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immunology Flashcards

1
Q

Why do we have an immune system

A

To protect against invasion by foreign organisms

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2
Q

What are the two types of immunity that we have

A

innate and adaptive

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3
Q

What is part of the innate immunity

A

Macrophages, granulocytes, NK cells, complement, physical barrier, ect.

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4
Q

What is part of the adaptive immunity

A

T and B cells

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5
Q

Compare innate and adaptive immunity

A

the response time of the adaptive immunity is day Vs hours of innate

Innate has a limited and fixed specificity while the adaptive is highly diverse, improves during the course of the response

the innate response to repeat infection is the same as the initial response while the adaptive response is more rapid

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6
Q

What is the first barrier to infection

A

Epithelial surfaces (mechanical protection) joined by tight junctions

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7
Q

What is the initial precursor to all cells in the immune system

A

The bone marrow: stem cells

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8
Q

What are the circulating cells in the blood divided into?

A

erythrocytes (red blood cells)

leukocytes (white blood cells)

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9
Q

classification of white blood cells (leukocytes)

A

Granular (eosinophils, basophils, neutrophils)

agranular (lymphocytes, monocytes)

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10
Q

What is a phagocyte

A

Type of cell that has the ability to ingest and sometimes digest foreign particles, such as bacteria, dust or dye.

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11
Q

what are the types of phagocytes in the immune system

A 
(monocytes:) 
macrophages 
dendritic cells 
(neutrophils)
Neutrophil
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12
Q

Difference between phagocyte macrophage/dendritic cells and neutrophils

A

Neutrophils are mostly short lived (60-70% of leukocytes) while macrophages/dendritic cells are long lived - can be fixed or migratory

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13
Q

What are the characteristics of inflammation

A
  • redness or vessel dilation
  • heat
  • swelling
  • pain
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14
Q

Describe the process that leads to inflammation

A
  1. bacteria trigger macrophages to release cytokines and chemokines
  2. vasodilation and increased vascular permeability cause redness, heat, and swelling (increased blood flow)
  3. inflammatory cells migrate into tissue, releasing inflammatory mediators that cause pain
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15
Q

what are the changes that occur to the local blood vessels during inflammation

A
  1. dilation of the blood vessel- increased blood flow
  2. changes in adhesion molecules- allows blood cells to ‘stick’
  3. increased permeability- blood cells can move into the tissue
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16
Q

How are pathogens recognised by phagocytes?

A
  1. the macrophage expresses receptors for many bacterial constituents= PAMPs (pathogen associated molecular pattern receptors).
  2. bacteria binding to macrophages receptors initiate the release of cytokines and small lipid mediators of inflammation
  3. macrophages engulf and digest bacteria to which they bind
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17
Q

What are PAMPs

example

A

Pathogen associated molecular pattern receptors - on macrophages
bind to receptors which result in the activation and secretion of inflammatory mediators

example Toll like receptors (TLR)

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18
Q

What are the different macrophages in the body

A

They are found all over-

microglia: phagocytose dying neurons
Alveolar macrophages: respond to local surface-acting stimuli e.g. Irritants, asbestos by cytokine release
Spleen macrophages: immune function. phagocytosis of naturally dying cells, clearance of particulate agents
kuppfer cells: Exposed to gut derived microbial products. Cannot mount a respiratory burst
joint: synovial A cells: responsible for cytokines in arthritis ..

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19
Q

What is Phagocytosis

A

It is the internalisation of particulate matter by cells

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20
Q

What are the 4 stages of phagocytosis

A
  1. Binding to surface receptors e.g. PAMP receptors
  2. Engulfment into vacuole/ phagosome
  3. Fusion of phagosome with lysosome
  4. killing and degradation of bacterium by lysozyme, proteases, acid hydrolases, free radicals.
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21
Q

Why don’t tattoos fade?

A

because long-lived macrophages take up colloidal ink by phagocytosis and endocytosis in situ. when they die, new macrophages move in to phagocytose the dead cells, resulting in a permanent colouration

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22
Q

What do macrophages secrete once activated?

