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3rd BDS IHD > Immunology > Flashcards

Immunology Flashcards

1
Q

what is passive immunity

A

administration of pre-formed “immunity” from one person or animal to another person

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2
Q

what are the advantages and disadvantages of passive immunity

A

Advantages:
-Gives immediate protection
-Effective in immunocompromised patients
Disadvantages:
-Only antibody mediated (not work if cell mediated !)
-Short-lived
-Possible transfer of pathogens
-“Serum sickness” on transfer of animal sera

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3
Q

what is HTIG

A

human tetanus immunoglobulin
passive immunity for tetanus

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4
Q

how is rabies treated

A

passive immunity of antibodies

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5
Q

what is HNIG

A

human normal immunoglobuilin
antibodies taken from 1000’s of donars
contains measles, mumps, varicella, hepatitis A

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6
Q

what can vaccinations be classified into (2)

A

non-living vaccines (whole killed and toxoids)
live attenuated vaccines. These stimulate a humoral response.

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7
Q

explain T cell priming of the humoral response (4)

A

Antigen bound to and internalised by APC (phagocytosis)
Antigen processed and peptide displayed on APC surface with MHC II
TCR of naïve T-cell (CD4) binds to Ag/MHC II complete
Naïve T-cell become activated and turn into primed Th2 cell

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8
Q

what is MHC and what is their use

A

major histocompatibility complex
display site for antigens on APC for T cell activation

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9
Q

explain T and B cell co-operation in humoral response

A

B-cells internalise and present the same antigen with MHC class II – to the primed Th2 cells.
Th2 cell now secretes cytokines – IL-4, IL-5, IL-10 and IL-13
These cause B cells to divide – Clonal Expansion and differentiate into plasma cells (AFC = antibody forming cell) and Memory B cells (Bm)
Plasma cells secrete antibody that have high specificity to the original antigen

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10
Q

what 2 cell types cna B cells differentiate into

A

Plasma cells - APC antibody producing cells
Bm cells - B memory cells

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11
Q

what are whole killed vaccines

A

where the organism/protein injected is dead/inactive
antigens still produce immune response
can be anti-toxoids

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12
Q

give an example of where cell-free toxoids are used

A

against the tetanus toxoid

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13
Q

how might we ‘inactivate’ a toxoid/organism

A

using formaldehyde or Β-propiolactone

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14
Q

what are some limitations of non-living vaccinations

A

The organisms must be grown to high titre in vitro (viruses and some bacteria difficult/expensive to grow in the lab)
Whole pathogens can cause excessive reactogenicity (i.e. adverse reactions, excessive immunological responses)
Immune responses are not always close to the normal response to infection, e.g no mucosal immunity, no CD8 Tc responses, slight change shape
Usually need at least 2 shots

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15
Q

give some examples of inactivated non-living viral vaccines

A

Polio vaccine (Salk)
Influenza vaccine
Hepatitis A vaccine
Rabies vaccine
SARS-Co-V2 (Valneva)

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16
Q

how do live attenuated vaccines work

A

The organisms replicate within the host and induce an immune response which is protective against the wild-type organism but does not cause disease.

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17
Q

what is ‘attenuation’ of a microbe

A

Attenuation - Where an organism is cultured in such a way that it does not cause disease when inoculated into humans. It has lost its pathogenicity but retains its antigenicity – (i.e., shape).

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18
Q

give 3 limitations of live attenuated vaccines

A

Often impossible to balance attenuation and immunogenicity
Reversion to virulence - live polio vaccine
Transmissibility
Live vaccines may not be so attenuated in immunocompromised hosts

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19
Q

give a viral example of a live attenuated vaccine

A

MMR measles mumps and rubella

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20
Q

why might we not have a vaccine for a pathogen

A

Pathogen too difficult to grow
Killed pathogen not protective (shape change)
Impossible to obtain attenuated and suitably immunogenic strain
Too many strains causing disease etc.
Usually tale 10-15 years to make

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21
Q

what are the 5 ways of vaccination and which has no examples on the market

A

Recombinant Proteins
Synthetic Peptides - no examples on the market
Live Attenuated Vectors
mRNA Vaccines
Polysaccharide-Protein Conjugates

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22
Q

what are recombinant protein vaccines and give examples/limitations

A

genetically modified proteins grown from yeast/bacteria
limitations: proteins don’t induce strong enough response
examples: HPV, Hep B surface antigen

