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Immunology Flashcards

1
Q

A normal immune response is composed of which three sequential phases?

A
  1. Immediate innate immunity - defensins, physical barrier
  2. Early induced innate immunity - PAMP/PRR interactions, mast cell activation, release of pro-inflammatory mediators
  3. Adaptive immune response - activation of naive T and B cells, production of antibodies and antigen-specific cells
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2
Q

What is vaccination?

A

Deliberate exposure to a pathogen-related antigen to induce immunological mediated response and to acquire immunological memory

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3
Q

What do memory cells allow for?

A

A rapid response when the same pathogen invades a second time

Symptoms will be eradicated or dampened down in second exposure

Memory cells can remain dormant and reactivate when foreign antigens previously detected are present

Effector cells are more quickly produced this way via clonal proliferation and differentiation of memory cells

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4
Q

What must occur for antibodies to be produced?

A

An antigen specific cell must be encountered

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5
Q

What is the first antibody produced in response to infection?

A

IgM

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6
Q

IgM production will change to production of what other antibody class during the adaptive response?

A

IgG

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7
Q

What is the reason for the change between IgM production to IgG production?

A

IgG has the same, but added functionality to IgM

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8
Q

What is the lag period?

A

This is the time when antibody levels are low as they gradually build

Pathogen proliferation is very high at this stage

Symptoms will likely be experienced at this stage

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9
Q

Where do long-lived plasma cell retreat after infection is eradicated and what do they do?

A

They retreat to the bone marrow

They will secrete antigen specific antibodies for an extended period of time

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10
Q

In a secondary response to an infection, which antibody class(es) are activated from the beginning?

A

IgG and IgM

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11
Q

How can IgG activate complement?

A

Via the classical pathway

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12
Q

Why is it often effective to swtich to IgA production during the secondary response?

A

IgA can form dimers which can cross epithelial tissues and that are able to block bacterial attachment to ucous membranes

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13
Q

What is unusual about how the immune system combats diptheria?

A

The toxin produced by the infection is targeted - not the microorganism

This means the toxin can be cleared, by the individual will still be a carrier

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14
Q

What happens to effector cells (non-memory B and T cells) when no antigen is present for binding?

A

They will undergo apoptosis

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15
Q

Why can memory B cells produce more functional differentiation than in the primary response?

A

They have already undergone Ig class switching (IgM to IgG) and hypermutation

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16
Q

How are memory cells superior to primary B cells produced?

A
  • They have already undergone Ig class switching
  • They have enhanced cell adhesion
  • They have enhanced chemotaxis properties
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17
Q

Why do memory cells encounter antigens faster?

A

They are present in secondary lymphoid tissues unlike naive cells

This is because they have receptors on their surface which allows for binding with chemokines which causes entrapment within such tissues

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18
Q

What is active immunity?

A

This is protection obtained solely from an individual’s own immune system and can be stimulated by vaccine or occur naturally

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19
Q

What is passive immunity?

A

This is temporary immune protection transferred form one individual to another such as secretory IgA in breastmilk

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20
Q

Describe the methodology behind inactivated vaccines?

A
  • These are termed attenuated vaccines
  • This involves the vaccine being made up of components that were never alive such and only exist to minic the real antigen - they can be “edited” versions of the real antigen
  • This will not produce immunity as effective as a live pathogen would
  • The immune response will be mostly B cell mediated and less activity of T cells will be present as a live pathogen is absent
  • Immunological memory will likely not last as long and repeat vaccine may be required
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21
Q

Why will there be a relatively weak T cell response to attenuated vaccines?

A

There are no live components for which T cells can act upon

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22
Q

How can an attenuated vaccine be created?

A
  1. Chemical fixatives - the structure can be preserved by formalin
  2. Heat denaturation
  3. Irradiation
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23
Q

What are the two main problems associated with attenuated vaccine preparation?

A
  • Under-inactivation - pathogen is not inactivated correctly and viable pathogens remain present
  • Over-inactivation - antigens on over-inactivated pathogens are too different from the real pathoegn and do not confer immunity against it
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24
Q

What are the main benefits to attenuated vaccines?

