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Phase 2a > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the key features of innate immunity?

A

instinctive
non-specific
doesn’t depend on lymphocytes
present from birth
response not improved by repeat infection
rapid response
involves phagocytes, NKC, lysosomes, complement, interferon

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2
Q

What are the key features of adaptive immunity?

A 
specific acquired/learning immunity
requires lymphocytes
antibodies
resistance improved by repeat infection
slower response (days/weeks)
involves B and T lymphocytes
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3
Q

What are the 3 layers of a blood sample?

A

top (yellow): plasma (90% water, electrolytes, proteins, lipids, sugar)
middle (white): buffy coat of wbc
bottom (red): 45%, rbc and platelets

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4
Q 
Neutrophils:
% of blood
lifespan
role
extra details
A 
65%
6hrs - 12 days
innate immunity: phagocytosis
2 intracellular granules
kill microbes by secreting toxic superoxides
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5
Q 
Monocytes:
% of blood
lifespan
role
extra details
A 
5%
months
innate immunity: phagocytosis
adaptive immunity: antigen presentation 
= remove foreign stuff
lysosomes contain peroxidase
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6
Q 
Macrophages:
examples
lifespan
role
extra details
A 
Kupffer cells, microglia (brain)
months/years
innate immunity: phagocytosis
adaptive immunity: antigen presentation to T cells
remove foreign and self debris
1st line of non-self recognition
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7
Q 
Eosinophils:
% of blood
lifespan
role
extra details
A

5%
8-12 days
granules contain Major Basic Protein: activates neutrophils, induces histamine release + bronchospasm: allergy
associated with allergic and parasitic infections

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8
Q

What do eosinophil granules stain for?

A

acidic dyes

eosin = red

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9
Q

Basophils:
% of blood
lifespan
role

A

2%
2 days
immunity to allergic reactions and parasitic infections

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10
Q

Basophils and mast cells are ver similar apart from what?

A

mast cells: fixed in tissue

basophils: circulate

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11
Q

What do basophil granules stain for?

A

basic dyes

haemotoxylin: blue

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12
Q

Monocytes differentiate into what when they reach tissues?

A

macrophages

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13
Q

What kind of high affinity receptors do basophils have? What happens when they are activated?

A

IgE receptors

when IgE binds: de-granulation = histamine release = allergic reaction

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14
Q

What is the role of a mast cell?

A

immunity to allergic reactions and parasitic infections

have high affinity IgE receptors like basophils

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15
Q 
T lymphocytes:
% of blood
lifespan
role
extra details
A

10%
hours to years
adaptive immunity: recognise APCs and bind antigens via specific TCRs
produce cytokines and oil infected host cells

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16
Q 
B lymphocytes:
% of blood
lifespan
role
extra details
A

15%
hours to years
adaptive immunity: recognise ACPs
differentiates into plasma cells which produce antibodies

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17
Q

Where are B lymphocytes found in the body?

A

blood, lymph nodes, spleen

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18
Q

What is the role of dendritic cells?

A

adaptive immunity: act as APCs and induce primary immune response in inactive T lymphocytes = ONLY CELLS THAT CAN DO THIS
produce cytokines = B cell activation and differentiation

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19
Q

Where are dendritic cells found?

A

in tissue that has contact to outside environment e.g. skin, lining of lung and nasal cavity

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20
Q

What is the role of natural killer cells?

A

recognise and kill virus infected cells and tumour cells by apoptosis
expressed CD56

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21
Q

Where are natural killer cells found?

A

spleen and tissues

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22
Q

What are the 4 types of T cell?

A
  1. T-regs
  2. T helper (CD4, Th1 and Th2)
  3. Cyotoxic (CD8)
  4. TH17
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23
Q

What do neutrophils look like?

A

3 lobes
lots of granules
neutral stains

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24
Q

What do eosinophils look like?

A

lots of granules
2 lobes
acidic stains

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25
Q

What do basophils look like?

A

basic stains

2 lobes

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26
Q

What do monocytes and macrophages look like?

A

monocytes: few granules

gain more granules and cytoplasm when they mature to macrophages

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27
Q

What do T and B cells look like?

A

little cytoplasm

T-cell: no indentation

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28
Q

What is complement secreted by?

A

liver

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29
Q

What needs to happen for complement to be functional?

A

must be activated

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30
Q

What are the 3 main things complement does? Which molecules carry out each property?