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23
Q

explain how viral vector vaccination works (4)

A

viral vector DNA is combined with antigen protein genes
when injected, taken up by APC
Viral DNA is taken up by nucleus and transcribed and translated
Presented on MHC and produces immune response

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24
Q

give an example of viral vector live attenuated vaccine

A

Oxford -Astra Zeneca covid 2 vaccine

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25
Q

explain advantages/disadvantages of DNA vaccines

A

Avoid the need to grow the pathogen, viral vector
No live organism involved
DNA is cheap to produce
DNA problem is often poor immunogenicity
None on the market

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26
Q

what is needed for DNA/mRNA vaccines to reach cells and why

A

lipid nanoparticles
stabilise and protect the mRNA from degradation and allow the mRNA to cross the plasma membrane

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27
Q

compare Oxford Astra-Zeneca and Moderna/Pfizer

A

OAZ - genetically modified viral vector and stored in regular fridge temp
Moderna/Pfizer - DNA/mRNA vector and stored in -20 to -70 degrees

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28
Q

compare DNA and mRNA vaccines and what common (dis)advntages

A

DNA needs to enter nucleus to be transcribed and translated
mRNA only needs to reach cytoplasm for translation
dis : store very cold
ad :Avoid the need to grow the pathogen, viral vector, No live organism involved, mRNA is cheap to produce

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29
Q

which 3 immunoglobulins have similar Y structure

A

IgG, IgE, IgD

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30
Q

what are the 5 immunoglobulins

A

IgA, IgG, IgM, IgE, IgD

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31
Q

which Ig is a pentamer

A

IgM

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32
Q

describe the structure of secretory IgA

A

dimer of 2 IgA components
with a secretory J chain

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33
Q

which Ig’s have the highest and lowest amounts in healthy blood

A

highest= IgG
lowest = IgE

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34
Q

what is the Hib vaccination and how does it work

A

Haemophilus influenzae type B vaccine
Hib polysaccharide and diphtheria toxoid bound together
Hib binds to cell wall and conjugates to a Hep B B cell
polysaccharide cannot be processed but diphtheria protein is and is expressed
Diphtheria T cell activates the Hep B B cell

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35
Q

how do protein conjugate vaccines work

A

they use a conjugate of a polyaccharide of the target pathogen and protein of helped pathogen
polysaccharide binds to wanted B cell but cannot be processed
helper protein is processed and expressed to get helper T cell
Activates the target B cell

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36
Q

give examples of conjugate vacciones

A

Meningitis C
Haemophilus influenzae type B Hib
Streptococcus pneumoniae 23-valent polysaccharide vaccine or 7-valent conjugate

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37
Q

give some reasons for not trusting vaccines

A

religion - acting against gods will
rumours around atusim, downs syndrome, neurological disorders with HPV (japan)

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38
Q

what percentage of population thin vaccine are safe

A

79%

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39
Q

what do all blood cells derive from

A

multipotent haematopoietic stem cells from bone marrow

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40
Q

what are the 2 classifications after a multipotent haematopoietic stem cell

A

common lymphoid progenitor cell –> lymphocytes
common myeloid progenitor cell –> RBC, platelets, neutrophils, macrophages

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41
Q

what are dendritic cells, where are they found

A

Dendritic Cells (often called Langerhans cells) reside in the oral mucosa, often seen as a band of cells in the spinous layer of the epithelium.

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42
Q

what do plasma cells look like histologically

A

lots and lots of RER for antibody production with very large nucleus
look like a fried egg

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43
Q

compare innate and acquired immunity

A

innate:
-First line of defence
-Is present from birth
-has no memory component
-Same speed, even if antigen is known
-is not specific and does not require lymphocytes.

Acquired:
-Response specific to a particular antigen
-involves memory to specific antigen (development of memory T and B lymphocytes)
-quicker response when the microbe/antigen is encountered the second time
requires the involvement of T and B lymphocytes
-not present from birth

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44
Q

what is an antigen

A

Anything that is recognised by the immune system as non-self

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45
Q

what is an antibody

A

proteins produced in response to an antigen. It can only bind to the antigen that induced its formation – i.e. specificity.

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46
Q

what is an Epitope

A

the specific part of the antigen that binds to the antibody.

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47
Q

what is affinity

A

measure of binding strength between an epitope and an antibody binding site. The higher the affinity the stronger the interaction.