A

a range of cytokines:

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

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23
Q

What secreted by macrophages can produce fever

A

IL-1, TNF- alpha and IL-6.

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24
Q

IL-6 function

A

Lymphocyte activation

increased antibody production

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25
Q

TNF-alpha function

A

aActivates vascular endothelium and increases vascular permeability, which leads to increased entry to igG, complement, and cells to tissues and increased fluid drainage to lymph nodes

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26
Q

IL-1 beta function

A

Activates vascular endothelium
activate lymphocytes
local tissue destruction
increased access of effector cells

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27
Q

What are neutrophils

A

They are the main line of defence against invading bacteria

belong to the innate immune system

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28
Q

Neutrophils structure

A

multi-lobed nucleus
granulated cytoplasm
stains with both acidic and basic dyes
phagocytic

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29
Q

In a normal adult how many neutrophils are produced?

A

1-3 10^10 / day from bone marrow

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30
Q

what is the primary function of neutrophils

A

Phagocytosis and killing of pathogens

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31
Q

First cells to bind to inflamed tissue

A

neutrophils

must leave bloodstream to gain access to tissues (extravasation)

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32
Q

How do the neutrophils and macrophages know where to go

A

chemotaxis (movement of an organism in response to a chemical stimulus).
They move up a gradient of attractive molecules towards the the source.

closer to source = high concentration of attractive molecules (chemokines)

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33
Q

What is the complement system

A

A set of plasma proteins (C1-C9) that act together as a defence against pathogens in extracellular spaces

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34
Q

What are the effector functions of complement

A

recruitment of inflammatory cells
killing of pathogens
coats microbes with molecules (opsonins) that enhances their phagocytosis.

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35
Q

What are the three ways that complement can bind bacteria

A
  1. classical pathway: Antigen: antibody complexes
  2. MB:lectin pathway: lectin binding to pathogens surface
  3. Alternative pathway: Pathogen surfaces

binding leads to complement activation–> effector functions

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36
Q

How are mast cells activated

A

FceRI are high affinity receptors for IgE on the surface of mast cells
when cross linked by allergen- antibody complexes, mast cells respond by degranulation

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37
Q

What are mast cells and Basophils primarily responsible for

A

type I (immediate) hypersensitivity ???

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38
Q

What do Mast cells release

A

granules containing histamine and active agents

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39
Q

what do Basophils do

A

promote allergic response and augment anti-parasitic immunity

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40
Q

What are NK cells

A

natural killer cells: they recognise infected cells or tumour cells and destroy them.

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41
Q

What to NK cells develop from where?

A

develop in the bone marrow from common lymphoid progenitor cells

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42
Q

How are NK cells different to T cells

A

They are larger with distinctive cytoplasmic granules

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43
Q

Describe the steps of NK cells encountering a normal cell

A
  1. MHC class I on normal cells is recognised by inhibitory receptors that inhibit signals from activating receptors
  2. NK cell does not kill the normal cell

MHC I acts as a inhibitory signal for NK cells

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44
Q

Describe the activation steps of NK cells

A
  1. ‘Missing’ or absent MHC class I cannot stimulate a negative signal. The NK cell is triggered by signals from activating receptors.
  2. Activated NK cells release granule contents, including apoptosis in the target cells.

NKC activated by the absence of MHC class I

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45
Q

What is NKC activation controlled by (summary)

A

The balance of signals from activating and inhibitory receptors
(absence of MHCI)

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46
Q

Describe the steps of Antibody dependent cell-mediated cytotoxicity (ADCC)

A
  1. Antibody binds antigens on the surface of target cells
  2. Fc receptors on NK cells recognise bound antibodies
  3. cross-linking of Fc receptors signals the NK cell to kill the target cell
  4. Target cell dies by Apoptosis.

Bound Antigens provide a +ve signal to the NKC to preform apoptosis

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47
Q

What are Fc receptors

A

FcERI- high affinity receptors for IgE on the surface of mast cells (cross link allergen antibodies: degranulation of antibodies)

Fc receptors on NKC recognise bound antibodies. Contribute to the protective function of the immune system.

