Immunology Flashcards

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1
Q

What are the two components that make up the immune system?

A

cellular and soluble

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2
Q

What cells are in the cellular component?

A
neutrophils
monocytes
macrophages
eosinophils
basophils
mast cells
t lymphocytes
B lymphocytes
natural killer cell
(9)
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3
Q

what type of cells are all the cells in the cellular component?

A

white blood cells (or originate from white blood cells)

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4
Q

what stem cell do all white blood cells come from?

A

haematopoietic pluripotent stem cell

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5
Q

What is the role of a neutrophil?

A

phagocytic, engulf and destroy bacteria

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6
Q

how many types of granules are in a neutrophil?

A

3

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7
Q

describe the primary granules’ role and what they contain

A

role: antibacterial, digest by combining with the phagosome
contain: lysosomes, acid hydrolases, defensins, superoxides, complement receptors.

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8
Q

what do superoxides do that assists break down of bacteria?

A

covert h2o2 to .oh which is a free radical which is toxic

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9
Q

what do defensins do that assists break down of bacteria?

A

insert into membranes of bacteria so killing it

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10
Q

describe the secondary granules’ role and what they contain

A

role: regulate inflammatory response
contain: lactoferrin and lysozyme

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11
Q

describe the tertiary granules’ role and what they contain

A

role: facilitate insertion of proteins into cell membrane of bacteria

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12
Q

describe the neutrophil nucleus

A

nucleus is multi lobar (2-5 lobes)

nuetrophils are polymorphonuclear leukocytes

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13
Q

What is the role of a monocyte?

A

remove foreign or dead madterial by phagocytosis.

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14
Q

how are monocytes important for both innate and adaptive immunity?

A

phagocytic - innate

antigen presenting cells- adaptive

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15
Q

what can monocytes differentiate into?

A

monocytes are immature cells. they differentiate into macrophages or dendritric cells once they enter connective tissue

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16
Q

where do macrophages live and what is their role?

A

in tissues

remove foreign microbes and dead/tumour self by phagocytosis

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17
Q

how do macrophages and monocytes phagocytose?

A

by using their lysosomes that have peroxidase

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18
Q

what are dendritic cells? give an example

A

fixed, differentiated macrophages

e.g. kupfer cells in liver

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19
Q

describe the shape of the nucleus of a monocyte

A

kidney shaped

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20
Q

what is the role of eosinophils?

A

phagocytose antigen-antibody complexes
are associated with parasitic infections
neutralise histamine so are also associated with allergic reactions

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21
Q

are eosinophils granulocytes?

A

yes

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22
Q

what do eosinophil granules contain?

A

major basic protein which is a potent toxin. it activates neutrophils, induces histamine release from mast cells

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23
Q

describe the eosinophil neucleus

A

polymorphonuclear, 2-3 lobed nucleus

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24
Q

what is the role of basophils?

A

main role in parasitic infections and allergic reactions

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25
Q

are basophils granulocytes?

A

yes

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26
Q

what do basophil granules contain?

A

histamine

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27
Q

how does histamine get released from basophils?

A

basophils have IgE receptors so when IgE binds to them degranulation occurs so histamine released from granules

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28
Q

describe the basophil nucleus?

A

polymorphonuclear but not multi-lobar

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29
Q

what cell has a similar role to basophils?

A

mast cells

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30
Q

where are mast cells found?

A

in tissues, their precursor (mast cell progenitor) is found in the blood

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31
Q

what is the role of mast cells?

A

parasitic infections

allergic reactions

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32
Q

what do mast cells have that allows them to be involved in allergic reactions?

A

high-affinity IgE receptors

histamine-containing granules

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33
Q

how do lymphocytes leave the blood? (3)

A

by extravasation they travel to infection site. mediated by:

  1. rolling of lymphocytes along activated vascular endothelium
  2. tight adhesion of lymphocytes
  3. chemokines
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34
Q

how many lymphocytes are there that are involved in immunity? Name them

A

3
T cells
B cells
Natural killer cells

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35
Q

where are T cells matured?

A

thymus

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36
Q

what is T cells major role? (3)

A

recognising antigens displayed on antigen presenting cells, stimulate antibody production from B cells, help kill pathogens

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37
Q

how many types of T cells are there? name them

A
4
t helper 1 cell
t helper 2 cell
cytotoxic t cell
T regulator cell
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38
Q

what is the role of each of the T cells?

