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HDT 2.1 > immunology > Flashcards

immunology Flashcards

1
Q

what are the consequences of having a penicillin allergy?

A
  1. significant restriction in available antibiotics
  2. potential harm from other drugs
  3. longer inpatient stays
  4. higher incidences of antibiotic resistant infections
  5. higher costs
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2
Q

what are the steps you can undertake to confirm penicillin allergy?

A
  1. retake history + timing of drugs + symptoms + other concurrent medical issues
  2. SPT/ID testing; intradermal tests and blood tests; take drug and put tiny amount on skin to see any reaction
  3. sIgE
  4. Drug challenge
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3
Q

why is Type 1 hypersensitivity symptoms reproducible?

A

as the Ig antibodies dont go away

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4
Q

What are the sid effects of penicillins, macrolides and opiates?

A

penicillins; nausea, diarrhoea, candida
macrolides; abdominal pain, nausea, diarrhoea
opiates; itch, sedation, hallucinations

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5
Q

what is the difference between side effects and allergies?

A

with allergies your immune system dictates the response to the allergy but does not for side effects

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6
Q

how do NSAIDs stop arachidonic acid from accessing catalytic site?

A

the NSAID will block both Cox1 and Cox2 inhibitors by binding at an arginine molecule halfway up the channel inhibiting the access of arachidonic acid and so inhibiting synthesis of prostaglandins PGI2 and PGE2, thromboxanes TGA2

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7
Q

how is red man syndrome caused?

A

due to the intake of vancomycin and its infusion; slow to <10mg/min and with an antihistamine
can happen first dose
- direct mast cell degranulation can occur
- if opiates are being taken this can cause mast cell degranulation also

vancomycin binds to mast cell and histamine is released into peripheral circulation

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8
Q

what are SJS/TEN?

A

severe adverse cutaneous reactions

- skin reaction seen by blistering rash

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9
Q

how can you treat SJS/TEN?

A
  • antibiotics
  • aromatic anticonvulsants
  • antiretrovirals
  • allopurinol
  • NSAIDs
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10
Q

if patients have TEM or Steven-johnson syndrome what should you do?

A

stop the drug

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11
Q

what is the definition of anaphylaxis?

A
  • an acute, severe, life-threatening allergic reaction in pre-sensitised individuals, leading to a systemic response caused by the release of immune and inflammatory mediators from basophils and max cells involving at least two organ systems
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12
Q

what symptoms will occur with patients with urticaria and angioedema?

A

urticaria: airway compromise
angioedema: rapid CV collapse

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13
Q

what is the process of the immune response for Type 1 hypersensitivity?

A
  1. T cells will help and Th2 cytokines will help B cells
  2. Class switches to produce antigen specific IgE
  3. the IgE binds to high affinity mast cells on surface of high affinity receptor on surface on mast cell
  4. the mast cells have granules with histamine
  5. the protein antigen will cross link the receptor and send signals to do the degranulation
  6. mast cell degranulation will occur causing histamine, tryptase and lipid mediators to be released
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14
Q

what causes symptoms for Type 1 hypersensitivity?

A

there is a sudden rise in histamine

most reactions will occur within minutes of allergen exposure

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15
Q

how does serum conc. work for histamine and mast cell tryptase change?

A

histamines conc goes up and down and peaks within 15 minutes
mast cell tryptase steadily increase and then decreases over 24 hours

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16
Q

how does histamine cause hypotension?

A

histamine increases NO release and so the BP will decrease

this causes organs to not be able to perfuse properly

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17
Q

how does histamine cause vascular leak (oedema)?

A

histamine will alter the permeability of tight junctions and so these will open and fluid leaks out and eventually causes angioedema

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18
Q

how does histamine cause bronchoconstriction/spasm?

A

it has direct and indirect effects on bronchial smooth muscle
- opens up the blood vessels and constricts airways and causes wheeziness

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19
Q

how does histamine cause mucus secretion?

A

histamine has a direct effect on goblet cells of respiratory mucosa
- histamine can cause mucus plugging in the lungs and there is difficulty recruiting alveoli to ventilator capacity so adult cant breathe properly

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20
Q

what can mucus plugging cause?

A

can cause patient to become rapidly hypoxic

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21
Q

what are common causes for anaphylaxis?

