different pathogens

295
Q

what do cytokines cause in Th0 cells?

A

them to differentiate into a specialised T helper phenotype

296
Q

what are the 4 main T helper cell phenotypes?

A

T helper 1 cells (Th1)
T helper 2 cells (Th2)
T helper 17 cells (Th17)
Treg

297
Q

what is the role of T helper 1 cells (Th1)?

A

help with responses to intracellular pathogens

298
Q

what is the role of T helper 2 cells (Th2)?

A

help with responses to extracellular pathogens

299
Q

what is the role of T helper 17 cells (Th17)?

A

help with fungi and bacteria that Th2 cannot manage

300
Q

what are Tregs?

A

a group of T lymphocytes which help to reduce or switch off immune responses when they are no longer needed, or when they are mistakenly directed at healthy cells

301
Q

what are Tregs a component of?

A

peripheral immune tolerance

302
Q

what happens to CD4+ T cells after priming?

A

divide to form a clone

303
Q

what happens once CD4+ T cells go elsewhere to produce more cytokines?

A 
support B cells at the germinal centre and tell them what antibody class to produce
support effector cells at the tissue and tell them to kill more effectively
304
Q

what do CD4+ T cells do once the pathogen has gone?

A

produce regulatory cytokines to switch off the immune response

305
Q

what is the role of IL-2?

A

makes T cells proliferate

306
Q

what is the role of IFN-gamma?

A

helps the Th1 immune response (involves killing of viruses and cancer)

307
Q

what is the role of IL-4?

A

helps Th2 responses (allergy and parasite infection)

308
Q

what is the role of IL-10 and TGF-beta?

A

produced by regulatory immune cells to switch off the immune response

309
Q

what is the role of chemokines?

A

circulate all around the body telling immune cells which tissue to go to (show where pathogen is)

310
Q

what cytokines induce Th1?

A

IFN-gamma

311
Q

what cytokines induce Th2?

A

IL-4

312
Q

what cytokines induce Th17?

A

TGF-beta and IL-6

313
Q

what cytokines induce Tregs?

A

TGf-beta and IL-10

314
Q

what cytokines does Th1 produce?

A

IL-2 (T cell proliferation)

IFN-gamma (support immune effector functions)

315
Q

what cytokines does Th2 produce?

A

IL-4 (B cell division and switch to IgE in germinal centre)

IL-5 (B cell division and switch to IgA in germinal centre)

316
Q

what cytokines does Th17 produce?

A

IL-17

317
Q

what cytokines does Tregs produce?

A

IL-10, TGf-beta, IL-35

318
Q

what cells are involved in Th1 immune responses?

A

innate - neutrophils, macrophages and NK cells

adaptive - CD8+ T cells

319
Q

what cells are involved in Th2 immune responses?

A

innate - neutrophils, eosinophils, basophils and macrophages

adaptive - B cells

320
Q

define immune memory

A

the ability of the immune system to remember antigens from pathogens and mount an immune response of greater magnitude with faster kinetics upon re-encounter of the same antigens

321
Q

what does vaccination involve?

A

showing a piece of the pathogen, or dead or inactivated pathogen, to the immune system in order to generate a primary immune response and an associated memory response

322
Q

what part of vaccination stops you from getting symptoms when exposed to the pathogen again?

A

immune memory response generated by the vaccine

323
Q

what processes prevent our immune system from attacking healthy self tissues?

A

immune tolerance

324
Q

what are the 2 types of immune tolerance?

A

central tolerance

peripheral tolerance

325
Q

when does central tolerance occur?

A

during T cell development in the thymus

326
Q

what happens in central tolerance during T cell development?

A

T cells which have receptors specific for antigens expressed on normal, healthy self cells are identified, those that react strongly to self-tissues are deleted

327
Q

what happens if there are no self reactive cells in the T cell repertoire?

A

none of our T cell responses will be directed at healthy self tissues

328
Q

what is peripheral tolerance?

A

immune tolerance that occurs in peripheral body tissues outside the thalamus

329
Q

when do peripheral tolerance mechanisms occur?

A

during the T cells lifetime not during development

330
Q

what are the main mechanisms of peripheral tolerance?