A
  1. Made quickly
  2. May elicit good antibody responses
  3. Easy to store and do not require refridgeration
  4. Usually safe to give to anyone - even the immunosuppressed
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25
Q

What are the main disadvantages to attenuated vaccines?

A
  1. Can be difficult to stimulate an immune response
  2. Poor at eliciting T cell responses
  3. May not give lasting immunological memory and require boosters
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26
Q

What are adjuvants?

A

A mixture of inflammatory substances to kick-start the immune system to activate B and T cells

This is required because a foreign antigen alone is not enough

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27
Q

What are the main downsides to the use of adjuvants in vaccines?

A
  • Toxicity
  • Altered immune response - the immune response may be directed aginst the pathogen/adjuvant conjugate rather than solely the pathogen
  • CD4+ cells may only be able to recognise the carrier and not the free vaccine
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28
Q

What is sub-unit vaccination?

A

Recombinant DNA technology allows for the genes for a sole antigen to be isolated

This involves using a sole antigen, menaing disease cannot be caused

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29
Q

What are polysaccharide vaccines?

A
  • These are vaccines directed against pathogens encapsulated by polysaccharide sugars
  • The polsysaccharide sugar is the antigenic material
  • To improve immune response, adjuvant toxoids can be added to this coating
  • This is important in allowing both B and T cell responses to the toxoid
  • This aids better class switching and antibody production
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30
Q

How can live attenuated vaccines be obtained?

A

Passaging

This is the process whereby attenuated strains are grown through repeated subculturing

The pathogen will become adapted to the environment it is grown in meaning it can be led down certain paths of adaptation to make it less effective in human tissues

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31
Q

What are the advantages to live attenuated vaccines?

A
  • Similar to natural infection
  • Both B and T cells are properly activated
  • There is a strong immune response initiated
  • Good immunological memory is conferred
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32
Q

What are the main disadvantages to live attenuated vaccines?

A
  • If immunocompromisation, patients can become very ill
  • Any circulating antibody can interfere with the immune response
  • The vaccine is fragile and refridgeration is key
  • The pathogen can acquire new mutations and become virulent again
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33
Q

What are the two types of passive immunity?

A
  1. Naturally acquired
  2. Therapeutic
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34
Q

What is naturally acquired passive immunity?

A

This is when a foetus or baby obtains maternal antibodies

Secretory IgA is given to babies through breastmilk

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35
Q

What is therapeutic passive immunisation?

A

This involves injecting antibodies to specific pathogens

This is effective but cannot last long since the antibodies cannot be produced by the body

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36
Q

When may it be difficult to produce vaccines?

A
  • The body can never clear infection (Tb and HIV)
  • When there are many different strains of a pathogen
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37
Q

Which acronym is used to remember types of infections associated with immunodeficiency?

A

SPUR

  • Serious (unresponsive to oral antibiotics)
  • Persistent (can cause structural damage and become chronic)
  • Unusual (may include opportunistic pathogens)
  • Recurrent
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38
Q

What is primary immunodeficiency?

A

This is caused due to the immue system having components “missing” or functioning incorrectly

This is most often due to genetic disorders

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39
Q

What is secondary immunodeficiency?

A

This is caused by environmental factors

Most often due to immunosuppressant drugs

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40
Q

Which cells make up the innate immune system?

A
  • Macrophages
  • Neutrophils
  • Mast cells
  • NK cells
  • Dendritic cells
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41
Q

Which proteins are involved in the innate immune system?

A
  • Complement
  • Acute phase proteins
  • Cytokines
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42
Q

What do macrophages do at the end of infection?

A

Produce cytokines and other molecules which promote wound healing and tissue repair

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43
Q

Which pathogens are likely to cause recurrent infection?

A
  • Staph aureus
  • Burkholderia cepacia
  • Mycobacteria Tb
  • Fungi - candida and aspergillus
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44
Q

Where are neutrophils produced?

A

Bone marrow

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45
Q

Which cells produce which pro-inflammatory mediators and cytokines that allow activation of specific adhesion molecules (on endothelium) and neutrophils to occur?

A

Macrophages and mast cells

IL-1, IL-6 and TNFα

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46
Q

Which cells secrete which cytokine to superactivate macrophages?

A

NK cells and T cells

Interferon γ

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47
Q

What is Kostmann syndrome?