A
  • cows milk
  • eggs
  • drugs and drug exposure
  • nuts
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22
Q

what are the co-factors for anaphylaxis?

A
  • drugs
  • antigen dose
  • ace-inhibitors
  • alcohol
  • route of delivery
  • hormones
  • infections
  • opioids
  • EtOH
  • exercise
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23
Q

what is the ABCDE process?

A 
A- airway
B- breathing
C- circulation
D- disability 
E- exposure
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24
Q

what are the airway, breathing and circulation danger signs for anaphylaxis?

A 
airway
- persistent cough
- vocal change
- difficulty swallowing 
- swollen tongue
breathing 
- wheezy 
- noisy breathing 
- stridor
circulation
- loss of consciousness 
- pre- syncope
- confusion
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25
Q

why should you lay a patient flat with their leg slightly up when having an anaphylaxis?

A

it helps blood reach the brain quicker

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26
Q

what is the purpose of the drug adrenaline?

A
  • increases peripheral vasoconstriction
  • increases peripheral vascular resistance
  • increases BP and coronary artery perfusion
  • decreases vascular permeability and angioedema
  • maintains bronchodilation
  • decreases inflammatory mediator release
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27
Q

how often should you administer an adrenaline after first dose? how should it be administered

A

5 mins after first dose if needed

and should be given IM

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28
Q

what is the adaptive immunity system made up of?

A

it is made up of T cells, B cells and high affinity antibodies

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29
Q

how long does the adaptive immunity take to activate?

A

4-6 weeks but is able to rapidly up regulate on re-exposure

has good memory and is highly tailored to infection

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30
Q

where are T cells derived from and where do they mature?

A

derive from stem cells in bone marrow and mature in the thymus

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31
Q

what type of T cells are there and what do they subdivide into?

A

there are CD4 T cells and CD8 T cells

CD4 T cells subdivide into Th1, Th2, Th17 and Treg based on cytokines they produce

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32
Q

where are B cells derived from and where do they mature?

what do they differentiate into?

A

derive from stem cells in bone marrow
mature in the bone marrow/spleen and then migrate to lymph node
terminally differentiate into long lived plasma cells
produce antibodies (IgM, IgE, IgA)

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33
Q

what are B cell receptors identical to?

A

the antibody it produces

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34
Q

why is the adaptive immunity system necessary?

A

bacteria can produce thousands of proteins and we dont have enough energy to fight all these bacteria that we consider as threats

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35
Q

how does the adaptive immune system actually work?

A

from the APC cells in the innate immune system they will send instructions to the CD4, CD8 and B cells
the CD8 cells are cytotoxic T lymphocytes, the CD4 cells co-ordinate and produce cytokines and the B cells will produce the antibodies which cause feedback to occur in the innate system

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36
Q

what occurs in the feedback process of the innate immune system?

A

there is a production of antibodies or cytokines

opsonisation can occur where a foreign cell is made more susceptible to phagocytosis

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37
Q

what is a T cell receptor made up of?

A

it has a section called the Fab fragment which is responsible for binding to antigens
it has a constant region
it has an alpha and beta chains

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38
Q

what is a B cell receptor made up of?

A

it is made up of a heavy chain attached to a light chain

it has two Fab fragments which allow immunogobulin of the T cells to bind to lots of high variable sets of targets

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39
Q

what is the T cell response in the adaptive immune system when it recognises proteins?

A

a linear peptide epitope( part of a foreign antigen/protein) is presented on the MHC
this binds to a T cell triggering a T cell response
the T cell response means T cell proliferation which occur and cytokine production will occur. Help to B cells will be given and cytotoxicity occurs

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40
Q

what is the B cell response in the adaptive immune system when it recognises proteins?

A

a conformational epitope will be recognised by the Fab fragments on the B cell receptors triggering a B cell response; can only occur when epitope is attached and is the right shape
B cell response in antibody production and antigen presentation

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41
Q

for each chain of the receptors what regions are present?

A

you have 1 variable region, 1 diversity regions and 1 joining region

these regions are created by shuffling and recombining different fragments of genes

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42
Q

what do B cells do in a typical immune response?