A 
lack of signal 2 and 3 during T cell activation
regulatory cells (Tregs)
331
Q

what type of cells are allowed to leave the thymus during central tolerance?

A

non self-reactive T cells and weakly self-reactive T cells

332
Q

why are weakly reactive self cells useful?

A

help in destruction of infected self cells

333
Q

what conditions must be met for a weakly self-reactive self cell to activate?

A

strong signal 2 and 3 from dendritic cells

334
Q

under what conditions will dendritic cells provide strong signal 2 and 3?

A

detection of PAMPs and DAMPs

335
Q

what is anergy?

A

T cell receptor binds to antigen presented on a dendritic cell (signal 1) without co-stimulation (signal 2) or stimulating cytokines (signal 3) the T cell then switches off instead of becoming activated.

336
Q

where are Tregs produced?

A

some in the thymus, others differentiate from CD4+Th0 cells

337
Q

what do Tregs do?

A

produce cytokines (e.g. IL-10 and TGF-beta) to switch off immune responses

338
Q

when do autoimmune diseases occur?

A

when immune tolerance is broken

339
Q

define autoimmune disease

A

clinical syndromes caused by a break in immune tolerance permitting immune responses directed at healthy self-tissues

340
Q

give 4 examples of autoimmune disease

A

type 1 diabetes
multiple sclerosis
immune mediated polyarthritis (IMPA)
auto-immune uveitis

341
Q

what normal immune response is an autoimmune response similar to?

A

Th-1 anti-viral response

342
Q

define hypersensitivity reactions

A

group of excessive immune responses to (usually harmless) molecules

343
Q

what are the 4 types of hypersensitivity reaction?

A

type 1: immediate hypersensitivity
type 2: antibody mediated hypersensitivity
type 3: antibody-antigen complex
type 4: delayed type hypersensitivity

344
Q

what are hypersensitivity types 1-3 driven by?

A

antibodies

345
Q

what cells is hypersensitivity type 4 driven by?

A

driven by T cells

346
Q

what can type 1 hypersensitivity be likened to?

A

an inappropriate Th2 response

347
Q

define allergen

A

a harmless molecule which should be ignored by the immune system but which initiates a allergic immune response in some individuals

348
Q

why is the response mild the first time the body meets an allergen?

A

because B cell differentiation to plasma cells and class switching to produce IgE in response to the allergen is not yet efficient

349
Q

what happens the second time a body meets an allergen?

A

memory B cells rapidly activate and produce large amounts of IgE, which produces an aggressive immune response

350
Q

what causes the itching, mucous production and vasodilation associated with an allergic response?

A

mediators in granules produced by mast cells eosinophils and basophils act on different aspects of the tissues

351
Q

when does anaphylaxis occur?

A

when the animal has a systemic allergic reaction

352
Q

what are the most common clinical signs of anaphylaxis?

A

itching, hives, swollen face, excessive salivation, vomiting, diarrhoea, difficulty breathing and cyanosis

353
Q

what happens during type 2 hypersensitivity?

A

free floating IgM and IgG antibodies bind to a tissue and cause recruitment and activation of neutrophils and macrophages

354
Q

what happens during type 3 hypersensitivity?

A

IgM/IgG antibodies bind to circulating antigen and form immune complexes which circulate in the blood. Causes recruitment and activation of neutrophils and macrophages.

355
Q

what happens during type 4 hypersensitivity?

A

CD4T cell produce cytokines that activate macrophages. CD8T cells direct killing granules at healthy self cells

356
Q

what is a clinical example of immediate (type 1) hypersensitivity?

A

seasonal allergies/ flea allergic dermatitis

357
Q

what is a clinical example of antibody mediated (type 2) hypersensitivity?

A

blood transfusion reaction (antibodies against donor cells)

358
Q

what is a clinical example of antigen-antibody immune complex mediated (type 3) hypersensitivity?

A

complexes tend to get stuck in glomerulus, joints or small blood vessel walls. Causes things refurred to as ‘autoimmune disease’

359
Q

what is a clinical example of delayed (type 4) hypersensitivity?

A

contact sensitivity

X Pre Clinical Science (17 decks)

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