A

T helper 1: produce IFN gamma to kill intracellular pathogens (e.g. virus)
T helper 2: stimulates antibody production
cytotoxic t cell: kills intracellular pathogens directly
T regulator cell: inhibitory role and controls level and quality of immune response

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39
Q

describe the T cell receptors (TCR)

A

TCR have transmembrane proteins that make CD3 thus forming the CD3-TCR complex. this complex recognises antigens when they are with major histocompatibility complex. but recognition is not enough to activate T cell, other signal needed e.g. interleukin and co-stimulatory molecules

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40
Q

how many classes of major histocompatibility complex are there?

A

3

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41
Q

what cells recognise MHC class 1?

A

cytotoxic T cells that have CD8

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42
Q

what cells can present MHC class 1?

A

all cells except red blood cells

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43
Q

what type of antigens do MHC class 1 use?

A

intrinsic e.g. virus

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44
Q

what cells recognise MHC class 2?

A

T helper cells that have CD4

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45
Q

what cells can present MHC class 2?

A

antigen presenting cells

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46
Q

what type of antigens do MHC class 2 use?

A

extrinsic e.g. microbe phagocytosed and antigen on surface

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47
Q

what type of molecules are MHC class 3?

A

secreted proteins with immune function e.g components of complement system

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48
Q

where do B cells mature?

A

bone marrow

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49
Q

what is B cells role in adaptive immunity?

A

recognise antigens by antigen presenting cells
express membrane bound antibodies on surface
differentiate into plasma cells that make lots of antibodies
differentiate into memory cells

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50
Q

What are natural killer cells a type of?

A

type of lymphocyte

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51
Q

where are natural killer cells found?

A

spleen and tissues

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52
Q

what is natural killer cells’ role in immunity?

A

innate immunity as they have no memory and need no prior activation. they kill virus infected cells and tumour cells by apoptosis.

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53
Q

what are the parts to the humoral component of immunity?

A

complement
antibodies
cytokines

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54
Q

what is the role of complements?

A

remove/destroy antigens by direct lysis or by opsonisation

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55
Q

define opsonisation

A

mechanism in which microbes become chemically modified to have stronger interactions with phagocytic cells

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56
Q

what are complements?

A

series of interacting plasma proteins that act as an enzymatic cascade i.e. they are mostly inactive and activation of one will lead to it activating the others.

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57
Q

what are the two steps in the activation of complement?

A

1) produce C3 convertase

2) C3 convertase cleave C3

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58
Q

how many pathways can produce C3 convertase? name them

A

3
classical
alternative
lectin

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59
Q

how does the classical pathway lead to C3 convertase?

A

activation by the antibody bound to the microbe

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60
Q

how does the alternative pathways lead to C3 convertase?

A

activation by the compliment binding to the bacterial cell wall

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61
Q

how does the lectin pathway lead to C3 convertase?

A

activation by mannose-binding lectin bound to the microbe (MBL promotes opsonisation)

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62
Q

what are some of the fragments produced from C3 cleavage?

A

C3a, C4a, C5a
C3b
C5, C6, C7, C8, C9

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63
Q

What is the most important and main fragment from C3 cleavage?

A

C3b

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64
Q

What do fragments C3a C4a C5a do?

A

involved in inflammation and immune cell recruitment

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65
Q

what does fragment C3b do?

A

involved in opsonisation and removal of immune complexes

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66
Q

what do fragments C5-C9 do?

A

involved in cell lysis

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67
Q

which fragments from c3 cleavage are involved in inflammation and immune cell recruitment?

A

c3a, c4a, c5a

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68
Q

which c3 cleavage fragment is involved in opsonisation?

A

c3b

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69
Q

which c3 cleavage fragments are involved in cell lysis?

A

c5-c9

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70
Q

are mast cells all the same? what is the name for this feature of mast cells?

A

no they are different slightly in different tissue types

this is called heterogeneity

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71
Q

which cell is the main effector cell in allergies?

A

mast cell

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72
Q

give a difference between mast cells and basophils

A

mast cells are characterised by c-kit protein on their surface

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73
Q

what can mutation of c-kit proteins lead to?

A

cancer

systemic mastocytosis

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74
Q

does IgE promote the compliment system?

A

no

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75
Q

what part of the antigen do antibodies bind to?

A

epitope

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76
Q

what does it mean that the antibodies are specific?