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48
Q

What are Fc receptors

A

FcERI- high affinity receptors for IgE on the surface of mast cells (cross link allergen antibodies: degranulation of antibodies)

Fc receptors on NKC recognise bound antibodies attached to infected cells or invading pathogens. Contribute to the protective function of the immune system.

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49
Q

What cells form part of the adaptive immune system

A

T cells and B cells

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50
Q

What cells form part of the innate immune system

A

NKC, Mast cells, Macrophages, dendritic cells, neutrophils…

Not specific to individual pathogens, rely on signals on the surface.

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51
Q

What do B-cells recognise Vs T-cells

A

T-cells recognise processed antigen fragments when bound to MCH molecules= antigen presentation
= a combination of peptides and the MHC complex
B cells recognise intact antigens directly through antibody molecules

t cells= fragments of antigens
B-cells= intact antigens

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52
Q

MHC?

A

Major Histocompatibility complex

main function of MHC molecules is to bind antigens derived from pathogens and display them on the cell surface for recognition by T-cells

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53
Q

T-cell recognition

A

TCR recognises antigen presenting cell: right MCH complex with bound peptide.

Highly specific

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54
Q

MCH class I structure

A

peptide binds though middle in peptide-binding cleft- formed by 2 alpha helixes. another alpha helixe and beta 2 microglobulin form base

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55
Q

Where are the peptides derived from for class I Vs Class II MCH molecules

A

Bind peptides from different compartments

MHC I : peptides derived from intracellular proteins- brought to the surface of the cell- displayed on the MCH I molecule
short peptides
> tells immune system a lot about what’s going on inside the cell.
MHC II: peptides are derived from extracellular or vesicle proteins- brought inside the cell in vesicles + bind to MHC II
long peptides

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56
Q

Viral proteins tend to invoke HMC class…

A

I: intracellular proteins

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57
Q

Extracellular bacteria tend to invoke MCH Class..

A

II: extracellular or vesicle proteins

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58
Q

What cells respond to peptide bound MHC

A

T-cells

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59
Q

what cells respond to MHC I

A

CD8 T-cell

60
Q

what cells respond to MHC II

A

CD4 T-Cells

61
Q

Where do T cells and antigen carrying cells first meet?

A

Antigens from sites of infection reach lymph nodes via lymphatic system

62
Q

What is a Naive T-cell?

A

T-cell that hasn’t been activated yet, it stays in blood and lymph

63
Q

How does a T-cell get activated

A

via a specific signal and co-stimulation
requires two signals
Signal 1 and signal 2.

64
Q

A naive T-Cell requires what to be activated

A

Signal 1 and 2 or else the cell will be silenced

65
Q

An effector T-cell requires what to trigger effector function

A

Signal 1 (T-cell receptor engagement)

66
Q

How do dendritic cells function in naive T-cell activation

A
  1. immature dendritic cells in the periphery continually sample antigens in the environment by phagocytosis, macropinocytosis and receptor mediated endocytosis
  2. Upon stimulation by ‘danger signals’ DCs stop antigen uptake, up regulate co-stimulatory molecules (signal 2) and migrate to the lymph nodes - express B7: B7 positive dendritic cells stimulate naive T-cells

Dendritic cells function to activate T-cells by providing signal 1 (MHC/ peptide) and signal 2 (B7).

67
Q

Where are T-cells educated?

A

Thymus

68
Q

What is the system that prevents T-cells from acting on ‘self’?

A

By testing the affinity of the TCR to self peptides

If they have a strong affinity, they are auto reactive thus by negative selection they are deleted.

Weak affinity: positive selection- cell survives

very weak affinity: death by neglect- cell is deleted.

69
Q

What are the two major subsets of T-cells?