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48
Q

what is polyclonal antiserum and how is it achieved

A

Inject Ag into the animal (large animals) and leave for 4 weeks for primary Ab response.
Give booster injection of the same Ag.
Leave 4 weeks for a secondary Ab response which is larger due to memory.
Collect blood and centrifuge to isolate serum.
Collect serum and check for Ab specificity and affinity.
Bind to different sites = polyclonal

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49
Q

explain production of monoclonal antibodies

A

Mouse immunised with antigen
Mouse produces Ab to Ag
Spleen removed to get plasma cells (NB. 1 plasma cell = 1 Ab = 1 specificity)
Plasma cells fused with immortal B cells using polyethylene glycol to produce immortal hybridomas
Cells are placed into 96-well plates containing HAT (hypoxanthine, aminopterin, thymidine).
This kills off non-fused cells so only hybridoma cells survive.
Dilute so have only 1 hybridoma per well – this will produce just a single mAb with 1 specificity.
Hybridomas secreting high affinity mAb selected using ELISA against original Ag.
End up with a limitless supply of high affinity mAb.

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50
Q

what is a hybridoma

A

immortalised cancer cell fused with a plasma cell

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51
Q

compare direct and indirect antibody tests

A

direct = testing antibody on the antigen
indirect = testing an antibody for an antibody of an antigen
using tagging of the antibody

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52
Q

what is the titre of an antibody

A

the lowest dilution of the sample that retains a detectable activity

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53
Q

what can serological dilution be used for (4)

A

Diagnose infections - only retrospective
Identify microorganisms
Quantify proteins in the serum ***
Type Blood – for blood banks and tissue transplantations

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54
Q

describe the ouchterlony diffusion test

A

Ab and Ag are placed into a well cut into agar gels.
The Ab and Ag diffuse through the gel and form a precipitate at the equivalence point (usually visualised by staining).

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55
Q

how do we test for antibodies for influenza

A

hemagglutination inhibition test

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56
Q

explain the hemagglutination inhibition test

A

Influenza has haemagglutinin molecules on their outer surface
Hemagglutinin binds the virus to red blood cells
When virus particles are mixed with red blood cells from patient with no antibodies they cause haemagglutination. This forms an aggregate
In the presence of specific anti-haemagglutinin Abs in blood from patient, binding of haemagglutinin to RBC is inhibited. RBC settle to bottom of tube

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57
Q

how do we test for influenzal meningitis

A

take CSF
Sample mixed with a suspension of latex beads coated with specific anti-H. influenzae Ab
Interaction between Ag and Ab causes agglutination of beads which can be seen by eye – positive diagnosis for H. influenzae.

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58
Q

when do we use the anti ASO test

A

detection of streptococcus antibodies

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59
Q

exaplin the ASO test

A

Serum taken from patient and diluted in tubes containing standard amount of sheep RBC and streptolysin O toxin.
If the patient has Ab to O toxin it will neutralise (inhibit) O toxin and stop it from lysing RBC (RBC settles to bottom of tube and the tube is clear).
At low Ab concentration there is not enough Ab to stop RBC lysis (RBC bust releasing haemoglobin – red tubes).
This gives the Ab titre

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60
Q

what blood groups are universal donor and universal acceptor and why

A

donor - O
Blood type O do not have A or B antigens on their surface so do not aggregate with antibodies in blood
acceptor - AB
AB do not produce antibodies for A or B or O

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61
Q

what would happen if you gave someone with blood Type A, some blood from a person with blood type B

A

blood type A will have anti-B antibodies in their blood
type B blood will express B antigens
Anti-B antibodies will aggregate with B antigens and cause an aggregation
This clots blood and can be fatal

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62
Q

why is ELISA used and what are the two types

A

to detect presence and levels of Ag, Ab or proteins in a sample
Used to accurately quantify levels of test molecule in a sample using a standard curve - very accurate
sandwich and antigen ELISA

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63
Q

explain sandwich ELISA test

A

Capture Ab bound to a plastic surface that is specific for desired Ag.
Add patient serum, CSF or supernatant (and standards to other wells)
Ab will bind specifically to Ag it is raised to. 1000s of other Ag are washed away.
Add Detection Ab – this has an Enzyme (usually HRP) conjugated to it for direct detection
Wash of excess detection Ab.
Add substrate for enzyme – this is colourless and turns blue in the presence of enzyme.
The more Ag the more colour is produced
Measure absorbance 450nm
Calculate concentration of Ag in the sample
E.g. for TNFalpha