A

they only bind with the antigen which induced their synthesis

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77
Q

How many classes of antibodies are there? name them

A
5
IgG
IgA
IgM
IgD
IgE
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78
Q

which antibody can cross the placenta?

A

IgG

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79
Q

Which antibody is the predominant Ig in mucous secretion?

A

IgA

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80
Q

describe the structure of IgA

A

two molecules of basic units (dimers) linked by a joining (J) chain

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81
Q

describe the shape of IgM

A

pentamer shape (five units with lots of J chains)

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82
Q

which Ig can never cross the endothelium?

A

IgM, too big

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83
Q

which antibody mostly acts as a cell surface receptor on B cells for antigens?

A

IgD

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84
Q

which antibody’s receptor is mostly expressed on basophils and mast cells?

A

IgE

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85
Q

which antibody is most associated with allergic reactions and parasitic infections?

A

IgE

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86
Q

what are cytokines?

A

proteins secreted to act as simulator or inhibitory signals between cells

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87
Q

what cells secrete cytokines?

A

immune cells and non-immune cells

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88
Q

what is a cytokine called if it is released from lymphocytes vs macrophages/monocytes?

A

lymphokines

monokines

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89
Q

give 5 examples of cytokines

A
interferons
interkeukins
colony stimulating factor
tumour necrosis factors
chemokines
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90
Q

what do interferons do?

A

induce state of antiviral resistance in unaffected cells to limit spread of viral infection

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91
Q

how many types of interferons are there and where are they produced from?

A

3
IFN alpha and beta-produced by virus infected cells
IFN gamma- produced by activated T helper 1 cells

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92
Q

what do interleukins do?

A

cause cells to divide, differentiate and secrete factors

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93
Q

what is the difference between interleukin 1 and 2?

A

IL1- pro-inflammatory

IL2- anti-inflammatory

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94
Q

what do colony stimulating factors do?

A

involved in directing the division and differentiation of bone marrow stem cells

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95
Q

what do tumour necrosis factors do?

A

mediate inflammation and cytotoxic reactions

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96
Q

what do chemokines do?

A

direct movement of leukocytes and other cells from blood to tissues or lymph nodes where infection or inflammation is occuring

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97
Q

where are chemokines produced?

A

site of inflammation/infection

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98
Q

what are some features all cytokines share? (4)

A

short half lives
rapid degradation
local action
may affect multiple organs

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99
Q

what are the two types of immunity we have?

A

innate and adaptive

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100
Q

give 10 features of the innate immune system

A
  1. not specific
  2. first line of defence
  3. instinctive
  4. primitive
  5. independent of lymphocytes
  6. provides barriers to antigens
  7. doesn’t have long lasting memory (only has evolutionary memory)
  8. supplement to adaptive response
  9. rapid response
  10. can be evaded
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101
Q

give an example of an anatomical, physical, chemical and physiological barrier that the innate system provides

A

anatomical-skin
physical- mucociliary lining of resp tract
chemical- acidic stomach
physiological-temperature

102
Q

what is PAMP and DAMP?

A

pathogen/ damage associated molecular patterns

103
Q

describe the evolutionary memory of innate immunity

A

microorganisms have similar characteristics which are unchanging. infection is also associated with damage and trauma so through evolution and natural selection our immune system has memorised PAMP and DAMPs

104
Q

what type of receptors does innate immunity use?

A

pattern recognition receptors

105
Q

what do pattern recognition receptors detect?

A

all microbes that share a specific pattern or characteristic

106
Q

what are the two divisions for pattern recognition receptors?

A
  • secreted and circulate in the body

- cell-associated

107
Q

give four examples of types of secreted PRR

A

defensins
lectins
collectins
pentraxins

108
Q

what are defensins?

A

antimicrobial peptides that are secreted in lining fluid from epithelium and phagocytes

109
Q

what do lectins and collectins do?

A

they are carbohydrate-containing proteins that bind to carbohydrates or lipids in bacterial walls and can activate complements and improve phagocytosis

110
Q

give an example of a lectin or collectin

A

mannose-binding lectin

111
Q

what can pentraxins do?

A

activate complement and promote phagocytosis

112
Q

give an example of a pentraxin

A

CRP

113
Q

where are cell-associated PRR found?

A

cell membrane or cytosol of cell

114
Q

what is the main family of cell-associated PRR?

A

Toll-like receptors

115
Q

what do TLR1 and 2 recognise?