A

CD8 T-cells: recognise MCH I + peptide in all nucleated cells

CD4 T-cells: recognise MHC II + peptide in professional APC (antigen presenting cell) (dendritic cells)

70
Q

How do CD8 T cells function

A

Cytotoxic T Lymphocytes (CTL)
kill virally infected cells
secrete cytokines

71
Q

How do CD4 T-cells function

A

produce Helper T- cells
TH1: secrete cytokine which activate macrophages, assist cellular immunity
TH2: provide signals for B-cell maturation
TH17: involved in inflammation
Treg: suppress immune response

72
Q

What are the mechanisms involved in CTL (CD8 + T cell) killing

A
  1. primary mechanism
    TCR triggering leads to the directed secretion of preformed lytic granules (5 min)= target cell death
  2. second mechanism
    membrane expression of FAS LIGAND causes cross linking of FAS on the target cell and triggering of apoptosis
73
Q

What are the two main proteins found in Lytic granules, what is their function?

What are lytic granules?

A

Preforin: polymerises to form a pore in the target cell membrane

Granzymes:

  • at least three serine proteases
  • activate apoptotic pathways in the cytoplasm of the target cell

Secreted by the CTL T cells in response to TCR triggering.

74
Q

where do T cells develop

A

in the thymus

75
Q

What is the function of CD4 + TH1 T cells

A

Secrete IFN-gamma, TNF- alpha to help macrophages.

The APC in tissues (dendritic cell become mature) express the two signals. activate CD4 T cell–> cause proliferation differentiation in lymph node and migration to inflammatory site—> TH1 connect to infected macrophage via signal 1–> activation of infected macrophage to kill intracellular pathogens

76
Q

What is the function of CD4 + TH2 cells

A

Help for B cells (secrete IL-4, IL-5)

TH2 cells bind B cell, signal 1, release IL-4, iL-5: causes proliferation, differentiation Ig production, Ig class switching in B cell bound antigen.

77
Q

Most antibody production is dependent on … help

A

T cell

78
Q

The balance of CD4 T Cell TH1 Vs TH2 affects disease outcomes
example

A

mycobacterium leprae infection- two forms of disease depending on which is primary response TH1 or TH2.

TH1 response: macrophage activation- Tuberculoid leprosy (eradicated)

TH2 response: antibody release: lepromatous leprosy- proliferate out of control

79
Q

lepromatous leprosy results from

A

mycobacterium leprae infection –> failed TH1 cells activation, thus fails to eradicate the disease

80
Q

What are antibodies or immunoglobins (Ig)

A

glycoproteins found on surface of B-cells (as part of B cell receptor =BCR) and in mammalian serum and tissue fluid

81
Q

What do antibodies recognise

A

‘epitope’ of an antigen (e.g. on pathogen)

each B-cell produces antibodies of a single specificity (recognise specific epitope of antigen)

82
Q

What do antibodies / immunoglobins do

A

they recruit molecules and cells to destroy pathogens

83
Q

What happens when antigen is recognised by BCR

A

The antibody must have same specificity as the membrane bound form.

B cells mature into antibody secreting = plasma cells

84
Q

What is the antibody structure

draw + describe

A

4 upper sections (Fab) and two lower sections (Fc) joined to mirror sections by disulphide bonds

An antibody has two basic regions : a variable region (N terminus) and a constant region ( C terminus) (variable region is the top of the two upper sections)

Also has light chain (2 outside top) and heavy chain (inside top and all bottom)

85
Q

Which past of the antigen is in contact with antigen

A

Variable region/ half light and half heavy chain

86
Q

What are the proteolytic cleavage molecules of antibodies

A

papain and pepsin

87
Q

Where does Papain cleave the antibody

A

at the disulphide bonds - one spot

88
Q

Where does pepsin cleave the antibody

A

below the disulphide bond- multiple cleavage points

89
Q

What are the primary 5 isotypes of antibodies

What changes

A
  1. IgG
  2. IgM
  3. IgD
  4. IgA1
  5. IgE
    heavy chain
    light chains are either kappa or lambda
90
Q

What determines the class/ isotype of an antibody

A

The heavy chain

91
Q

What multimer does IgM form

A

pentomeric structure-
5 basic IgM units linked
10 identical binding sides
linked by J chain

92
Q

What multimer does IgA form

A

Dimeric IgA
2 basic units of antibodies linked
4 identical binding sites
linked by J chain