A

A syndrome affecting only the end part of the myeloid lineage that allows for neutrophil differentiation

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48
Q

How is Kostmann syndrome treated?

A

Since the immune system is weakened (no neutrophils) prophylactic antibiotic and antifungals can be given

Stem cell ransplants can also occur

Granulocyte colony stimulating factor can allow for maturation of neutrophils

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49
Q

What are some types of PRRs?

A
  • Toll like receptors
  • Scavender receptors
  • Lectin receptors
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50
Q

Macrophages have what receptors that can bind to an opsonin/pathogen complex?

A

Fc receptors

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51
Q

When complement is bound to a protein, it can bind to a macrophage via which receptor?

A

Complement receptor 1 (CR I)

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52
Q

Why will a defect in the mechanism of one opsonin not necessarily be severly detrimentral to phagocytosis as a functional process?

A

There are many opsonins available

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53
Q

A chronic granulomatous disease may be due to what?

A

A genetic defect in the production of the NADPH oxidase complex

This means reactive oxygen and nitrogen species cannot be produced and pathogens are not so easily killed

Systematic infection may occur

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54
Q

How can chronic granulomatous disease be tested for?

A

The nitroblue tetrazolium test

This determines in neutrophils can kill pathogens by producing oxygen free radicals

Bacteria are exposed to patient neutrophils and production of hydrogen peroxide is tested for using a dye

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55
Q

How can granulomatous disease be treated?

A

Supportive

  • Prophylactic antibiotics and antifungals

Definitive treatment

  • Stem cell transplantation (bone marrow)
  • Gene therapy
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56
Q

Infected macrophages produce which cytokine?

A

IL-12

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57
Q

IL-12 produced from infected macrophages has what effect?

A

It induces TH1 cells to secrete interferon gamma which can stimulate macrophages and neutrophils to produced TNF which can activate the oxidative pathways for producing NADPH

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58
Q

What will the neutrophil count be in:

  1. Congenital neutropaenia?
  2. Leukocyte adhesion defect?
  3. Chronic granulomatous disease?
A
  1. Absent
  2. Increased
  3. Normal
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59
Q

Will there be pus formation in:

  1. Congenital neutropaenia?
  2. Leukocyte adhesion defect?
  3. Chronic granulomatous disease?
A
  1. No
  2. No
  3. Yes
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60
Q

What will the level of leukocyte adhesion markers be in:

  1. Congenital neutropaenia?
  2. Leukocyte adhesion defect?
  3. Chronic granulomatous disease?
A
  1. Normal
  2. Absent
  3. Normal
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61
Q

What is the result of the nitroblue oxidative killing test in:

  1. Congenital neutropaenia?
  2. Leukocyte adhesion defect?
  3. Chronic granulomatous disease?
A
  1. Usually absent (lack of neutrophils)
  2. Normal
  3. Abnormal
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62
Q

The repertoire of cells in the adaptive immune system is:

a) Genetically encoded
b) Developed over time through maturation

A

b)

The repertoire is developed over time through maturation

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63
Q

Pre T-cells mature in the thymus gland by which process?

A

Thymopoeisis

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64
Q

What occurs during the T cell maturation process?

A

The cells have their alpha/beta chain genes rearranged allowing or specificity to a specific antigen

Only 10% of cells survive this process

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65
Q

Helper TH1 cells (CD4+) secrete which mediator which will activate whihc type of cell?

A

They release interferon gamma to activate macrophages

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66
Q

Which type of T cells aid the activation of B cells?

A

T follicular helper cells

67
Q

Describe how B cells present antigens

A

They bind to a specific antigen, engulf it, and then present it on their cell surface in complex with HLA class II

(MHC class II is the same as HLA class II)

68
Q

How do TFH cells activate B cells?

A

They bind to the peptides in complex with the HLA class II

This interaction reactivates the B cells

Specific cytokines are released by TFH cells which influence B cell class switching

69
Q

CD8+ T cells can recognise antigens in complex with what?

A

HLA (MHC) class I molecules

70
Q

CD8+ T cells destroy infected host cells by which three main processes?