A

gram positive bacteria’s lipopetides

116
Q

what does TLR3 recognise (exogenous and endogenous)

A

exogenous-double stranded RNA

endogenous- mRNA

117
Q

what does TLR4 recognise (exogenous and endogenous)?

A

exogenous- viral proteins

endogenous-heat shock proteins

118
Q

what does TLR5 recognise?

A

flagellin of microorganism

119
Q

what do TLR7 and 8 recognise?

A

single stranded RNA (exogenous)

120
Q

what does TLR9 recognise?

A

endogenous DNA

121
Q

what PRR are used for intracellular pathogens?

A

Nod like receptors

Rig like receptors

122
Q

what is PRR roles (3)?

A

recognition of PAMP recognition of DAMP

haemostasis

123
Q

how does PRR contribute to haemostasis

A

tlr4 signalling controls neutrophil numbers

PRR can control number of commensal organsims

124
Q

how does PRR contribute to damage recognition and repair?

A

PRR recognise substances not meant to be outside of their cell or in unfamiliar places so TLR activated
TLR activation can activate tissue repair

125
Q

how does PRR contribute to adaptive immunity?

A

TLR can increase cytokine production by antigen presenting cells so increase t cell activation

126
Q

give 5 features of adaptive immunity

A
  1. specific
  2. acquired
  3. required immune recognition by lymphocytes
  4. requires antibodies
  5. has memory
127
Q

why do we need adaptive immunity?

A

microbes can evade innate immunity

we need memory for specific antigens so second response is faster

128
Q

what are the two components of adaptive immunity?

A
cell mediated (t cells interacting with APC, MHC, antigens)
humoral (b cells)
129
Q

what are three antigen presenting cells?

A

dendritic cells
macrophages
B cells

130
Q

describe t cell selection, thymus tolerance

A

t cells that recognise and bind with low affinity to self-antigens are positively selected and mature
t cells that don’t recognise self-antigens apoptosis occurs
t cells that are recognise and bind with high affinity to self-antigens are negatively selected and apoptosis occurs

131
Q

what are the primary lymphoid organs?

A

thymus and bone marrow

132
Q

what are secondary lymphoid organs?

A

those that have antigen reactive cells in the process of recirculating around the body

133
Q

give three examples of secondary lymphoid organs?

A

lymph nodes
spleen
mucosa-associated lymphoid tissue

134
Q

what is the difference between primary and secondary follicles in lymph nodes?

A

primary: B cells have more IgD and IgE
secondary: B cells have more IgG

135
Q

how do primary follicles become secondary follicles in lymph nodes?

A

antigen challenged

136
Q

how do antigens get presented?

A

antigen-presenting cell will phagocytose microbe. Antigen processed in golgi body to form complex with MHC. this complex goes to surface of APC.

137
Q

how does a T cell interact with an APC?

A

T cell recognises antigen bound to MHC and binds.

Co-stimulatory pathway also needed e.g. interleukin production

138
Q

can antibodies be produced without an APC contributing? Why?

A

no, because for a T cell to recognise an antigen on a B cell it must have first bound to that antigen whilst it was on an APC

139
Q

Which cell synthesises antibodies?

A

B cell

140
Q

what is isotype switching?

A

B cell switch from making one type of antibody e.g. IgM, and make another e.g. IgG

141
Q

What is required for isotype switching?

A

CD4 on B cell
CD4 ligand on activated T cell
interkeukin

142
Q

How can a T cell recognise and activate a B cell for a specific antigen?

A

B cell must present antigen.

143
Q

How does a B cell present an antigen?

A
IgM on B cell surface binds to antigen, internalises it.
antigen processed in golgi body to form complex with MHC class 2 that goes to surface.
144
Q

What does the activation of B cells by T cells lead to the formation of?

A
Plasma cells (antibodies)
Memory cells
145
Q

What are plasma cells?

A

B cells that all produce the same type of antibody for one specific antigen.

146
Q

how are plasma cells made?

A

contact with antigen on surface of B cell and T cell and interleukin (produced by T cell)

147
Q

What is the process called of making lots of memory and plasma cells?

A

clonal expansion

148
Q

what can antibodies do to fight microbes?

A

neutralise toxins by binding to them
increase opsonisation so increase phagocytosis
activate complement cascade

149
Q

what are the two ways of acquiring adaptive immunity?

A

passive and active immunity

150
Q

what is passive immunity?