A

direct lysis (MAC)
attract more leukocytes to infection site (chemotaxis) and enhance inflammation (C3a and C5a)
opsonisation (C3b)

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31
Q

What 3 main properties do immunoglobulins have?

A

soluble
secreted
bound to B cells

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32
Q

What type of protein are Igs?

A

glycoproteins

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33
Q

What is an epitope?

A

part of the antigen that binds to the antibody

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34
Q

What are the 5 immunoglobulins?

A

IgG, IgA, IgM, IgD, IgE

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35
Q

What are the key properties of IgG?

A

most predominant
goes everywhere in body due to small size
only one too ross placenta to give neonates immunity

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36
Q

What are the key properties of IgM?

A

mainly found in blood: too big to cross endothelium
have multiple complement binding sites
primary immune response: initial contact with antigen
main role = intravascular neutralisation

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37
Q

What are the key properties of IgA?

A

predominant Ig in mucous secretions: milk, saliva, bronchiolar, genitourinary
SECRETORY

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38
Q

What are the key properties of IgE?

A

basophils and mast cells express IgE specific receptors
binding = histamine release
associated with hypersensitivity allergic reactions and parasitic infections

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39
Q

What are the key properties of IgD?

A

on naive B cells

acts as B-cell antigen receptor

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40
Q

What are the 5 main functions of immunoglobulins? Which Ig is associated with each function?

A

neutralise toxins by binding to it (IgA, IgG)
immobilise motile microbes (IgM)
increase opsonisation: aids phagocytosis
activates complement using Fc receptors (IgG, IgM)
bind Fc receptors: phagocytes (IgG, IgA), mast cells (IgE), natural killer cells (IgG)

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41
Q

What is a cytokine?

A

soluble proteins secreted by lymphocytes, monocytes or macrophages that act as stimulation or inhibitory signals to cells

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42
Q

What are the 4 types of cytokine?

A

interferons (IFN)
interleukins (IL)
colony stimulating factors
tumour necrosis factors (TNF alpha and beta)

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43
Q

What do interferons do?

A

induce state of antiviral resistance in uninfected cells

= limits spread of viral infection

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44
Q

What are the 3 types of interferon? What are they produced by?

A

IFN alpha and beta produced by virus infected cells

IFN gamma released by activated Th1 cells

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45
Q

What do interleukins do?

A

act between cells of the immune system

cause cells to divide, differentiate and secrete factors

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46
Q

What are they 2 types of interleukin?

A

pro-inflammatory (IL1)

or anti-inflammatory (IL10)

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47
Q

What do colony stimulating factors?

A

direct division and differentiation of bone marrow stem cells
= precursors of leukocytes

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48
Q

What do tumour necrosis factors do?

A

mediate inflammation and cytotoxic reactions

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49
Q

What are chemokines?

A

chemotactic cyotkines

direct movement of leukocytes from blood to tissues by binding to specific receptors on cells

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50
Q

What are the 4 key chemokines?

A

CXCL: mainly neutrophils
CX3CL: T lymphocytes and NKC
CCL: monocytes, lymphocytes, eosinophils, basophils
XCL: mainly T lymphocytes

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51
Q

What are the 3 key parts of innate immunity?

A 
physical and chemical barriers
phagocytic cells (neutrophils and macrophages)
blood proteins (complement, acute phase)
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52
Q

What are the physical and chemical barriers of the body used in innate immunity?

A

anatomical barriers: skin
mucous membranes: saliva and tears: lysozyme (cilia)
commensal colonies: mouth, vagina, skin, gut
pH: gastric acid, decreased in vagina

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53
Q

What are the hallmarks of inflammation?

A

increased blood supply
increased vascular permeability
increased leukocyte transendothelial migration extravasation

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54
Q

Which immune cells are found in the blood and which are in the tissues?

A

blood: monocytes, neutrophils
tissues: macrophages, dendritic cells

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55
Q

What is a Pathogen Associated Molecular Pattern (PAMP)?

A

on microbes
innate immunity depends on an immune cell recognising some general molecular features common to lots of pathogens = PAMP
e.g. a lipopolysaccharide

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56
Q

What is a Pattern Recognition Receptor (PRR)?

A

recognise and bind to variety of pathgogen ligands

activation drives cytokine production by APCs that increases T cell activation

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57
Q

What are Toll-like Receptors?