A
  1. Producing pore forming molecules such as perforin
  2. Triggering apoptosis
  3. Secreting cytokines such as interferon gamma
71
Q

Upon reactivating B cells, what do TFH cells ensure about the subsequently generated B cells in relation to their affiity to the pathogen antigen?

A

They ensure that the affinity is greater compared with the original receptors

72
Q

Antibodies have three main functions, what are these?

A
  1. Identify pathogen
  2. Recruit other immne system components such as complement, phagocytes, NK cells
  3. Neutralise toxins
73
Q

What is reticular dysgenesis?

A

The failure of haematopoetic stem cells to differentiate further

Hence, myeloid cells (lymphocytes, neutrophils, macrophages etc.) cannot be produced

This is fatal unless a bone marrow transplant is received

74
Q

What is the treatment for reticular dysgenesis?

A

Bone marrow transplant

75
Q

What is SCID?

A

Severe combined immunodeficiency

An umbrella term for many conditions involving problems with stem cells and their differentitaion to lymphoid progenitors

In short, lymphocytes cannot be produced

76
Q

What are some signs of SCID?

A

“SPUR” infections - Severe, Persistent, Unusual and Opportunistic

  • Persistent diarrhoea
  • Failure to thrive
  • Infection of all types - normal (increased severity), unusual and opportunistic
  • Unusual skin disease
77
Q

Why is SCID not easily picked up immediately after birth?

A

Circulating IgG from colostrum (in breastmilk) and IgA will deplete over time yet provides protect for a while

78
Q

What is hypoglobulinaemia?

A

Low levels of antibodies circulating the body

79
Q

What may be the cause(s) of SCID?

A
  • Deficiency of cytokine receptors
  • Deficiency of signalling molecules
  • Metabolic defects
  • Defective receptor arrangements
80
Q

What is the most common form of SCID?

A

X-linked SCID

81
Q

What causes X-linked SCID?

A

Mutation of the IL-2 gene meaning the normal function of IL-2 (instructs proliferation of lymphocytes) cannot occur

Without IL-2 there will be too few effect cells and not enough T cells will mature

82
Q

In which to ways can SCID be treated?

A
  1. Prophylactically
  2. Definitively
83
Q

Describe prophylactic treatment of SCID

A

Antibiotics and antifungals are given in anticipation of infection

No vaccines are given - especially attenuated vaccines

Antibody replacement therapy can be given

84
Q

Describe definitive treatment of SCID

A
  • Stem cell transplant from HLA identical sibling
  • Stem cel, transplant from other sibling, parent or other donor
  • Potentially gene therapy using genetically altered stem cells - but this is difficult and has its own issues
85
Q

What is DiGeorge syndrome characterised by?

A

A lack of thymus gland

86
Q

What causes DiGeorge syndrome?

A

Chromosomal deletion (22q11)

87
Q

What is the over-arching consequence of DiGeorge syndrome?

A

Lack of a thymus gland means T cells have nowhere to mature

88
Q

What are some signs of DiGeorge syndrome?

A
  • Failure of thymic development
  • Congenital heart defects (chromosomal deletion affects heart too)
  • Cleft palate
  • Hypocalcaemia secondary to hypoparathyroidism
  • Developmental delay
  • Psychiatric disorders (OCD, Schizophrenia)
89
Q

What are the main symtoms of DiGeorge syndrome?

A
  • Recurrent viral infection
  • Recurrent bacterial infection
  • Frequent fungal infection
90
Q

Which lab investigations can lead to a disgnosis of DiGeorge syndrome?

A
  • Absent or very low T cell count
  • Normal, or slightly elevated B cell count
  • Low antibody count
  • Normal NK cell count
91
Q

How can DiGeorge syndrome be treated?

A
  • Correct any metabolic or cardiac abnormalities
  • Prophylactic antbiotics
  • Immunoglobulin replacement
  • T cell function can improve naturall with age as the body adapts
92
Q

Which cytokine is released by infected macrophages which will cause T cells to secrete which cytokine?

A

Infected macrophages release IL-12

T cells secrete - INF gamma

93
Q

Interferon gamma release from T cells has what effect?

A

Recruitment of macrophages and neutrophils

Causes macrophages and neutrophils to release TNFa

This allows NADPH oxidase activation

94
Q

The IL12-INFgamma network can be activated by which pathogens?