93
Q

Where does B cell development occur

A

in the bone marrow

94
Q

Describe the steps of B cell development

A
  1. B cell precursor rearranges its immunoglobulin genes- bone marrow stromal cell= generation of B cell receptors in the bone marrow
  2. Immature B cells bound to self cell- surface antigen is removed from the repertoire- negative selection in the bone marrow (testing step- ensure not autoimmune)
  3. mature B cell bound to foreign antigen is activated- B cells migrate to the peripheral Lymphoid organs
  4. activated B cells give rise to plasma cells and memory cells - Antibody secretion and memory cells in bone marrow and lymphoid tissue.
95
Q

IgM is primarily involved in which part of an immune response

A

the initial part

96
Q

Draw the antibody levels during an immune response

A

Antigen A introduced–> lag phase of 4 ish days –> primary response by IgM

Antigen A introduced again–> no lag response–> secondary response by IgG, IgA, IgE. (a lot more antibody in serum)

97
Q

Describe Isotope switching

A

Switch from IgM production to other isotypes (IgG, IgA)
need the variable region- VDJ + elements to encode constant region.

genetic elements called switch elements loop out parts of the sequence. Realigns the variable region with a different element.

Directional process, can only happen downstream.

Switching the heavy chain- determines the isotype

98
Q
  • heavy chain

- light chain

A
  • All constant elements
    Variable region in heavy chain made of 3 regions: VDJ (variable diversity join) - body will randomly chose one section in each region.
  • variable region in light chain made from 2 regions: VJ

variable regions= where diversity comes in, so you can recognise numerous antigens

99
Q

What mechanisms are responsible for antibody diversity

A
  1. Heritable V/D/J gene segments and somatic recombination
  2. Junctional diversity
  3. pairing of different heavy and light chains
  4. somatic hypermutation (not part of development- an enzyme will come in and try and increase affinity of antibody to antigen)
100
Q

In a lymph node, what are the different sections

A

paracortical area= mostly t cells
Secondary lymphoid follicle with germinal centre (B cells)
Medullary cells= macrophages and plasma cells
????

101
Q

What is required for B cell activation

2 mechanisms for antibody production

A

Signal 1 and 2

  1. T-cell dependent antibody production
    antigen provides signal 1
    signal two comes from helper T-cell (CD40, cytokines)
  2. T- cell independent antibody production
    > rare in nature
    get signal 1 and 2 from antigen
102
Q

What are the antibody effector functions

A
  1. Neutralisation (Fc independent). Bind antigen and block function e.g. prevent entry into cell, block toxicity.
  2. Opsonisation (coating of microbe with molecules to allow its destruction by phagocytes). Promotes phagocytosis of antibody coated pathogens
  3. Complement activation. Recruits/ activates phagocytes, directly kill pathogen, opsonisation.
  4. ADCC (antibody-dependent cell-mediated cytotoxicity). NK cells destroy coated cells
  5. Triggering of mast cells, basophils and activated eosinophils.
103
Q

What are some features unique to IgM antibody isotype

A

main antibody in primary immune response

104
Q

What are some features unique to IgG antibody isotype

A

Transport across the placenta

105
Q

What are some features unique to IgE antibody isotype

A

Sensitisation of mast cells, involved in allergy

106
Q

What are some features unique to IgA antibody isotype

A

transport across epithelium, main antibody found at mucosal sites and mucosal secretions

107
Q

What are some features unique to IgD antibody isotype

A

No know functions

108
Q

What do B-cells produce that are important for recognition of diverse array of foreign antigens

A

antibodies

109
Q

What are the research uses of antibodies

A
  1. Polyclonal Antibodies
  2. Monoclonal Antibodies
  3. Antibodies made by phage display
110
Q

Polyclonal Antibodies

A

Animal Immunised (antigen/ adjuvant), followed by boosters.
serum (containing complx mixture of antibodies) is collected.
Antibody can be affinity purified
Antibody is heterogeneous, limited supply, batch specific

111
Q

Monoclonal Antibodies

A

Animal immunised as in polyclonal antibodies
spleen cells harvested and fused with myeloma cells
single cell clones screened for reactivity against antigen
unlimited supply of antibody with defined specificity

112
Q

Antibodies made by phage display

A

cDNA libraries generated (PCR)- H and L Chains V regions
these are fused to bacteriophage coat protein
Bacteriophage library screened for reactivity to antigen

113
Q

Other applications for antibodies???