A
  1. a naive B cell receptor will be engaged by antigen
  2. B cell will present the antigen in MHC II to T cells
  3. B cell can also also allow IgM production ( rapid and low affinity)
  4. after antigen is presented, T cells can give help to cognate the B cells and this causes the B cells to switch to high affinity antibody producing plasma cells
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43
Q

how do T cells help B cells?

A

when T cells help B cells this means that B cells can switch the type of antibody they produce to tailor it to the pathogen

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44
Q

what is the role of CD4 Th cells in the T cell response for the immune response?

A

on the surface of the APC there is a MHC II which has a peptide that is presented
the CD4 Th cell will recognise the peptide and differentiation will occur to produce Th1, Th2 and Th17
Th1; macrophages will be produced to target intracellular bacteria
Th2; eosinophils will be produced to target worms parasites
Th17; neutrophils will be produced to target extracellular bacteria

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45
Q

what is the role of CD8 CTL cells in the T cell response for the immune response?

A

on the APC there is a MHC I which has a peptide binded to it that is presented on cell surface
the CD8 recognises the dangerous green peptide
it will then seek out other cells containing and presenting this peptide and destroy these cells
it kills virally infected cells that are MHC-I dependant

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46
Q

what are antibodies made up of?

A

it has 2x heavy chains binded by disulphide bridges to 2 x light chains
each light chain has a Fab fragment which binds to the antigen
the heavy chains have the Fc fragment which contains the antibodies; IgM, IgD, IgG, IgE and these bind to receptors and determine their function

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47
Q

what do antibodies do?

A
  1. neutralise toxins
  2. opsonise pathogens
  3. agglutinate; stick to pathogens and sticks them together to make complexes
  4. blocks viral entry
  5. antibody dependant cellular cytotoxicity; stick to target and facilitate cytotoxicity from NK cells
  6. activate complements
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48
Q

what are the different classes of antibodies?

A

IgA, IgG, IgM, IgE
IgE; mast cell affinity and anaphylaxis
IgA; mucosal, lung and gut

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49
Q

what does the heavy Fc chain do? how is it involved and differ with B cell and T cell responses?

A 
determines function of the antibody 
for early B cell response the default immunoglobulin class is IgM and response is rapid and has lower affinity; fixes complement 
for later T cell response the Fc fragment will change to IgG, IgE or IgA to refine the antibody response; the Fab fragment stays the same
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50
Q

what are the characteristics of adaptive immunity?

A
  1. highly specific; generates a clone of T cells with receptors or B cells with antibodies specific to proteins in a specific pathogen
  2. allows memory; once clone of a specific T cells has developed these become memory cells that can respond rapidly upon re-exposure
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51
Q

what are MHC’s?

A

molecules that bind to peptides of foreign cells/pathogens to display on cells so T cells can recognise these dangerous peptides

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52
Q

what is polyclonal immunoglobulin?

A

it is when thousands of B cells with different receptors all produce a different immunoglobulin molecule

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53
Q

what is monoclonal immunoglobulin?

A

it is when there is a single B cells and so produces identical immunoglobulins with same target and functions

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54
Q

what do monoclonal antibodies look like and consist of?

A

has a Fab domain which is engineered to bind any protein target
has a Fc domain that can engage specific receptors and generate specific immune functions
has conjugation where a drug will stick on and can go wherever the antibodies bind to

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55
Q

how do you make monoclonal antibodies?

A

place an antigen with epitopes in an animal and you isolate the serum first and then also isolate spleen cells to get the plasma cells and myeloma cells
then you hybridise the plasma and myeloma cells to produce hybridomas and select which clones to place into solution

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56
Q

what are some blockbuster drugs?

A
  • anti-TNF-alpha

- anti CD20 B cell depletion

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57
Q

what is the drug Rituximab and how does it target the B cells?

A

it is a anti-CD20 monoclonal antibody
has a fab domain target CD20 where a protein is expressed on all B cells until they become plasma cells
has a FC domain that is IgG1- binds to CD20 the domain interacts with receptors to activate complement

rituximab can directly kill CD20 expressing cells too

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58
Q

where do immunoglobulin products come from?

A
  1. people give blood
  2. get their red blood cells and the plasma
  3. IgG fractionated, nanofiltered, pasteurised and gets turned into the immunoglobulin

these products are not generic but are interchangeable
only contain IgG
can be given IM, IV or SC

59
Q

what are the clinical uses for immunoglobulins?