A

type of PRR
proteins that recognise and bind to PAMPs
2nd messenger is generated = inflammatory mediators released

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58
Q

Where are toll-like receptors found?

A

on macrophages, dendritic cells and neutrophils

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59
Q

What are the 3 activation pathways for complement?

A
  1. classical (Ab bound to microbe)
  2. alternative (C’ binds to microbe)
  3. lectin (mannose-binding lectin binds to microbe)
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60
Q

How does the classical activation pathway of complement work?

A

IgM or IgG binds to an antigen and reveals a binding site for C1 = antibody dependent
Attachment to Fc region on 2 Ig molecules is required
C4bC2a is formed when C1r and C1s bind together
C4bC2a complex has enzymatic action on C4 and C2 = splits these into a and b
C4b and C2 combine to form C4bC2a aka C3 convertase
Cleaves C3 into C3a and C3b
C3 convertase remains on surface of pathogen to cleave C3
regulated by C1 esterase inhibitor

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61
Q

How does the lectin pathway of complement activation work?

A

independent of antibodies: activated when mannose-binding lectin binds to mannose on bacterial cell walls, yeast walls or viruses
joins classical pathway: forms C3 convertase to cleave C3

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62
Q

How does the alternative pathway of complement activation work?

A

activated by microbial cell surfaces
generates C3 convertase without the need for C1, C4 or C2
spontaneous cleavage of C3 occurs: C3b and B combine to form C3bB
converted to C3bBb = C3 convertase
cleaves C3 into C3a and C3b
regulated by factors H and I which cleave and inactivate displaced C3b

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63
Q

What do all forms of A complement do?

A

enhance inflammation

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64
Q

Explain the membrane attack complex pathway

A
  1. C3b can bind to C3 convertase (C4bC2a) to form C3/C5 convertase (C4bC2aC3b)
  2. this cleaves C3 into C3a and C3b or C5 into C5a and C5b
  3. C5b initiates formation of MAC
  4. with other complement proteins, MAC is formed and destroys pathogens
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65
Q

Explain how extravasation is used to attract wbc from the blood to the tissue?

A
  1. macrophage secretes pro-inflammatory molecule once it binds to a pathogen = attracts more immune cells
  2. TNF Alpha activates endothelium so it becomes sticky
  3. neutrophils bind to the endothelium = tethered: they roll along it to slow down initially
  4. TNF alpha causes chemokines to be released = stick to molecules on endothelial surfaces
  5. neutrophils interact with the chemokines, they tell neutrophils to stop
  6. neutrophil binds to integrin: holds it in place and signals it to move to the tissue
  7. squeezes between gaps in the endothelium, up a chemokine gradient
  8. most chemokines are by the site of infection where they are released = neutrophils move here
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66
Q

What are the 2 methods of microbial killing b neutrophils and macrophages?

A
  1. oxygen dependent: reactive oxygen intermediates (ROI)
    superoxides > H202 > OH radical
    nitric oxide: vasodilation increases extravasation and is anti-microbial
  2. oxygen independent
    enzymes: lysozyme
    proteins: defensives, TNF
    pH
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67
Q

What are the hallmarks of adaptive immunity?

A

specific
quicker response
response and memory specific to antigen
requires lymphocytes

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68
Q

What is the difference between cell-mediated and humour adaptive immunity?

A

cell mediated: involves T cells for intracellular microbes

humour: involves B cells for extracellular microbes

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69
Q

Why do we need adaptive immunity?

A

microbes evade innate immunity (proteases etc)
intracellular viruses and bacteria hide from innate immunity
need memory to specific antigens

70
Q

What are the 3 key players in adaptive immunity?

A

T cells
B cells
APCs: dendritic cells, macrophages and B cells

71
Q

Where are T cells produced? Where do they mature and travel to?

A

produced in bone marrow > primary lymphoid: mature in thymus > secondary lymphoid

72
Q

Where are B cells produced? Where do they mature and travel to?

A

primary lymphoid: produced and mature in bone marrow > secondary lymphoid

73
Q

Where are APCs produced? Where do they mature and travel to?

A

primary lymphoid: produced in bone marrow > tissue > recirculates to secondary lymphoid

74
Q

What do adaptive immunity cells accumulate in the body?

A

secondary lymphoid tissue e.g. spleen, lymph nodes, MALT

75
Q

What is MALT?