A
  • Tb
  • Atypical mycobacteria
  • BCG infection after immunisation
  • Deep fungal infections such as aspergillus
95
Q

How can T cell deficiencies be investigated in the lab?

A
  • Total white cell count
  • Serum Ig levels by protein electrophoresis
  • Quantitation of lymphocyte subpopulations
  • Functional tests of T cell activation and proliferation
  • HIV test
96
Q

Recurrent bacterial infections may be a sign of what?

A

Deficiency in B cells

(may be as a result of T cell deficiency)

97
Q

How can B cell deficiencies be investigated?

A
  • Total white cell count
  • Serum Ig
  • Serum and urine protein electrophoresis
  • Quantitation of B and T cells
  • Measure antibody responses to known pathogens
98
Q

How can B cell deficiencies be treated?

A
  • Treatment of current infection
  • Ig replacement (IV every 3-4 weeks for life)
  • Stem cell transplantation - can fully resolve condition
99
Q

What is immune hypersensitivity?

A

This is a term used to describe the immune over-reaction to a innocuous antigen that causes damage deterimental to the body

100
Q

What are the four types of hypersensitivity?

A
  1. Immediate
  2. Direct cell killing
  3. Immune complex mediated
  4. Delayed type
101
Q

Immediate hypersensitivity encompasses what?

A

Allergic diseases

102
Q

Immediate hypersensitivity involves an ____ mediated response

A

IgE

(it is possible for IgE to not be involved by this is very rare)

103
Q

What are some examples of immediate hypersensitivity?

A

Asthma, hayfever, eczema, food allergies and anaphylaxis

104
Q

What are two examples of non-IgE mediated allergies?

A
  1. Coeliac disease
  2. Eosinophilic gastroenteritis
105
Q

Which factors will generally cause allergic disease?

A

Environmental factors

106
Q

What is the “hygiene hypothesis”?

A

Due to living in a more unnatural environment in the Western world, more antigens are exposed to that can be detected as foreign

The immune system is not required as often leading to over-reactions when it is activated

107
Q

TH2 cells ca activate which cell types?

A
  • B cells
  • Eosinophils
  • Mast cells

(can also recruit monocytes)

108
Q

How do TH2 cells activate B cells?

A

Release of IL-4, IL-5 and IL-13

109
Q

How do TH2 cells activate eosinophils?

110
Q

How do TH2 cells activate mast cells?

A

IL-4 and IL-13

111
Q

Which three cytokines are effective at telling plasma cells to swtich their heavy chain to epsilon to produce IgE, and no longer IgM?

A
  1. IL-4
  2. IL-5
  3. IL-13
112
Q

What are the clinical features of type 1 hypersensitivity?

A

Acute onset (seconds, to minutes)

The site of contact is the area whih usually experiences the reaction presentation

113
Q

Immediate hypersensitivity reactions can be inlfuenced by what?

A
  • Exercise
  • Alcohol
  • Temperature
114
Q

Granulated material can cause an inflammatory response, it is present in which immune cell types?

A
  1. Mast cells
  2. Basophils
  3. Eosinophils
115
Q

In granular cells which types of granulated material is preformed?

A
  • Histamine
  • Tryptase
  • Heparin
116
Q

In granular cells which types of granulated material is not preformed?

A
  • Leukotrienes
  • Prostaglandins
  • Cytokines (IL-4, TNF, etc.)
117
Q

The inflammatory cascade can cause many change to the body such as what?

A
  • Increased blood flow
  • Contraction of smooth muscle
  • Increase in vascular permeability
  • Increase in secretions at mucosal surfaces
118
Q

Mast cells function well when defending the body against ________

119
Q

Which receptor is present on mast cells (also basophils and eosinophils) to interact with IgE, and which region does IgE bind by?

A

Fcε R1 receptor

Binds to Fc region of IgE

120
Q

What happens on a first encounter with an allergic antigen?

A
  • IgE binds to the antigen
  • IgE/antigen complex causes mast cell degranulation
  • Residual IgE binds on the surface of mast cells via Fc receptors
  • When re-encountered, the antigen bind to IgE on mast cells causing disruption of the cell membrane
  • This causes release of many vasoactive mediators
121
Q

What is anaphylaxis?