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64
Q

what enzyme is usually used for detection in ELISA tests

A

HRP

65
Q

what are the two types of ELISA tests used for

A

sandwich : used to measure cytokines, virus, bacterial products etc in serum and lab
Antigen: used to measure concentration of human antibody in serum to bacteria - antibodies to Strep. Pneumoniae

66
Q

explain the antigen ELISA test

A

Bind Ag/bacteria to solid phase
Wash off excess Ag
Add primary Ab specific for the Ag
Wash of excess primary Ab
Add secondary Ab. This is specific for the primary Ab and is conjugated with an enzyme (HRP)
Wash off excess secondary Ab
Add substrate
Substrate turns from colourless to blue.
Measure absorbance on spectrophotometer
Calculate concentration of Ag if it has a std curve.
Indirect detection

67
Q

explain flow cytometry

A

Widely used to analyse cells and cell surface receptors in clinic and research
Uses Ab that are conjugated with a fluorescent tag (can be direct or indirect)
A laser is used to excite the FL tag
The emission intensity given by the FL tag is recorded
More emission intensity the more receptors on the cell
Up to 18 colours can be detected simultaneously – so you could measure expression of 18 cell surface receptors all at the same time.
Can also measure the size and granularity of cells

68
Q

how is HIV monitored

A

Flow Cytometry of CD4 and CD8 cells
CD4 : CD8 ratio as HIV affects CD4, T-helper cells

69
Q

what are the two types of diagnostic microscopy and compare (2)

A

Immunohistochemistry – staining of sections of tissues (wax or frozen)
Immunocytochemistry – staining of cells
Wax perseveres the tissue architecture better than frozen
Not as many Ab can be used in wax so must be used in frozen

70
Q

how do we ‘snap freeze’ tissues for microscopy

A

liquid nitrogen

71
Q

how can we get cells to be ‘splat’ onto glass slide

A

very fast ‘cytospin’

72
Q

explain how we do Immunocytochemistry

A

cells taken from patient and grown in culture
cells mixed with markers for secifics e.g. VWBF
cells put on cytospin to ‘splat’ cells onto slide
microscopy

73
Q

what are some problems with therapeutic monoclonal antibodies and give solutions

A

Most monoclonal Ab are raised in mice
These are NOT human (not-self)
The human immune system will raise Ab to the therapeutic Ab and will inactivate it.
solution = humanised monocloncal antibodies

also can cause MRONJ
solution = prevent need for XLA with good OH

74
Q

what are humanised monoclonal antibodies

A

These are Ab where only the Ab binding site is mouse, the rest has been engineered to be human
Enough of the therapeutic Ab is human for it not to be recognised as non-self

75
Q

how does Herceptin work

A

Trastuzumab
humanized monoclonal antibodies
blocks HER2 receptors which usually bind to growth factors which cause breast, ovarian, stomach and endometrial cancer

76
Q

what does the suffix omab mean

A

rat - murine monoclonal antibodies

77
Q

what does the suffix zumab mean

A

humanized monoclonal antibodies

78
Q

what does the suffix Mumab mean

A

Human monoclonal antibodies

79
Q

what does the suffix ximab mean

A

Chimeric monoclonal antibodies - more than 1 animal involved

80
Q

what is a common protein that monocloncal antibodies attack when used against cancer

A

PD-1 and PDL-1
tumour cells express PDL-1 this which bionds to PD-1 on T cells
deactivates and prevents T killing
inhibition of these sites leads to T cell killing

81
Q

why is hypersensitivity a problem in general and dental surgery

A

general:
-growing autoimmunity to lactose/glucose
-growing allergic reactions

dentistry:
-patients and staff allergy to latex
-allergies to dental materials e.g. zinc

82
Q

how do T killer cells act

A

CD8+ cells
when activated by the cell mediated response they release granulysin, perforin and IFNgamma
granulysin and perforin lyse cells and kill them
IFNgamma recruits macrophages

83
Q

what is a hypersensitivity and when does it occur

A

an overactive, damaging immune response e.g. allergy
occurs due to a stimulus, usually on second exposure