A

protection provided by transfer of antibodies from immune individuals to non-immune individuals

151
Q

give three examples of passive immunity

A

across placenta/ via breast milk
transfusion of blood
injection of human immunoglobulin

152
Q

give five infections that are protected against by antibodies that cross the placenta or enter individual via breast milk

A
tetanus
rubella
mumps
poliovirus
streptococcus
153
Q

give three scenarios where passive immunity is provided

A

infection by toxins from tetatnus
infection from hepatitis, measles, rubella (antibodies given as prophylactic)
exposure to venom e.g. snake bite

154
Q

what are two negative points to passive immunity?

A

protection temporary

doesn’t activate immunological memory

155
Q

what is active immunity?

A

protection provided by an individual’s own immune system

156
Q

what substances are involved with active immunity?

A

cellular responses

antibodies

157
Q

give two benefits to active immunity

A

long-lasting protection

immunological memory activated

158
Q

what kind of immunity do vaccines provide?

A

active immunity

159
Q

why do we use vaccinations to provide active immunity instead of natural infection?

A

vaccination provides similar immunity as infection naturally but without any risks from the actual disease

160
Q

what are the first antibodies produced when first vaccinated? what are the second?

A
  1. IgM

2. IgG

161
Q

what can vaccinations be made from?

A
  1. whole organism
  2. subunits
  3. recombinant components
162
Q

what are the two ways of delivering whole organisms in vaccines?

A

inactivated/dead organism

attenuated (altered so not harmful) live organism

163
Q

what are the advantages of using inactivated whole organisms in vaccines?

A

no risk of infection

less critical storage

164
Q

what are the disadvantages of using inactivated whole organisms in vaccines?

A

lack of T cell involvement

repeated booster needed

165
Q

give three examples of vaccines that use inactivated whole organisms

A

cholera
hepatitis a
polio salk

166
Q

what are the advantages of using whole attenuated live organisms in vaccines?

A

full natural immune response
prolonged contact with immune system
stimulates T and B cell memory
single immunisation needed

167
Q

what are the disadvantages of using whole attenuated live organisms in vaccines?

A

immunosuppresed patients may become infected, attenuated can become virulent (harmful again), transport difficult because fridge needed

168
Q

give four examples of vaccines that use whole attenuated live organisms

A

tuberculosis
measles
mumps
polio sabin

169
Q

give four types of subunits that can be used in vaccines

A

secreted products from that organism e.g. exotoxins (heat treated toxins to remove toxicity)
antigenic extracts
capsular polysaccharide on cell wall
peptides

170
Q

give advantages of using subunits in vaccines

A

safer than whole pathogen, no risk of infection, easy storage

171
Q

give disadvantages of using subunits in vaccines

A

less powerful immunity, repeat vaccines needed, adjuvant needed

172
Q

what are adjuvants

A

substances added to vaccines to stimulate immune system

173
Q

give advantages of using recombinant components of organisms

A

create ideal, flexible, produces memory, safe in relation to live pathogen

174
Q

give disadvantages of using recombinant components of organisms

A

requires fridge, can cause illness in immunosuppressed

175
Q

why are booster vaccines needed?

A

some pathogens mutate regularly
some diseases have such rapid onset that even activated memory takes too long to be set off, so need constant high levels of antibodies

176
Q

define allergy

A

abnormal response to harmless foreign material

177
Q

what is allergy also known as

A

hypersensitivity

178
Q

what is atopy?

A

hereditary tendency to develop immediate hypersensitive reaction against common environmental antigens.

179
Q

What are the four things that are involved in allergic responses?

A

antibodies
genetics (immune and non-immune related genes)
cells
mediators

180
Q

what is the main antibody involved in allergic reactions

A

IgE

and IgG4, IgA

181
Q

what cells are involved in allergic responses?

A
immune cells (mast cells, eosinophils, TH2, dendritic cells (APC))
non-immune (smooth muscle, fibroblasts, epithelia, neurons)
182
Q

what makes a substance an allergen (4)

A

delivery of antigen (through respiratory system more likely to be allergen)
presence of PAMP
low doses makes substance allergen (high doses-desensitisation)
substance must induce TH2 formation

183
Q

name the two types of receptors that IgE bind to

A

high affinity receptors (FcER1)

low affinity receptors (FcER2)

184
Q

where can high affinity receptors of IgE be found?

A

eosinophils, basophils, mast cells

185
Q

what happens when IgE binds to a high affinity receptor on a mast cell?