A

An extreme immediate hypersensitivity reaction

122
Q

Which types of drugs may cause asthma?

A

Non-steroidal anti-inflammatory drugs

  • Aspirin
  • Ibuprofen
123
Q

Which tests can be used to determine the presence of an allergic reaction?

A
  • Skin prick test - tissue is exposed to antigen through break in the skin
  • Quantitative specific IgE investigation
  • Exposure to putative (suspected) antigen
124
Q

How can evidence of mast cell degranulation be monitored during an acute anaphylactic shock, and why is measuring total IgE levels an inaccurate test?

A

Serum mast cell tryptase levels - only occurs in anaphylaxis

There are many causes for IgE production - it is a poor test to monitor anaphylaxis

125
Q

How can mast cell activation be blocked?

A

Cromones

These are mast cell stabilisers

Sodium chromoglicate is an example

126
Q

How can the effects of mast cell activation be counteracted pharmacologically?

A
  1. Anti-histamines
  2. Leukotriene receptor antagonists
127
Q

What are anti-histamines?

A

H1 receptor antagonists which will block the effects of histamine upon its release

128
Q

How do leukotriene receptor anatagonists function?

A

They block the binding sites of leukotrienes

This means the synthesis of mast cell mediators is stopped because they cannot be activated

129
Q

Give an example of a leukotriene receptor antagonist

A

Montelukast

130
Q

How is anaphylaxis treated in emergencies?

A

Adrenaline

This is administered via an Epi-Pen

It acts on B2 adrenoceptors to constrict arterial smooth muscle raising blood pressure and decreasing leakiness

Dilation of bronchial smooth muscle will also occur decreasing obstruction

131
Q

Immunotherapy is a treatment option for anaphylaxis, how does it work?

A

There is controlled exposure to the antigen in sequentially increasing doses designed to train the immune system

Over time CD4+ T cells increase in number, and regulatory CD4+ T cells secrete anti-inflammatory IL-10

132
Q

What is type II hypersensitivity?

A

Direct cell killing

Antibodies come in direct contact with host cells via antigens activating complement and acting as opsonins which leads to cell lysis

133
Q

Which antibodies may be used in a type II hypersensitivity reaction?

A

IgG or IgM

(both are effective at activating complement)

134
Q

Where is complement produced?

A

The liver

(around 20 different types are produced here as inactive precursors)

135
Q

What are the three pathways by which complement can be activated?

A
  1. Classical pathway
  2. Alternative pathway
  3. Mannose-binding lectin pathway
136
Q

Describe the classical pathway of activating complement

A
  • This is triggered by the activation of the C1 complex
  • IgG or IgM can complex with antigens on host cells or pathogens and the C1 complex can bind and become activated
  • Upon activation it can cleave C4 into C4a, C4b and also C2 into C2a and C2b
  • C4b and C2a form C3 convertase (C4b2a) which allows C3 to be cleaved into C3a and C3b
137
Q

Describe the mannose-binding lectin pathway for activating complement

A

Mannose is a bacterial carbohydrate and can be detected as a foreign antigen

Mannose-binding lectin is produced in the liver and can bind to mannose and then initiate the breakdown of C3a and C3b

138
Q

Describe the alternative pathway for complement activation

A

C3 spontaneously breaks down into C3a and C3b

139
Q

When produced what does C3 allow for?

A
  • Chemotaxis - stimulates migrationof macrophages and neutrophils to the inflammation site
  • Solubilisation of immune complex
  • Direct killing - aids in the formation of the membrane attack complex
  • Opsonisation - enhances phagocytosis by macrophages and neutrophils
140
Q

In basic terms why does the membrane attack complex do?

A

Punches holes in the membrane of the bacterium

141
Q

What role do C3a and C5a have in common?

A

They both increase vascular permeability

This aids the transport of immune cells to the site of infection

142
Q

Antibodies produced by B cells can have what 3 main effects against pathogens?

A
  1. Complement activation and osmotic lysis of cells by binding to cell surface antigen
  2. NK cell and eosinophil activation by binding to cell surface antigens
  3. Antibodies can act as opsonins for phagoctes allowing for phagocytosis
143
Q

Give an example of a type II hypersensitivity disease?