84
Q

what are the 4 types of hypersensitivity

A

Type I - Immediate/anaphylaxis - antibody mediated
Type II - Cytotoxic - antibody mediated
Type III - Immune complex - antibody mediated
Type IV - Delayed -T cell mediated

85
Q

what is an allergen

A

antigen that gives rise to a type I immune hypersensitivity

86
Q

describe type I hypersensitivity

A

IgE mediated
very fast onset
allergic reaction

87
Q

A person with high IgE levels is…

A

more likely to be susceptible to type I hypersensitivity

88
Q

explain mast cell degranulation

A

Mast cells contain high amounts of granules that contain histamine
Fc3 receptors on surface can bind to the ligand IgE on 1st exposure of allergen
After a second exposure, the antigen cross-links the Fc3 receptors on the cells - clustering - signals
This causes histamine release and IL-5 release stimulating eosinophils

89
Q

what receptors on mast cells lead to degranulation

A

Fc3 receptors for IgE

90
Q

what are 6 results of histaminerelease

A

Vascular dilatation
Increased Vascular permeability i.e. oedema
Bronchospasm
Urticarial rash – nettle rash
Increased nasal and lacrimal secretions

91
Q

what are the two phases to type I hypersensitivity

A

immediate phase: initial swelling, erythema
Lag Phase: generalised swelling due to oedema and leukocyte infiltration

92
Q

what is the wheel and flare skin test

A

skin test for type I hypersensitivity
Apply a small amount of allergen just under the skin using a needle prick.
Skin response is fast (5 min)
WHEEL caused by extravasation of serum into skin due to histamine – angio-odema.
Must be supervised in hospital
FLARE (erythematous red patch) caused by axon reflex.
Late Phase (6 h+) due to leukocyte infiltrate + more oedema

93
Q

give 4 ways to treat type I hypersensitivity

A

Adrenaline (epinephrine)
Anti-histamines
Corticosteroids - much more side effects
Avoidance of allergen

94
Q

what antibodies are involved in Type II hypersensitivity

A

IgG or IgM

95
Q

explain type II hypersensitivity

A

antibody mediated hypersensitivity
antibodies target cell surface self antigens (auto-antibodies) due to shape change
Usually IgG or IgM
The antibodies induce: cell damage and Inflammation

96
Q

when do we see type II hypersensitivity

A

Acute transplant rejection / blood transfusion
Haemolytic disease of the new-born: Rhesus + or -
Autoimmune diseases e.g. coeliac

97
Q

what Type II hypersensitivity affects the oral cavity and explain (3)

A

Pemphigus
Auto-antibodies against desmoglein-1&3
Ab prevents formation of junctions between epithelial cells
Epithelial shedding – mainly mucosal

98
Q

what is Pemphigoid

A

Auto-antibodies against hemidesmosomes
Ab prevents binding of epithelium with dermis at basement membrane
Epithelial shedding – skin and mucosal - left with connective tissue
ulcerations

99
Q

what is an immune complex

A

the complex formed by antibody and antigen

100
Q

what is a type III hypersensitivity

A

an immune complex-mediated hypersensitivity
they can stay for too long and line blood vessels in different parts of the body e.g.
The lining of blood vessels, Glomeruli, Lung
Here they induce:
Complement activation, Leukocyte binding, Inflammation
cannot be phagocytoses but continue causing inflammation, neutrophils release mediators causing more tissue damage

101
Q

how do you treat type III hypersensitivity

A

immunosuppressant - steroids

102
Q

what problems does type III hypersensitivity cause

A

Immune complex mediated vasculitis
-Erythema multiforme
-Systemic lupus erythematosus (SLE

103
Q

what is Erythema multiforme

A

Common skin condition mediated by deposition of an immune complex in the superficial microvasculature of the skin and oral mucosa that usually follows an infection or drug exposure.
Often has a classical “target lesion” appearance - don’t confuse with Limes disease

104
Q

what makes type IV hypersensitivity different to others

A

T cell mediated as opposed to humeral response mediated
Haptens activate e.g. small antigen e.g. Ion

105
Q

explain how we know a reaction is Type IV hypersensitivity (3)

A

Slow to develop (12-48 h)
Slow to resolve
Localised

106
Q

what is a hapten

A

very small antigen e.g. ion

107
Q

explain how type IV hypersensitivity

A

Langerhans cells internalise antigen/hapten and move from epidermis to lymph nodes.
They present Ag to memory CD4+ T cells in lymph nodes
These are activated, travel to the dermis and secrete IFNγ and TNFa
This increases expression of ICAM-1 and MHC II on Keratinocytes (which usually don’t have antigen presenting complexes)
And causes secretion of pro-inflammatory cytokines
More leukocytes are attracted to site
Neutrophils arrive after 4 h, monocytes and T cells after 12 h & secrete tissue damaging cytokines