A

more IgE will come and bind to the other receptors so that the mast cell becomes covered with IgE

186
Q

What happens when an IgE (already bound to high affinity receptor via body) binds to an antigen

A

the high affinity receptors will cluster and receptor cross-linking will occur

187
Q

what type of hypersensitivity reaction is the one mentioned of an antigen binding to an IgE bound to a mast cell?

A

type 1

188
Q

describe type 1 hypersensitivity

A

immediate hypersensitivity due to antigen interacting with IgE bound to mast cell/basophil
OR
overproduction of IgE on mast cell/basophil

189
Q

what happens after receptor cross-linking occurs?

A

cascade of signalling cellular events will be initiated which lead to degranulation

190
Q

where are low affinity receptors found?

A

B cells, T cells, monocytes, eosinophils, platelets, neutrophils

191
Q

what is FcER2 role?

A

regulate IgE synthesis
trigger cytokine release from monocytes
present antigens on cells

192
Q

which IgE receptors mentioned don’t cross-link?

A

FcER2 (low affinity receptors)

193
Q

what are the three types of susbtances (or what event occurs) after/during granulation? and when are they released?

A
  1. pre-formed compounds released (within seconds)
  2. lipid derived mediators released (within minutes)
  3. transcription/ translation occurs (within hours (of mast cell still alive and degranulating)
194
Q

what are the four preformed compounds that are released from mast cells?

A

histamine
chemotactic factor
proteases
proteoglycans

195
Q

what does histamine do?

A

lead to arteriole dilation
capillary leakage
bronchoconstriction

196
Q

what do chemotactic factors do?

A

lead to eosinophil attraction and activation

197
Q

give an example of two proteases released from mast cells during degranulation

A

tryptase

chymase

198
Q

give an example of a proteoglycan that is released from mast cells during degranulation

A

heparin

199
Q

what do the proteoglycans do?

A

they were involved with the packaging of the granules

200
Q

name three lipid derived mediators released from the mast cells during degranulation

A

leukotrienes
prostaglandin D2
platelet activating factor

201
Q

what do leukotrienes do?

A

capillary endothelial contraction

vascular leakage

202
Q

what does prostaglandin D2 to?

A

smooth muscle contraction

203
Q

what does platelet activating factor do?

A

increased platelet aggregation
degranulation
activation of neutrophil secretion

204
Q

what is being transcribed, translated during the transcription event that occurs within hours of degranulation?

A

new proteins: forms of mediators to control wider immune system
cytokines (leads to more IgE so more mast cell activation)

205
Q

what can activate mast cells?

A

indirect and direct activators

206
Q

give three classes for indirect activators

A

allergens
bacterial/viral antigens
phagocytosis of enterobacteria

207
Q

how do indirect activators work?

A

via IgE and high affinity receptors, prior sensitisation is required

208
Q

give six examples of allergens

A
latex
wasp venom
foods
drugs
pollen
house dust mite faeces
209
Q

give three examples of direct activators

A

cold/mechanical deformation
aspirin
preservatives

210
Q

give three examples of allergic diseases

A

anaphylaxis
allergic asthma
allergic rhinitis hay fever

211
Q

what happens during anaphylaxis

A

vasodialtion, low BP, bronchial constriction
rashes- urticarial
swelling- oedema because more vascular permeability
pain
vomiting

212
Q

how many classes of hypersensitivity are there, name them

A
4
type 1: immediate hypersensitivity
type 2: antibody to cell-bound antigen
type 3: immune complex reaction
type 4: delayed hypersensitivity mediated by T cells
213
Q

describe type 2 hypersensitivity

A

antibody to cell-bound antigen
antibodies bind to antigenic determinants on cell membrane
(e.g. drug incorporated into RBC so antibody binds to drug (so cell-bound antigen)) and causes bystander lysis (damage to RBC)

214
Q

what type of hypersensitivity does autoimmunity use?

A

type 2

215
Q

what antibodies are involved in type 2 hypersensitivity?

A

IgM and IgG

216
Q

give an example of type 2 hypersensitivity

A

RBC in autoimmune haemolytic anaemia

217
Q

describe type 3 hypersensitivity

A

immune complex reaction

deposition of immune complexes (e.g. antigen-antibody complex) in tissues

218
Q

give an example of type 3 hypersensitivity

A

nephritis

219
Q

describe type 4 hypersensitivity

A

delayed hypersensitivity mediated by T cells
T cells sensitised to antigen during primary exposure and produce interleukin 2 etc. in secondary exposure there is a delay before action.
delay can be 2-3 days and involves inflammatory responses

220
Q

give an example of type 4 hypersensitivity

A

contact dermatitis

221
Q

what does immunodeficiency present as?