A

mucosal associated lymphoid tissue: patches of specialised tissue e.g. in mouth, tonsils, gut

76
Q

Which cells are involved in cell-mediated immunity?

A

APCs: dendritic cells, macrophages, B cells

T cells

77
Q

What are the 5 key requirements for cell-mediated immunity?

A
  1. intimate cell to cell contact: to control Ab response via contact with B cells + recognise and kill viral infected cells
  2. a Major Histocompatibility Complex
  3. intrinsic/endogenous (intracellular) antigens
  4. extrinsic/exogenous (extracellular) antigens
  5. recognise self and non-self proteins
78
Q

What is a Major Histocompatibility complex?

A
  • present antigenic peptides from self or non-self proteins to T cells
  • antigenic specific receptor of the T cell only recognises antigens if they are part of a complex with an antigenic peptide and it’s specific MHC
  • safety: stops immune system getting activated too easily
79
Q

What kind of antigens do T cells and B cells respond to?

A

T cells DO NOT respond to soluble antigens, B cells do

T cells ONLY respond to intracellular presented antigens

80
Q

The structure of a T cell receptor is similar to what?

A

Fab region of Igs

81
Q

What do T cell receptors recognise and bind to?

A 
T cells are committed to an antigen
TCR recognises small antigen peptides in association with EITHER a major histocompatibility complex class I (cytotoxic T cell CD8) or class II (T helper CD4)
82
Q

What are Major Histocompatibility complexes coded by?

A

Human Leukocyte Antigen genes

83
Q

Major Histocompatibility complex class I is associated with what kind of antigens and T cells? Where is it found? What is its function?

A

intracellular antigens e.g. virus
Tc (CD8)
found on the surface ALL nucleated cells e.g. all cells but erythrocytes
kill infected cell with intracellular pathogen

84
Q

Major Histocompatibility complex class II is associated with what kind of antigens and T cells? Where is it found? What is its function?

A

extrinsic antigens e.g. phagocytosis
Th (CD4)
found only on APCs: macrophages, B cells, dendritic cells
HELP B cells make Ab kill extracellular pathogens and HELP directly kill

85
Q

Explain how T cells recognise an antigen and are then activated?

A
  1. APC presents antigen with a Major Histocompatibility complex to the T cell receptor
  2. CD4 or CD8 binds to this complex: required for full T cell activation
  3. once bound: send intracellular signals inside T cell
  4. intracellular signals tell T cell to release IL-2
  5. IL-2 acts on IL-2 receptor on same T cell: receptor activated and can send signals to T cell
  6. tells T cell to divide: more T cells to kill cells expressing this antigen = CLONAL EXPANSION
    also tells them to differentiate: more mature + active, gives effector functions, some become memory cells
86
Q

How do naive T cells become functional T cells? Explain the 2 pathways.

A

becomes activated and follows 1 of 2 pathways
1. naive T cell becomes CD8 (cytotoxic T cells): kill intracellular pathogens directly

  1. naive T cell becomes CD4
    in high levels of IL-12, CD4 then becomes Th1: helps kill intracellular pathogens by secreting IFN-gamma and IL-2 = helps viral response
    in low levels of IL-12, CD4 becomes Th2: produces antibodies, secretes IL-4, 5 and 10
87
Q

What are CD8 T cells also called?

A

cytotoxic T lymphocytes (CTL)

88
Q

How are CD8 cells activated?

A
  1. virus-infected cell contains viral proteins: broken down in cytosol
  2. peptides transported to endoplasmic reticulum and binds to Major Histocompatibility complex class I on cell surface
  3. naive CD8 cells activated by antigens presented on the MHC class I molecules
89
Q

How do CD8 cells kill infected host cells once activated?

A
  • mature cytotoxic T cells (Tc) provide protection: release pro-inflammatory and macrophage activating cytokines
  • kill infected host cells by forming proteolytic granules and releasing perforin and granulysin: form holes in cell membrane of pathogens and kill them
  • CD8 also induce apoptosis
90
Q

How are CD4 cells activated?

A
  1. APC presents an antigen with MHC II to a naive CD4 cell

2. High levels of IL-12 activate naive cells to CD4 Th1 cells

91
Q

After activation, what happens to CD4 Th1 cells to allow them to carry out their function?