108
Q

how long does it take for type IV Hypersensitivity tissue damage

A

12 hours
+

109
Q

how can we test for type IV hypersensitivity and why is this relevant in dentistry

A

skin patches of e.g. nickel for 72-96 hours
common reaction to denture materials e.g. ions in materials

110
Q

explain how we can tell if a patient has a type IV hypersensitivity to their denture

A

Red areas due to uncontrolled inflammation and tissue damage
Epidermal thickening due to leukocytes, inflammation & proliferating keratinocytes trying to repair damage

111
Q

Explain Lichenoid reactions to amalgam

A

Type IV contact hypersensitivity response to mercury or amalgam ions
Lesions closely associated with amalgam fillings
Positive skin patch test response to mercury or amalgam
Lesion resolves on removing the filling

112
Q

what type of reaction can we get from amalgam

A

type IV hypersensitivity lichenoid reaction

113
Q

explain the difference between the two types of immunodeficiency

A

Primary Immunodeficiency
Intrinsic genetic defects in the immune system affecting T & B cells (Ab production), complement, phagocytes etc.
Absence or failure of NORMAL function in one or more elements of the immune system

Secondary Immunodeficiency
External factors that can deleteriously affect the immune system
Drugs, Malnutrition, Viral Infection etc

114
Q

what are the two types of primary immunodeficiency

A

Specific Immunodeficiency e.g., abnormalities of T or B cells – adaptive immune system
Non-Specific Immunodeficiency e.g., abnormalities of phagocytes or complement – innate immune system

115
Q

if you have immunodefiency in complement, Ig and phagocytes, what are you more susceptible to

A

susceptible to recurrent bacterial infections ( H. Influenzae, S. Pneumoniae, S. Aureus)
Termed: Pyogenic Infections – pus formation

116
Q

what are people with Defects in cell-mediated immunity (T cells) more prone to

A

Susceptible to commensal organisms (eg. Candida, Viruses)
Termed: Opportunistic Infections

117
Q

what is XLA in immunity and what 2 types are there

A

X- Linked agammaglobulinemia - affects men on X linked
primary B cell Immunodeficiency
Patients have: No B-cells, no plasma, No Tonsils, Little IgG in serum (usually 70%), (But have other Ig’s)
XLA recessive and XLA dominant (less prevalent)

118
Q

what causes XLA immunity

A

Defective btk gene that encodes a B cell tyrosine kinase
btk Important in maturation of B cells
No B cell maturation so no IgG – poor Ab responses
First 6-12 months of life have protective maternal IgG
Get recurrent pyogenic infections

119
Q

what gene does XLA affect

A

B cell Tyrosine Kinase BTK
used for maturation of B cells

120
Q

what is Hyper IgM immunodeficiency

A

Deficient in IgG and IgA but hyper IgM (large amounts of IgM) X-linked recessive condition with mutations in CD40 - IgM very large cannot go into tissues
CD40 important for ‘class switching’
Where IgM turns to IgG (Ab has same specificity)
So can not switch from IgM to IgG = more IgM and less IgG
Susceptibility to pyogenic infections & autoimmune disease (form auto-IgM antibodies to neutrophils & platelets)

121
Q

what gene is affected with patients with Hyper IgM immunodeficiency

A

mutations in CD40
CD40 important for ‘class switching’
Where IgM turns to IgG (Ab has same specificity)
So can not switch from IgM to IgG = more IgM and less IgG

122
Q

what is the most common immunodeficency

A

Most common immunodeficiency (1 in 700 Caucasians)
IgA deficiency

123
Q

if a pt has hyper IgM immunodeficiency, what can this lead to

A

Susceptibility to pyogenic infections & autoimmune disease (form auto-IgM antibodies to neutrophils & platelets)

124
Q

what causes to IgA deficiency an what can this lead to

A

Failure in terminal differentiation of B cells to plasma cells
Individuals develop Type III hypersensitivity (immune complex)
Susceptibility to pyogenic infections

125
Q

what is SCID in immunology

A

severe combined immunodeficiency
Individuals with no or poor T cell function
BUT - B cell function depends on T cell function
SO - T cell deficient individuals have poor T cell and humoral functions

126
Q

what are SCID patients likely to get in the mouth

A

People with SCID suffer from commensal organism infections e..g candida is in 50% of mouths
eg. Oral Candidiasis due to Candida albicans infection
SCID have very few lymphocytes = blood stream = 50% mortality.