A
  1. used as post-exposure prophylaxis for certain infectious diseases
  2. anti rhesus D immunoglobulin is used to prevent rhesus negative mothers from being immunised against RBC surface antigens of rhesus +ve baby
60
Q

what are the therapeutic uses of immunoglobulins?

A

can be used as a replacement product

  1. general population exposed to many pathogens
  2. immunoglobulins product contains IgG antibodies against multiple pathogens
  3. antibody deficiency so individual receives protection from product

short-lived protection

61
Q

what are the different types of antibody deficiencies?

A

when you have low IgG, IgA and/or IgM
primary antibody deficiency
- usually genetic but rare
- no B cells and no T cell help and no class switch
secondary antibody deficiency
- common
- causes are renal loss of IgG or GI loss of IgG and immunosuppression or B cell depletion

62
Q

what is the definition of vaccination?

A

the administration of antigenic material to stimulate an individuals immune system to develop adaptive immunity to a pathogen

63
Q

what prevents the eradication of polo worldwide

A

political factors

64
Q

how do vaccines work?

A

they exploit the immunological memory of the innate and adaptive immune system
with naive CD8, CD4 and B cells, after stimulation they clone and expand
most will die by apoptosis
but some become memory with a long-life span and can upregulate more quickly and response superiorly

65
Q

how does the immune response change with memory cells?

A
  • for the second re-exposure antibodies go up rapidly and faster response
  • higher affinity of IgG anitbody
66
Q

what types of vaccines can you have?

A
  1. live attenuated; capable of replication but not causing full disease; cant go in lung and replicate and produces strong immune response
  2. killed/inactivated; incapable of replication and safe to give immunocompromised patients; produces strong immune response
  3. toxoid; produces disease; bacteria produces pathogenic toxins; conjugate it the bone to generate the protein and put this protein into patient through vaccination; the toxoid is inactivated but body still produces antibodies against it neutralising and produces memory cells for re-exposure
  4. subunit; target of vaccine response is a subunit of the virus which can be made by recombinant protein technology
67
Q

how does a cell wall protect the cell?

A

the polysaccharide cell wall protects it from complement binding and neutrophil killing
antibodies bind to the cell wall and we want the antibodies to be produced against the cell wall to mimic natural immunity

68
Q

how do vaccines allow replication of natural immunity to pathogens in cells occur?

A
  • antibodies targeting the capsule and bind to help activate the complement cascade and facilitate neutrophil killing via opsonisation
    vaccines are designed to facilitate production of anti-polysaccharide antibodies
69
Q

what is a T-cell independent B cell response?

A

a repetitive pattern of sugars can cross link the B cells receptors
these receptors can activate without T cells and produce antibodies
shows a strong signal

70
Q

after how old does a patient have to be for T-cell independent response to be efficient?

A

after 2 years of age and quality of response in low affinity antibody and limited memory

71
Q

what role do adjuvants play in the immune response?

A

adjuvants stimulate an immune response by providing an additional signal to APC to provide instruction to adaptive system to present antigen and therefore activate a response

they augment the immune response to the protein target by:

  1. depot of antigen
  2. facilitating APC recruitment activation
  3. local cytokine + chemokine release
72
Q

what are some artificial adjuvants?

A
  • Alum; hydrated double sulphate salt of aluminium as it allows a more potent and long lasting immunity response
  • emulsified squalene; organic compound in oils, olives and rice bran
  • live attenuated; naturally immunogenic as they contain pathogen associated molecular patterns
73
Q

what is meant by herd immunity?

A

where enough of a population is vaccinated against an infectious organism
so prevents transmission of the pathogen

74
Q

what are the factors affecting herd population?

A
  1. coverage rates
  2. susceptibility of hosts
  3. vaccine effectiveness
  4. force of transmission
  5. crowding
  6. nasopharyngeal carriage
75
Q

what are some flu vaccines?

A

Influenza A; you have two major proteins present called heamaglutinin and neuraminidase
influenza can undergo both antigenic drift and antigenic shift

76
Q

what is antigenic drift? vs antigenic shift?