A
  1. Th1 cells travel to secondary lymphoid tissues - spleen, lymph nodes
  2. Proliferate: CLONAL EXPANSION (more Th1 cells available to recognise this specific antigen)
  3. Th1 cell recognises antigen on infected cells with MHC II via TCR
  4. Can then carry out various functions
92
Q

What is the function of Th1 CD4 cells?

A

Mediates functions associated with cytotoxicity and local inflammatory reactions
Produces IL-2, IFN-gamma, TNF beta
- IFN-gamma stops virus spreading and causes apoptosis = kills IC pathogens
Activates macrophages by producing cytokines = triggers inflammation
Helps CD8 develop into effector cells: kill virally-infected target cells and activate macrophages infected with intracellular pathogens
Induce B cells to make IgG

93
Q

What is the function of Th2 CD4 cells?

A

Produce IL-4, 5, 6, 10 and 13
Activate eosinophils and mast cells
Important in helminth infections and allergies
Induce B cells to make IgE: promotes release of inflammatory mediators
Stimulate B cells (by IL-4, 5, 10) to proliferate and produce antibodies, especially IgE

94
Q

B cells express membrane bound Ig. Which types of Ig?

A

IgM or IgD

95
Q

What happens to B cells that recognise self?

A

Killed in bone marrow

96
Q

In the first state of their activation, B cells present an antigen to what? Explain the process.

A

T cells.
1. IgM (or IgD) binds to the antigen
2. Phagocytosis occurs
3. Peptide is displayed on the surface of the naive B cell with MHC II
4. TCR of naive Th CD4 binds to MHC II
Lots of other co-stimulators molecules are needed

97
Q

Once the naive Th CD4 cell is bound to the B cell, what happens for B cells to become activated?

A
  1. Th cells become primed Th2 cells on binding to the APC
  2. Th2 now secretes cytokines (IL-4, 5, 10 and 13)
  3. Cytokines cause B cells to divide: clonal expansion
  4. B cells differentiate in plasma cells (AFC): make antibodies and memory B cells (Bm)
98
Q

What is the exact stage at which B cells are said to be activated?

A

On binding with the complementary antigen

99
Q

Where do activated B cells go for clonal expansion?

A

Lymph nodes

100
Q

What type of antibodies do plasma cells usually produce?

A

IgM initially

Later turn into IgG

101
Q

What are the primary lymphoid organs?

A

Thymus

Bone marrow

102
Q

Name the secondary lymphoid organs and tissues?

A 
Waldeyer’s ring: tonsils and adenoids
Bronchus associated lymphoid tissue
Lymph nodes
Bone marrow
Spleen
Lymphoid nodules
Mesentery lymph nodes
Peyer’s patch
Urogenital lymphoid tissue
103
Q

How do we handle bacteria and fungi?

A

Phagocytosis and killing

104
Q

How do we handles viruses?

A

Cellular shut down
Self sacrifice
Cellular resistance
Apoptosis

105
Q

What are the main problems with immunity?

A

Immunological memory is very protective but takes weeks whereas infections arrive quickly and unpredictably

Adaptive memory is highly specific: cross reacting or self targeting is a risk

106
Q

What is pattern recognition? What properties do these patterns have so that so many can be recognised?

A

Recognise patterns associated with particular organisms

Patterns have limited characteristics and are shared across organisms

107
Q

Give 3 examples of where similar patterns are distinguished in the body.

A

Gram positive and negative bacteria show different patterns
Double stranded RNA is used for detecting viruses
CpG motifs: part of DNA where cytosine and guanine are separated and have a phosphate group

108
Q

What are the main 2 types of pattern recognition receptor?

A
  1. Secrets and circulating PRRs

2. Cell associated PRRs

109
Q

What are secreted and circulating PRRs? Where are they found? What are they secreted by?

A

Antimicrobial peptides
Found in lining fluids of epithelial and mucosal surfaces and phagocytes
Cells there and immune system components secrete them

110
Q

Give 3 examples of groups of secreted and circulating PRRs?

A

Human defence proteins eg defending, cathelicidin
Lectins and collectins
Pentraxins

111
Q

What 2 ways do human defence protein PRRs cause pathogen clearance?

A
  1. Direct killing: interrupt metabolic activity by bilateral disruption, binding to specific lipid receptors, disruption of membrane bound channels
  2. Immune modulation: recruitment and activation of immune cells leads to inflammation, enhanced pathogen killing and assists phagocytosis
112
Q

What are lectins and collectins? Give an example of each.