A
  • immunoflurorescence microsopy.
  • immunoelectron microscopy
  • immunoprecipitation
  • immunohistochemistry
  • immunoblotting
  • flow cytometry
  • purification of cells (magnetic beads)
114
Q

What are the two major categories of immune deficiencies?

A 
1. primary immune deficiency 
> may be hereditary or acquired 
> immune deficiency is the cause of the disease 
2. secondary immune deficiency 
> result of another disease or condition
115
Q

What is the difference between how primary and secondary immune deficiency are acquired?

A

Secondary is the result of another disease, primary causes a disease

116
Q

What does primary immune deficiency involve? (like cause?

A

50% involve antibody deficiency
20% involve combined Ab and cell mediated immunity deficiency
18% involve phagocytic disorders
10% involve cell mediated immunity deficiency
2% involve complement deficiency

117
Q

Give example of a primary immune deficiency + cause

A

X-linked hyper IgM syndrome, involved defective CD40 ligand, implies there are no isotope switching. so extracellular bacteria can get in?

118
Q

what are Secondary immune deficiency disorders a consequence of

examples

A

consequence of another disease or condition, generating further complications

  • burns
  • leukaemia (malignant cells replace functional T and B cells)
  • Chemotherapy
  • deliberate immunosuppression of transplant recipient
  • certain infections (e.g. HIV)
119
Q 
Draw the curve of HIV infection
effect on: 
Antibodies against HIV
HIV specific CTL
infectious virus in plasma 
CD4
A

Antibodies against HIV- rise quickly in the first 8 weeks- 2 years then drop quickly 1 year before death
HIV specific CTL- rise quickly in the first 8 weeks to 2 years- drop a bit 2-12 years in
infectious virus in plasma- significant in the first 4 weeks-8weeks then drops as protective functions come in- rise steadily 2-3 years before it takes over
CD4- initial drop then gradual decrease before being under protective level

120
Q

What causes allergic rhinitis, asthma, systemic anaphylaxis

A

type 1 hypersensitivity

immune reactant: IgE
antigen: Soluble antigen
effector mechanism: mast cell activation

121
Q

Immune reactant in type 1 hypersensitivity

A

immune reactant: IgE

122
Q

Effector mechanism in type 1 hypersensitivity

A

effector mechanism: mast cell activation

123
Q

What causes some drug allergies (e.g. penicillin)

A

type 2 hypersensitivity

immune reactant: IgG
antigen: cell or matrix associated antigen
effector mechanism: complement, FcR+ cells (phagocytes, NK cells)

124
Q

What causes chronic urticaria (antibody against FCeR1alpha)

A

type 2 hypersensitivity

immune reactant: IgG
antigen: cell- surface receptor
effector mechanism: antibody alters signalling

125
Q

Immune reactant in type 2 hypersensitivity

A

IgG

126
Q

Effector mechanism in type 2 hypersensitivity

A

complement, FcR+ cells (phagocytes, NK cells) or antibody alters signalling

127
Q

what causes serum sickness, arthus reaction

A

type 3 hypersensitivity

immune reactant: IgG
antigen: soluble antigen
effector mechanism: Complement, phagocytes

128
Q

Immune reactant in type 3 hypersensitivity

A

IgG

129
Q

Immune reactant in type 4 hypersensitivity

A

Th1 cells, Th2 cells (ass. CD4)

CTL (ass. CD8)

130
Q

what causes contact dermatitis

A

type 4 hypersensitivity

immune reactant: Th1
antigen: soluble antigen
effector mechanism: macrophage activation