A

antigenic drift makes new influenza viruses with slightly modified antigens while antigenic shift will make viruses with entirely new antigens

with drift it is a random genetic mutation which changes the AA and so the protein

77
Q

how was COVID vaccines designed?

A

designed to target the spike protein on the outside of the virus to prevent infection

78
Q

how does spike protein on COVID virus mediate infection?

A

binds to ACE2 receptor

79
Q

before giving vaccination what should you consider about the patient?

A
  • any previous vaccination
  • any previous reactions
  • any immunosuppression history
  • immunocompromised?
80
Q

what is the overall purpose of the immune system?

A
  • to maintain tissue homeostasis and allow tissue healing

- make patient free of germs

81
Q

what is the process of a typical immune system when pathogens break down( adaptive) ?

A
  1. the pathogen has breached the barrier
  2. the pathogen can be broken down and these soluble antigens can travel to lymph nodes through lymphatic vessels
  3. B cell recognition will occur as B cell receptors on naive B cells recognise soluble pathogens
  4. the B cells will present the antigen to T cells in MHC II and need T cell help for activation and antibody production
  5. B cells can either die or turn into plasma cells and go into bone marrow to produce same antibody
  6. after presentation of antigen the B cells drags antigen inside and puts it on surface ti produce high affinity antibodies
82
Q

what is the process of a typical immune system with dendritic cells (innate) ?

A
  1. when pathogen breaches barrier, dendritic cells will sample pathogen and then gobble it up and stick it on surface in MHC
  2. PAMPS will recognise the danger and cause activation to occur of phagocytosis
  3. antigen presentation in MCH II will occur as well as costimulation is unregulated; it will tell other cells what is dangerous
  4. the PAMPS set off a signal that allows pathogen to be taken up and broken down into tiny peptides placed in MCH on cell surface and dendritic cell eventually takes them to the lymph node
  5. in lymph node dendritic cell will meet the naive T cells looking for peptide
  6. this causes CD8 CTL activation + proliferation and these cells travel to tissue to deliver cytotoxicity and kill any virally infected cell
  7. another route is CD4 Th cell activation and proliferation can occur and these cells replicate and produce cytokines to help immune response
  8. when CD4 Th cells are activated they provide T cell help to B cells also
83
Q

how does the immune system achieve maintaining homeostasis and tissue healing?

A

our cells have barriers e.g. mucus, epithelium to help prevent entry to bacteria and viruses and allow compartmentalisation
we have sentinel cells which keep an eye out for anything passing the barriers
the action of inflammation releases cytokines, chemokine and complements is a breach occurs; they can act systemically to produce an acute phase response
granulocytes such as neutrophils, eosinophils and basophils are there to destroy bacteria/viruses and allow acute phase response to occur

84
Q

what is involved in the process of innate immune response?

A
  1. neutrophils, monocytes, mast cells
  2. complements, CRP, cytokines
  3. dendritic cells

triggered in seconds
no memory

85
Q

how do barriers act as a first line of defence and what are some barriers?

A
  • we have cilia to help waft mucus up
  • anti-microbial peptides are released by the epithelial surface to kill pathogens before any entry
  • in the GI system we have Hal and proton pumps
  • the proton pumps secrete protons into gastrofungus
  • lowers pH and prevents bacteria living/multiplying
86
Q

how can barriers be disrupted?

A
  1. through physical disruption
    - > IV access devices
    - > catheters
    - > burns
  2. pharmacological disruption
    - > anti-cholinergics
    - > PPI and CDI use
87
Q

what happens when there is a breach of the epithelium?

A
  • the epithelium is breached
  • bacteria can get inside and the epithelium is broken down
  • acute inflammation will occur and neutrophils will be recruited from the blood
  • complement will also be activated
  • rapid, no memory, low specificity
88
Q

what are PAMPs? how are they recognised?

A

PAMPs are pathogen associated molecular patterns that the immune system is programmed to recognise and trigger a response to.
PAMPs are recognised by TLR and PRRs
immune system is set up to recognise things that are common to non-human cells

89
Q

what cells are involved in innate immunity?