A 
Carbohydrate containing proteins 
Type of PRR
Bind carbohydrates or lipids in microbe walls
Eg mannose binding lectin 
Eg surfactant proteins A and D
113
Q

What are the 2 main roles of lectins and collectins?

A

Activate complement

Improve phagocytosis

114
Q

What are the 4 main roles of pentraxins? Give an example of a pentraxin.

A

Have some antimicrobial actions
Can react with C protein of pneumococci
Activate complement
Promote phagocytosis

Eg proteins like c-reactive protein

115
Q

Where are cell-associated PRRs found?

A

Cell membranes or in the cytosol

116
Q

What is the main family of cell-associated PRRs?

A

Toll-like receptors

117
Q

Which 3 TLRs respond to viral components? What do they do? Where are they found?

A

TLR 3, 7 and 9
Trigger anti-viral immune response
Not on cell surface but in endoscopes where viral components can be endocytosed

118
Q

What exogenous and endogenous ligand activate TLR-3?

A

Exogenous: double stranded RNA
Endogenous: mRNA

119
Q

Why is TLR-4 important?

A

As little as 10 cells of lipopolysaccharides (LPS) or other activators can lead to the induction of TLR-4

Components of LPS sensed by CD14 (adaptor molecule) > TLR-4 is oligomerized > signal induced

120
Q

What endogenous and exogenous ligand activate TLR-4?

A

Exogenous: lipopolysaccharides, pneumolysim, viral proteins
Endogenous: heat shock proteins, HMGB1, hyaluronan, fibrinogen

121
Q

Give 3 examples of other membrane bound PRRs?

A

Receptors that sense fungi: eg mannose receptor on macrophages
Dectin -1: on phagocytes, helps recognise beta glucans in fungal walls
Scavenger receptors: non-specific, on macrophages cell surface

122
Q

How do PRRs target intracellular pathogens? Give 2 examples of pathogens which multiply inside cells.

A

Have receptors in cytoplasm not just on the cell surface or in endoscopes

Eg viruses multiply in the cytoplasm
Bacteria such as salmonella burst of out phagolysomes and multiply in the cytoplasm

123
Q

What are nod-like receptors? Give 3 examples of the most common.

A

PRRs found in the cytoplasm - target intracellular pathogens
Can detect components of bacterial cell walls
Eg NOD1 and 2, NLRP3

124
Q

What is significant about the NOD-2 intracellular PRR? What is its main function?

A

Widely expressed
Recognises breakdown projects of peptidoglycan such as MDP (pep is found in gram pos and neg bacteria)
Activates inflammatory signalling pathways

125
Q

What diseases are associated with NOD-2 when it is non-functioning and when it is hyper functioning?

A

Non functioning: associated with Crohn’s

Hyper functioning: Blau syndrome

126
Q

What are rig-like helicases? What do they do? Where are they found? Give 2 examples.

A

Intracellular PRRs in the cytoplasm
Especially for viruses
Activate interferon production = antiviral response
Eg RIG-1, MDA5: detect intracellular double stranded viral RNA and DNA

127
Q

In what 4 ways do TLRs play a role in homeostasis?

A
  1. Independent of lipopolysaccharides, TLR-4 plays a role in the number of neutrophils circulating
  2. Endotoxin tolerance in the gut: gut has a lot fo bacteria, don’t want the body to react to them all
  3. Maturation of the immune system: mediate macrophage activation
  4. Maintain balance with commensalism organisms: don’t overreact to pathogens that routinely colonise the skin, gut etc
128
Q

How are PRRs involved in damage recognition?

A

When cells are damaged, they release products that can be sensed by PRRs
In unfamiliar contexts, these molecules can activate TLRs
= activates immunity to initiate tissue repair and increase local antimicrobial signalling

129
Q

What extracellular and intracellular products to cells release when they are damaged?

A

EC: fibrinogen, hyaluronic acid, tenascin C - from EC matrix, coagulation system
IC: HMGB1, mRNA, heat shock proteins, uric acid, strathmin

130
Q

In what 2 ways are PRRs involved in adaptive immunity?

A
  1. activation of PRRs drives cytokine productions by APCs = increases successful T cell activation
  2. TLR-4 agonists can be used alongside vaccines to enhance immune responses
131
Q

How are PRRs linked to disease?