127
Q

what causes SCID

A

due to defective IL-2R gene affecting inflammation
it is 50% X linked so occurs more in males

128
Q

what are the consequences of SCID

A

death before 2 years old without a bone marrow transplant
50% mortality

129
Q

what is DiGeorge Syndrome

A

T cell deficiency because of affected Thymus in foetal development - Education of Thymus in development.
Distinctive facial features:
Wide-spread eyes
Low set ears
Upper lip shortened
Abnormal aorta – also have cardiovascular disorder

130
Q

what is MHC II Deficiency

A

Type of T cell immunodeficiency
Deficiency in MHCII leads to failure to express MHC II antigens on APC
Because CD4+ cells require MHCII for positive selection in the thymus
Infants deficient in MHC II = Have no CD4+ cells
Lack of CD4 cells leads to deficiency in Ab

131
Q

what is complement deficiency

A

Deficiencies in C3b, Factor H and Factor I – increased susceptibility to pyogenic infections as affect the innate immune response
Deficiencies in MAC increase in susceptibility to Neisseria infections (N. meningitidis, N. gonorrhoeae)
Most common is: Hereditary Angioneurotic Oedema (HAE)

132
Q

what is Hereditary Angioneurotic Edema (HAE) and what causes it

A

Most important Complement deficiency
C1 inhibitor- inhibits activation of C1 ( first initiator of Complement pathway) - inhibitor mutation
Inhibits Complement activity and elements of the kinin/clotting system
Allows severe oedema due to plasma leakage

133
Q

what are the symptoms and signs of Hereditary Angioneurotic Edema (HAE)

A

Recurrent swelling
Intestine – abdominal pains & vomiting
Upper airways – choke and death due to obstruction

134
Q

give three immunodeficiencies involving phagocytes

A

neutropenia is a severe lack of neutrophils = pyogenic infection
Two genetic defects that are often fatal:
-Chronic Granulomatous Disease (CGD)
-Leukocyte Adhesion Deficiency (LAD)

135
Q

what is Chronic Granulomatous Disease CGD

A

Defective NAPDH oxidase
Phagocytes CANNOT form superoxide ions & H2O2 (ROS - Reactive Oxygen Species) to kill microbes
Organisms remain alive in phagocytes – persistent intracellular infections & granulomas form

136
Q

what infections do patients with CGD chronic granulomatus disease get

A

Infections with S. Pneumoniae & abscesses in liver, skin etc.

137
Q

what is not working in patients with chronic granulomatous disease

A

Defective NAPDH oxidase
Phagocytes CANNOT form superoxide ions & H2O2 (ROS - Reactive Oxygen Species) to kill microbes

138
Q

what dye is used to diagnose CGD chronic granulomatous disease

A

Nitroblue Tetrazolium
Inability of phagocytes to reduce nitroblue tetrazolium (NBT) dye
NBT is pale yellow when taken up by phagocytes during phagocytosis.
In healthy phagocytes it is reduced by ROS to a purple colour
In patients with CGD the dye remains yellow

139
Q

what is Leukocyte Adhesion Deficiency LAD type 1 and what is the main factor deficency

A

Deficient for CD18 (integrin β chain)
Defective Complement Receptor 3 (CD18/CD11b) - This binds bacteria opsonized with C3bi – increase phagocytosis
Can not phagocytose opsonized bacteria – recurrent infections

ALSO Defective CD18/CD11c
Important in leukocyte adhesion (CD18/CD11c binds to ICAM-1)
Phagocytes not able to bind to the endothelium and extravasate

140
Q

what is leukocyte adhesion deficiency type 2

A

Defective receptors (CD15) that bind selections
Phagocytes can not roll on the endothelium

141
Q

what are the two main deficiencies involved with LAD leukocyte adhesion deficiency

A

LAD type I = CD18 complement receptor and affects extravasation
LAD type II = CD15 e-selectins