A
  1. dendritic cells; sits between mucosal surfaces and recognises threats via PAMPs and DAMPs; primes adaptive immune response by travelling to lymph node
  2. phagocytes; recognise pathogens, phagocytose and destroys pathogen as well as helping to resolve inflammation
  3. granulocytes; recognise pathogen; granules contain enzymes + peptides to destroy pathogen
90
Q

how do phagocytes work in the immune response?

A
  1. phagocyte migration; attracted to site of inflammation by chemokine that are released at inflammation site
    - > have receptors to recognise antibodies
  2. pathogen recognition; antibody/complement receptors
  3. phagocytosis and killing; internalisation of pathogen triggered by respiratory burst
91
Q

what is PUS?

A

pus is an accumulation of dead neutrophils (too many for macrophages to clear)

92
Q

what is neutropenia?

A

this is when you have too few neutrophils

  • often induced
  • due to this bacteria can go straight into the bloodstream
  • high risk of sepsis
93
Q

how can you boost neutrophil production?

A

G-CSF

94
Q

what is the treatment for neutropenia?

A
  • you can take drugs to boost production from bone marrow
  • a stem cell can differentiate into a common myeloid progenitor and lymphoid progenitor
  • get these cells to differentiate to produce neutrophils to start working
95
Q

what can a common lymphoid progenitor differentiate into?

A

a NK cell and a small lymphocyte

a small lymphocyte can differentiate into a T and B lymphocyte and B lymphocyte can differentiate into plasma cells

96
Q

what can common myeloid progenitor differentiate into?

A

can differentiate into a megakarocyte and erythrocyte, mast cells and myeloblast
megakarocytes differentiate into thrombocytes
myeloblasts differentiate into basophils, neutrophils, eosinophils, and monocytes
monocytes differentiate into macrophages

97
Q

what molecules are involved in the innate immune system?

A

mediator (substance P); neuropeptide to induce pain -> DOLOR
histamine, bradykinin, NO (local vasodilation, leak); capillaries open up, trying to get as many immune cells in -> TUMOR, RUBOR
cytokines (IL-1, IL-6); raise body temp -> CALOR

98
Q

how does the acute inflammatory response work?

A

when a fluid leak occurs it causes a neutrophil influx and they migrate
histamine (mast cells) will cause vasodilation and endothelial junctional widening which increases permeability
complement (C3, C5) causes vasodilation
cytokines act locally and they drive systemic response to the inflammation by increasing DC activation
lipid metabolites released from macrophages prolong oedema by causing vasodilation and bronchoconstriction

99
Q

where do cytokines act and what do these actions cause?

A
  • hypothalamus; fevers, rigors, anorexia
  • liver; acute phase proteins
  • bone marrow; increase mobilisation
  • fat and muscle; metabolism change
100
Q

what is the acute phase response?

A

when a quick response occurs to an infection or injury
acute phase proteins are produced by the liver
these proteins increase in response to infectious and inflammatory stimuli

101
Q

what is the complement cascade?

A
  • classical pathway (antibody)
  • mannose binding lectin pathway
  • alternative pathway
  • C1-C9
  • enhances ability of microbes and phagocytic cells to clear microbes and damaged cells from an organisms
  • C3a- histamine release
  • C5a- neutrophil chemoattractant
  • C3b- opsonin + enzyme
  • C5b - opsonin + enzyme
102
Q

what is the terminal complement complex?

A

the TCC is C5b-C9
ring shaped molecules that punches holes through membranes killing them
- regularity proteins stop lysis of human cells

103
Q

what occurs with congenital complement deficiency?

A

genetic deficiency in any of C5-C9

membrane attack complex cannot form properly and so susceptibility to recurrent meningococcal meningitis

104
Q

what occurs with acquired complement deficiency?

A
  • eculizumab blocks C5
  • membrane attack cant assemble properly
  • susceptibility to recurrent meningococcal meningitis
105
Q

what is the process of direct pharmacological inhibition of cytokine axes?

A
  1. monoclonal antibody to block cytokine
  2. soluble version of receptor
  3. monoclonal antibody to block receptor
  4. mimics of natural antagonist to receptor
  5. small molecule inhibitors of signalling molecules
  6. gene expression occurs
106
Q

what are some symptoms of rheumatoid arthritis?

A
  • nail infection
  • thin, aged skin
  • joint deformity and swelling
107
Q

what does TNF- alpha cause in rheumatoid arthritis?