A

recognition of host molecules: hyper functioning PRRs in autoimmune disease
failure to recognise pathogens
increased inflammatory response = increased likelihood of sepsis
abnormal immune responses can perpetuate damage: atherosclerosis, arthritis, COPD, IBD

132
Q

How can PRRs be used in therapy to treat disease?

A

increase TLR signalling: improve immunity and adjuvants in vaccines
inhibit TLR signalling in sepsis, inflammation or arthritis
modify adaptive immune responses e.g. in cancer

133
Q

According to immunological theory, what are the 4 key ways that a vaccine effects the immune system?

A

manipulating an immune item to generate a persistent protective response
immunisation that can trigger an immune response and safely mimic an infection
mobilise appropriate arms of the immune system to form immunological memory
can be transferred to others: passive immunity

134
Q

What is passive immunisation?

A

the transfer of preformed antibodies

135
Q

What is natural passive immunisation?

A

transfer of maternal antibodies across the placenta to the developing foetus/breast milk

136
Q

Which diseases does natural passive immunisation protect against?

A 
diphtheria
tetanus
rubella
mumps
poliovirus
137
Q

What is artificial passive immunisation?

A

treatment with pooled normal human IgG or immunoserum against pathogens or toxins

138
Q

When is artificial passive immunisation used?

A
  • individuals with agammaglobulinaemias (especially B cell defects)
  • exposure to a disease that could cause complications e.g. immunocomprised patients to measles
  • when there is no time for active immunisation to give protection (e.g. a pathogen with a short incubation time like rabies)
  • acute danger of infection
  • anti-toxins and anti-venins
139
Q

What is the biggest downside to passive immunisation?

A

doesn’t activate immunological memory so doesn’t provide long term protection

140
Q

With some pathogens, the main hazard is not the primary infection. What is it? Give 2 examples of diseases like this.

A

the effect of toxins released by bacteria
the primary infection can be eliminated by the immune system
e.g. tetanus, botulism

141
Q

What are deactivated toxins called?

A

toxoids

142
Q

Why is natural immunity to toxins very difficult to achieve?

A

toxins are very lethal at very low doses

143
Q

What treatment used to be used to neutralise toxins? Why was this a problem?

A

antisera
possibility of a reaction to anti-sera: it is non-self so the 2nd time it is used it will be immune to itself which can lead to anaphylaxis

144
Q

What effect do botulum and tetanus toxins have?

A

prevents fusion of vesicles at NMJs so NTs can’t cross the synapse

botulum: Ash
tetanus: glycine and GABA

145
Q

Passive immunisation is used when the body is exposed to which diseases? Name the type of passive immunisation used for each one.

A

botulism, tetanus, diphtheria = anti-toxins
hepatitis, measles, rabies = used prophylactically to reduce chance of establishing infection after exposure
snake bite, insects, jellyfish = anti-venin

146
Q

What is the 5 step process in forming active immunity?

A
  1. engage innate immune system
  2. elicit danger signals that activate system e.g. PAMPs
  3. engage TLR receptors via the PAMPs
  4. activate specialist APCs e.g. Langerhans cells
  5. engage adaptive immune system: generate memory T and B cells, activate T helper cells
147
Q

What is active immunity? (5 characteristics)

A

challenging immune system to induce state of immunity
production of high affinity protective antibodies against the immunogen
produced by own immune system
usually long lasting
achieve initial exposure without risks of actual infection

148
Q

What happens in the primary response to an antigen? Which Ig predominates?

A 
relies on innate immune system
no of antibodies is low
low affinity IgM predominate
essentially germline repertoire
memory T and B cells generated
149
Q

What happens in the secondary response to an antigen? Which Ig predominates?

A 
rapid and large reaction
high levels of high affinity IgG predominate
somatic hypermutation
T cell help
does not rely on innate immune system
150
Q

What are the 5 things that make a perfect vaccine?

A

achieve long term protection
stimulate B AND T cells
induce memory B and T cells
stimulate protective high affinity IgG production
importance of memory B cell response depends on nature of pathogen

151
Q

What is the time of onset for the influenza virus? What does this mean for influenza vaccines?

A

rapid onset - can be established before immunological memory can be activated
important to maintain high levels of antibody = annual boosts needed
mutates often so requires generation of new vaccines constantly

152
Q

What is the time of onset for polio? What does this mean for polio vaccines?