142
Q

what factors cause secondary immunosuppression

A

Drugs (hormones, cancer therapy, transplants)
Nutrition
Viruses
Burns

143
Q

explain corticosteroids affect on immune response

A

Prevent phospholidpid –> arachidonic acid –> prostoglandins
Significant changes in leukocytes in circulation after treatment
Lymphocytopenia - T cells (especially CD4) affected more than B cells
Monocytopenia – very quick ( 2 h) but back to normal by 24 h
Neutrophilia – due to release of mature neutrophils from the bone marrow
Repeat dose – leads to low lymphocytes, lack of Ab and defective cytokine synthesis

144
Q

how does cancer treatment lead to immunodeficiency

A

Radiotherapy:
-Causes strand breaks in the DNA
-Increases apoptosis and stops proliferation
-Targeted at cancer cells (high proliferation rates) but also affects the bone marrow and lymphoid tissue
-Stops immune cell production, proliferation and differentiation

Chemotherapy:
-chemicals that prevent cell proliferation and initiate apoptosis causing cell death

145
Q

how does IL-2 work in the MHC

A

after phosphorylation of T cell in MHC
T cell secretes IL-2 & bind to IL-2R on T cells
Leads to: division, differentiation, effector functions, memory

146
Q

what is the most common cause of immunodeficiency and why

A

nutritional deficiency
Malnutrition damages lymphoid tissues - lymphoid atrophy
nutrients are needed for production of lymphocytes and other immune cells

147
Q

what can lymphoid atrophy be caused by (1) and give consequences of this (5)

A

Caused by malnutrition

Thymus severely affected in children – T cell abnormalities
Reduced number of CD4+ cells
Reduced SIgA (mucosal infections)
Reduced C’ levels
Reduced microbial killing by phagosomes

148
Q

what vitamins are required for good immune health

A

zinc
iron
Folate
b6

149
Q

what is HIV and AIDs

A

Acquired Immune Deficiency Syndrome (AIDS)
Due to Human Immunodeficiency Virus (HIV) infection
immunosuppressive virus HIV that attacks CD4+ cells leading to opportunistic death AIDS

150
Q

what cells can HIV bind to (2) with their receptor

A

CD4+ cells
X4 (T-cell tropic) – CXCR4
R5 (Macrophage tropic) – CCR5

151
Q

what is the progression of attack of HIV (2)

A

In asymptomatic stage CCR5 predominates affecting macrophages
As infection proceeds HIV uses CXCR4 affecting T cells

152
Q

why is their less AIDS in Scandinavian countries

A

CCR5 32 deletion is common in scandinavian populations which inhibits infection
because the receptor is CCR5 that HIV would bind to is non-functional and rapidly degraded
no HIV invasion

153
Q

how many years may it take to show symptoms of AIDs

A

10 years

154
Q

why is it hard to immunise HIV

A

it hides within immune cells
envelope proteins continuously changing which means Ab always need to be made new

155
Q

what can HIV lead to

A

AIDS-
Oral candidiasis
Varicella-Zoster infection (Shingles)
Herpes Simplex Virus (oral & genital)
Cutaneous skin infections
Kaposi’s Sarcoma - Tumour of endothelial cells – widespread in skin, mucous, visceral (gut & lungs) and lymph node disease occurs
Pneumonia - Due to Pneumocystis jirovecii (formally P. carinii), Mycobacterium tuberculosis & fungal infections, enlarged heart
Enteric bacteria – cause weight loss
Toxoplasmosis – protozoan infection – causes brain & neurological problems
Cryptococcus neoformans – fungus that causes meningitis
Cytomegalovirus – inflammation of brain & spinal cord

156
Q

what is Kaposi sarcoma

A

Tumour of endothelial cells – widespread in skin, mucous, visceral (gut & lungs) and lymph node disease occurs
caused by HIV

157
Q

does IgM or IgG come first

A

MaGic
IgM is generally produced the first time a host is exposed to an antigen.
IgM will eventually decline, and then the host produces IgG, which lasts much longer.
Detection of IgM indicates acute or primary infection, IgG indicates past infection or immunity.

158
Q

if a patient has high IgM or IgG, are they infected now or have they previously been infected

A

IgM is generally produced the first time a host is exposed to an antigen.
IgM will eventually decline, and then the host produces IgG, which lasts much longer.
Detection of IgM indicates acute or primary infection, IgG indicates past infection or immunity.

3rd BDS IHD (14 decks)

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