A
  1. causes endothelial activations; increases inflammation
  2. positive feedback on inflammatory cytokine cascades
  3. causes bone erosion; via osteoclasts
  4. causes cartilage destruction; via MMPS; joint lining produces proteases that chew cartilage
  5. systemic effects
108
Q

when given TNF, what risk is there?

A

there is risk of reactivation of TB when given TNF

TB is common and hard to clear entirely as it is contained within granulomas

109
Q

what do mucosal surfaces help do?

A

they help establish tolerance to antigen

110
Q

what is the role of epithelium and tight junction? what is the role of sentry cells?

A

epithelium + tight junctions; prevent access of protein antigen to immune system
sentry cells; guard mucosal surfaces

111
Q

how does Type 1 hypersensitivity process work?

A
  1. with T cell help and Th2 cytokines this changes B cell production of IgN- to IgE and so antigen specific IgE antibodies are produced
  2. these antibodies attached to receptors on the mast cell surface
  3. mast cells have granules that contain histamine
  4. protein antigens will bind to the IgE on the mast cells surface and the receptors are cross linked
  5. this leads to mast cell degranulation and so histamine, tryptase, lipid mediators are released into circulation
112
Q

what drugs are used to manage type 1 hypersensitivity?

A
  • desensitisation; antigen
  • anti-IgE; omalizumab
  • mast cell stabiliser; sodium chromoglycate and steroids
  • histamine receptors; antihistamines
  • physiological stability; adrenaline
113
Q

what lab testing can be done for Type 1 hypersensitivity?

A
  • measure allergen specific IgE

- measure mast cell tryptase levels

114
Q

how does anti-parasite immunity work?

A
  • parasites are too large for phagocytes
  • so IgE attaches to helminth
  • eosinophils bind to IgE
  • helminth is killed with toxic granules and O2 and nitrogen radicals
  • IL-13 increases goblet cell mucus production to expel the parasite
115
Q

symptoms of type 1 hypersensitivity?

A
  • nasal congestion
  • runny nose
  • sneezing
  • throat scratchiness
  • itchy eyes
  • exaggerated asthma
116
Q

what are the three seasons of allergies?

A
  • tree pollen
  • grass pollen
  • weed pollen
117
Q

what is allergic rhinitis treatment?

A
  1. PRN non sedating AH
  2. regular OD non-sedating AH
  3. add topical intranasal steroid
  4. increase non sedating AH to BD/ montelukast if asthmatic
  5. antigen desensitisation
118
Q

if treatment fails, what should you look at?

A
  1. right diagnosis?
  2. treated too late?
  3. compliance?
  4. try immunotherapy?
119
Q

when standard optimal therapy has failed what should be used for treatment?

A

desensitisation treatment

  • not suitable for patients with poorly controlled asthma or CVD
  • can have SC or sub-lingual
  • induction occurs for twelve weeks and specific maintenance dose is given for 3-5 years
120
Q

what are the antigen desensitisation mechanisms?

A
  1. you get a minute doses of the antigen which causes the mast cell to undergo piecemeal degranulation; the allergen specific IgE is replaced by other IgE increasing the activation threshold
  2. a dendritic cell will have expansion of allergen specific Tree and reduction in Th2 due to the antigen
  3. the antigen will cause reduced IgE and increased IgG4; this is inert and unreactive and blocks the update of antigen and interaction of antigen with immune system
121
Q

what kind of immunotherapy is available?

A

SC immunotherapy

  • used for venom immunotherapy
  • small risk of systemic reaction and death; very labour intensive

sublingual immunotherapy

  • efficacious
  • cheaper; first dose at hospital but then daily tablets at home
  • safer; Grazax is licensed
122
Q

how does Type IV hypersensitivity occur?

A
  • it is mediated by T cells causing inflammation and oedema in the skin
  • symptoms occur 24-72 hours following exposure
123
Q

what is acute/chronic urticaria?

A

bacteria and viral infections, allergens, autoantibodies, cytokines affect basophils and cause histamine, pre-formed lipid mediators, IL-4, GM-CSF and PAF release

124
Q

where is the T cell conditioned and how?