A

can take 3 days to establish infection in NS
lag gives time for memory to be activated and to generate antibodies
boosts not needed

153
Q

What are the 5 types of vaccine?

A 
whole organism
subunit
peptides
dna vaccines
engineered virus/recombinant vector
154
Q

What are the 2 types of whole organism vaccines?

A

live attenuated pathogen

killed inactive pathogen

155
Q

Give 2 examples of live attenuated vaccines. Explain how they are produced.

A

TB: grown for 13 years on medium containing bile > adapts with reduced virulence
Polio sabin: grown on monkey kidney epithelial cells > prolonged culture > adapts with lower virulence

156
Q

What is the TB vaccine called?

A

BCG vaccine: Bacillus Calmetie-Guerin

157
Q

What are the advantages and disadvantages of live attenuated pathogen vaccines?

A

+ set up transient vaccine
+ activates full natural immune response
+ prolonged contact with immune system
+ stimulation of memory response in T and B cells
+ often only a single immunisation is required

  • immunocompromised patients may become infected
  • in some vaccine it can revert to its virulent form e.g. measles
  • complications e.g. encephalomyelitis in measles vaccine
  • needs to be refrigerated for storage
158
Q

Give 3 examples of killed inactivated pathogen vaccines.

A

anthrax, cholera, hep A

159
Q

What are the advantages and disadvantages of inactivated pathogen vaccines?

A

+ no risk of infection
+ storage less critical
+ good immune response possible

  • tends to just activate humoral response
  • lack of T cell involvement
  • without transient infection, immune response can be weak
  • repeated boosters needed - problems with patient compliance
160
Q

What are the 3 types of subunit vaccines? Give examples for each and briefly how they work.

A

a. toxoids (inactivated exotoxins): pathogens often produce symptoms as a result of exotoxins e.g diphtheria, tetanus
b. antigenic extracts/capsular polysaccharides (block opsonisation) e.g. Men C
c. recombinant proteins: cloning and expression of a single gene in a recombinant host e.g. Bexsero

161
Q

What are the advantages and disadvantages of subunit vaccines?

A

+ theoretically safer than active/inactive pathogens
+ no risk of infection
+ easier to store

  • immune response less powerful than live
  • repeat vaccinations and adjuvants needed
162
Q

What is an adjuvant in a vaccine?

A

substance added to a vaccine that stimulates the immune system

163
Q

Give 6 examples of adjuvants in vaccines.

A

whole killed organisms: not used in humans
toxoids: trigger immune system and send out danger signals
proteins
chemicals e.g. aluminium salts (potentiate opsonised phagocytosis), paraffin oil
TLR agonists
saponins

164
Q

What are peptide vaccines?

A

field advancing slowly
needs to include immunodominant B cell epitopes
stimulate T memory cell development

165
Q

What are the difficulties with peptide vaccines?

A

can be stimulatory or suppressive
most B cell epitopes are conformational
knowledge of HLA presentation of peptides essential

166
Q

What are DNA vaccines? How do they work?

A

transiently express genes from pathogen to host cells
generates immune response similar to natural infection = produces T and B cell memory
expression vector > transfected into muscle cells

167
Q

What are the advantages and disadvantages of DNA vaccines?

A

+ don’t require complex storage
+ safe
+ delivery can be simple: no refrigeration needed

  • no transient infection
  • limited to proteins: can build up tolerance or anti-DNA antibodies
  • mild immune response = needs boosters
168
Q

Which cell types can take up DNA from a DNA vaccine?

A

usually muscle cells

other types can e.g. APCs

169
Q

What is a engineered virus vaccine? How does it work?

A

initiate effect of transient infection with pathogen but using a non-pathogenic organism
genes for pathogenic antigens introduced into a non-pathogenic/attentuated microorganisms > then introduced to a host

170
Q

Give a viral and bacterial example of an engineered virus vaccine?

A

viral: attenuated poliovirus
bacteria: attentuated strains of salmonella

171
Q

What are the advantages and disadvantages of engineered virus vaccines?

A

+ produce immunological memory
+ flexible: components can be engineered in
+ safe relative to live vaccines

  • requires refrigeration
  • immune response to virus can negate effectiveness
  • illness in immunocompromised

Phase 2a (5 decks)

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