A

specific,
persistent,
unusual,
recurrent infection (SPUR)

222
Q

what is the reason for immunodeficiency?

A

missing or reduced or malfunctioning vital parts of the immune system (specific and/or non-specific)

223
Q

what are the two types of defects that can cause immunodeficiency

A

primary and secondary defects

224
Q

what are primary defects due to?

A

intrinsic defects with immune system

225
Q

what are the three types of primary defects?

A

primary antibody deficiencies
primary cell-mediated immunity defects
primary defects of phagocytic function

226
Q

what is primary antibody deficiency?

A

defects in synthesis of all classes of antibodies or only in some (selective deficiency)

227
Q

what signs will patients with primary antibody deficiency have? (4)

A

recurrent respiratory tract bacterial infections
skin sepsis -boils
gut infections
meningitis

228
Q

what is the most common family that infects patients with primary antibody deficiency? give an example

A

pyogenic bacterial

streptococcus pneumonia

229
Q

why do viral/fungi infections not commonly occur with patients with primary antibody deficiency?

A

cell-mediated is fine

230
Q

do primary cell-mediated immunity defects occur on its own?

A

mostly occurs with B cell defects because t cells needed to activate B cells

231
Q

do primary phagocytic cell defects occur on their own?

A

antibody synthesis usually occurs too

phagocytic cells are needed to removeantigen-antibody complexes

232
Q

give an example of a disease that is caused by primary phagocytic defects. explain

A

chronic granulomatous disease
inability to produce radical oxygen species during phagocytosis
caused by staphylococcus aureus commonly

233
Q

what causes secondary defects?

A

underlying conditions

234
Q

what can the underlying conditions do to cause immunodeficiency

A

decreased production of vital parts of immune system

increased loss of vital parts of immune system

235
Q

give three examples of conditions that cause decreased production of vital parts of immune system

A

malnutrition (protein-energy malnutrition)
infections : HIV, measles, rubella
bone marrow infiltration

236
Q

give three examples of conditions that cause increased loss of vital parts of immune system

A

nephrotic syndrome
protein-losing enteropathy
inflammatory disease- crohn’s disease, ulcerative colitis

237
Q

what is hypogammaglobulinemia?

A

reduction in antibodies

238
Q

what is autoimmunity

A

immune response to self-antigens, breakdown of tolerance to self-antigens

239
Q

what is autoimmune disease?

A

damage to tissues or disturbed physiological function after autoimmune response

240
Q

what method does autoimmunity use to attack self-antigens

A

same as that for any immune response for non-self antigens

241
Q

what are the two types of autoimmunity

A

organ specific

non-organ specific

242
Q

what is organ specific autoimmunity

A

restricted to a single organ, usually involved endocrine organs

243
Q

what are the common antigens for organ specific autoimmunity

A
surface proteins e.g. hormone receptors
intracellular molecules (intracellular enzymes)
244
Q

what is non-organ specific autoimmunity

A

involves auto-antigens widely distributed all around the body

245
Q

what antigens are commonly used for non-organ specific autoimmunity

A

molecules invpolved in translation and transcription of DNA

246
Q

what is t cell tolerance

A

down-regulation or removing T cells that react to self-antigens

247
Q

what is thymus tolerance

A

positive and negative selection

248
Q

why do we need periphery tolerance

A

because in thymus not all self-antigens are present to negatively select T cells against e.g. self-antigens in brain

249
Q

how does periphery tolerance occur? (4)

A
  1. some self-antigens in avascular areas away from immune cells
  2. MHC2 needed for T cell recognising antigens so MHC2 presentation only occurs on antigen presenting cells
  3. self-antigens kept away from antigen presenting cells by debris from cell death being cleared quickly
  4. self-reactive T cells inhibited by T regulator cells
250
Q

give three examples of autoimmune diseases?

A

multiple sclerosis
rheumatoid arthritis
insulin-dependent diabetes (type 1)

251
Q

how fast does anaphylaxis occur and for how long

A
within minutes (or hours if allergen exposure via GI)
lasts 1-2 hours
252
Q

what is anaphylactoid reactions?

A

non-immune anaphylaxis

direct mast cell degranulation without previous exposure