A

conditioned in the thymus

  • in the bone marrow there are T lymphocyte precursors that go to the thymus
  • T cells undergo development steps to produce naive T cells
  • and these T lymphocytes CD4 and CD8 enter the blood and go to the lymph node
125
Q

how does T cell antigen recognition occur?

A

T cells only recognise the antigen when presented in the context of MHC

  1. the T cell receptor recognises peptide when presented in the context of the MHC
  2. CD4 cells that has to be in APC
126
Q

how are antigen recognised by CD8 and CD4 cells?

A

recognised by TCR of CD8 T cells ; all nucleated cells

recognised by TCR of CD4 T cells ; professional APC

127
Q

what is MHC I made up of?

A

all nucleated cells
it has 6 alleles in total
have the ability to bind to slightly different peptides

HLA-A, HLA-B & HLA-C

128
Q

what is MHC-II made up of?

A

made up of
HLA-DP, HLA-DQ and HLA-DR
6 alleles in total
allows broad of range of peptides to be presented within them

129
Q

what causes autoimmune disease?

A

auto reactivity + environmental, genetic, epigenetic factors

130
Q

what is autoreactivity?

A

when the antibody binds to something within the nucleus of the cell
- more common than autoimmune disease

131
Q

what does it mean when the thymus selection is positive?

A

there is enough contact to between alpha and beta chains from the MHC II and alpha and beta TCR from T cells to bind together
this means that T cell receives survival signals and can progress

132
Q

what does it mean if the thymus selection is negative?

A

this means there is too much contact here, the self peptide bound too tightly to MHC II
so T cell is killed and potentially auto reactive cell is purged

133
Q

what are the outcomes of negative thymus selection?

A
  1. deletion
    - too tightly bound so T cell recognises this peptide and is extremely autoreactive
  2. release to periphery
    - weakly binding and is safe so can be released and no auto reactivity danger
  3. produce a regulatory T cell
    - not tight and not loose and risk of regulatory T cell regulated other T cells
134
Q

what happens in the thymus?

A
  1. precursor T cells enter the thymus
  2. precursor T cells begin to rearrange their T cell receptor; beta chain first
  3. the rearranged beta chain is bound to a generic alpha chain and tested to make sure it can bind to MHC (+ve selection)
  4. then a proper alpha chain is rearranged to make a full TCR
  5. new TCR is checked to make sure that it doesn’t bind self peptide presented by MHC too tightly (-ve selection)
  6. if not then naive T cell is released into the circulation
135
Q

what are Nk cells and what do they do?

A

NK cells are able to kill target cells that have lost expression of MHC class I “missing self”

136
Q

how do viruses and tumours hide from CTLs?

A

by downregulating MHC I and this means NK cells can kill

137
Q

what do regulatory cells do?

A

produces immunosuppressive cytokines that suppress local immune responses
produce immunosuppressive molecules and this is when receptor T cell is engaged
it direct killing of other immune cells
it causes metabolic disruption

138
Q

how are immunosuppressive cytokines produced?

A

the dendritic cells have pMHC which are peptides from the environment stuck in MHC
self-antigen expressed by dendritic cell without DAMPs and PAMPs
the naive T cell will recognise the MHC and an induced antigen specific regulatory T cell is produced releasing cytokines

139
Q

what is an autoimmune disease?

A

an inappropriate, self-directed inflammation caused by autoreactive T cell and B cell responses, which arise from failure of immune tolerance to self antigens

140
Q

what factors can break tolerance?

A
  • genes
  • environment
  • immune regulation
141
Q

what are some immune suppression strategies?

A
  • generic
  • cell specific
  • pathway specific
  • molecule specific
142
Q

what do glucocorticoids do?

A

the glucocorticoids bind to the receptor in the cytoplasm and It modulates gene expression

143
Q

what are antimetabolites?

A

they block pathways involved in nucleotide synthesis
lymphocyte turnover in autoimmune disease so more susceptible to drugs apoptosis

drugs that are anti-metabolites

  • methotrexate
  • azathioprine
144
Q

what can calcineurin inhibitors cause?

A

can cause chronic renal toxicity
the calcineurin integrates signal from T cell receptor to a transcription factor
this leads to IL-2 receptor expression
and the IL-2 governs T cell proliferation

HDT 2.1 (11 decks)

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