131
Q

What causes chronic asthma, chronic allergic rhinitis

A

type 4 hypersensitivity

immune reactant: Th2
antigen: soluble antigen
effector mechanism: IgE production, Eosinophil activation, mastocytosis

132
Q

what can also cause contact dermatitis

A

type 4 hypersensitivity

immune reactant: CTL
antigen: cell associated antigen
effector mechanism: cytotoxicity

133
Q

What occurs in type I hypersensitivity

A

IgE immune reactant and the allergen cause the mast cell to activate and release histamine and leukotrienes

134
Q

What are some clinical tests for allergy

A

Skin prick test

skin path test - application of allergen

135
Q

type 4 hypersensitivity is also known as

A

delayed type hypersensitivity (DTH)

136
Q

what is different about type 4 hypersensitivity compared to the others

A

It is antibody independent- T cell mediated

reactions develop hours to days after contact with antigen

137
Q

Describe the steps in a DTH reaction

A

= type 4 hypersensitivity over the course of 24-72 hours:

  1. Antigen is injected into subcutaneous tissue and processed by local antigen-presenting cell
  2. A Th1 effector cell recognises antigen and releases cytokines which act on vascular endothelium = recruitment of previously primed Th1 cells.
  3. Recruitment of phagocytes and plasma to site of antigen injection causes visible lesion = recruitment of phagocytes and inflammatory cells
138
Q

What is autoimmunity

A

An induction of an immune response against ‘self’

may be organ-specific, localised or systemic
consequences may be minimal or lethal

139
Q

What is Autoimmunity related to

A

the breakdown of tolerance

140
Q

What are tolerance mechanisms

A

the mechanisms to prevent autoimmunity

  1. Central tolerance/ negative selection (thymus)
  2. Antigen segregation (physical barrier, no access)
  3. Peripheral anergy (no costimulation)
  4. regulatory T-Cells
  5. Cytokine deviation
  6. Clonal exhaustion (apoptosis of cells after continuous stimulation)
141
Q

Examples of autoimmune diseases
organ specific
systemic

A 
organ specific 
type I diabetes mellitus 
Goodpasture's syndrome 
Multiple sclerosis 
Grave's disease 
systemic 
Rheumatoid arthritis 
scleroderma 
systemic lupus erythermatosus 
Primary Sjogren's syndrome 
polymyositis
142
Q

Cause of cancer

A

the progressive growth of the progeny of a single transformed cell
transformation can be spontaneous, or as the result of exposure to certain viruses, ionising radiation or mutagenic chemicals

143
Q

what is the theory of ‘immune surveillance’

A

proposes that the immune system continually surveys the body for the presence of abnormal cells, which are destroyed when recognised
also proposes that the immune system plays an important role in the regression of established tumours

144
Q

What are the types of tumour antigens

A
  1. Mutated proteins
  2. re-expressed developmental antigens
  3. differentiation antigens (e.g. Tyrosinase)
  4. Over -expressed self antigens (e.g. Her2)
  5. Modified self antigens
  6. Oncoviral proteins (e.g. HPV)
145
Q

What are the mechanisms by which tumours avoid immune recognition

A
  1. Low immunogenicity: immune system doesn’t realise. NO peptide: MHC ligand
    no adhesion molecules
    No co-stimulatory molecules
  2. Tumour treated as self antigen: antigen but no co-stimulation (signal 2)
  3. Antigenic modulation: T-cells may eliminate tumours expressing immunogenic antigens, but not tumours that have lost such antigens. change antigens.
  4. Tumour induced immune suppression: factors secreted by tumour cells inhibit T cells directly, expression of PD-L1.
  5. Tumour induced privileged site: Factors secreted by tumour cell create a physical barrier to the immune system
146
Q

What are some immunotherapies of tumours

A
  1. non-specific immune activating substances (e.g. adjuvant: stimulate APCs and NK cells)
  2. cytokine therapy (interferon for some leukaemia and carcinomas)
  3. monoclonal antibodies
  4. transfer of cytotoxic T- cells
  5. Vaccines (e.g. cervical cancer)

BIOM2011 (6 decks)

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