A

Good pasture’s syndrome

Antibodies bind to the glomerular basement membrane causing direct cell biological effects

(also blood type rections when the wrong type is administered)

144
Q

What is haemolyic disease of the newborn?

A
  • Mother RhD negative
  • Baby RhD positive
  • Mother generates antibodies against RhD +ve
  • Subsequent foetuses will be affected
145
Q

How can type II hypersensitivity reactions be managed?

A
  • Removal of antigens - via cell separator
  • Immunosuppression
146
Q

What is type III hypersensitivity?

A

Antibodies will bind to soluble antigens which forms many small immune complexes which can become trapped in blood vessels, joints and glomeruli

Immune complexes activate complement and attract macrophages and neutrophils

Enzymes from these imflammatory cells break down the immune complexes and also cause damage to nearby cells

147
Q

Hypersensitivity pneumonitis involves which type of hypersensitivity reaction?

148
Q

Give an example of a condition involved with type III hypersensitivity

A

Types of hypersensitivity pneumonitis:

  • Farmer’s lung
  • Bird fancier’s lung
  • Malt worker’s lung
  • Cheese worker’s lung
149
Q

How long does it take for symptoms to appear in a type III hypersensitivity (hypersensitivity pneumonitis) reaction?

A

4-8 hours

Wheezing and malaise will be present as well as breathlessness, a dry cough and pyrexia

150
Q

Why does SLE cause a butterfly pattern of inflammation on the face?

A

Vasculitis

151
Q

What is lupus and how does it manifest?

A

It is an autoimmune disease caused by type III hypersenitivity reaction

When cells break down normally, their contents are released into the extracellular space

Antibodies are produced againt these soluble antigens and immune complexes are deposited around the bodyin small vessels in the skin joints or kidney

Inflammation, complement activation and recruitment of inflammatory cells occurs

152
Q

What symtpoms does lupus (SLE) have?

A
  • Fever
  • Renal impairment
  • Vasculitic skin rash
  • Arthralgias
153
Q

Type III hypersensitivity reactions are all _________ unlike type II which are all __________

A

Systemic

Localised

154
Q

How can type III hypersensitivity be diagnosed?

A

The presence of IgG antibodies in the blood specific to the putative antigen

The presence of complement aids diagnosis

155
Q

How is a type III hypersensitivity reaction treated?

A
  • Avoidance of antigen
  • Corticosteroids
  • Immunosuppressants
156
Q

What drives a type IV hypersensitivity reaction?

157
Q

Give examples of type IV hypersensitivity reactions that are autoimmune

A
  1. Type 1 diabetes
  2. MS
  3. Rheumatoid arthritis
  4. Psoriasis
158
Q

Give examples of non-autoimmune type IV hypersensitivity reactions

A
  1. Tb
  2. Leprosy
  3. Sarcoidosis
159
Q

Why does a type IV hypersensitivity reaction occur?

A

Antigen presentation will cause CD4+ and CD8+ T cells to be produced

TH1 cells are produced from CD4+ cells and so are memory cells

On the first exposure there is little inflammation

In subsequent exposures, effector TH1 cells are available to secrete cytokines (IFN gamma) immediately after antigen detection

This recruits macrophages, lymphocytes and neutrophils

Proteolytic enzymes will cause damage to the surrounding cells as well as destroying the pathogen

160
Q

What is sarcoidosis and where do most instances infect?

A

Type IV hypersensitivity reaction

(90% of cases affect the lungs)

161
Q

Describe how sarcoidosis can damage the lungs

A

A non-specific immune response occurs to a foreign antigen

CD4+ and CD8+ T cells (and macrophages) become activated

The stimulus is not removed so persistent INF gamma production occurs

Collections of activated cells accumulate leading to tissue damage and potentially fibrosis

162
Q

How is sarcoidosis managed?

A
  • NSAIDS
  • Systemic corticosteroids - blocks T cell activation, blocks macrophage activation
163
Q

How can types I, II, III and IV be remembered?

A

ABCD

  • A - Allergic, anaphylaxis, atopy
  • B - B cells produce antibodies
  • C - Complexes (immune)
  • D - Delayed

Respiratory (16 decks)

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