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Immunology Flashcards

1
Q

What is SPUR?

A 
Serious infections 
Persistent infections 
Unusual infections 
Recurrent infections 
When you see a patient with SPUR think about immune deficiency
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2
Q

What are clinical features suggestive of immunodeficiency?

A 
SPUR
Weight loss or failure to thrive 
Severe skin rash (eczema)
Chronic diarrhoea 
Mouth ulceration 
Unusual autoimmune disease
Family history
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3
Q

What is the classification of immunodeficiencies?

A

Secondary or primary

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4
Q

What are the characteristics of a secondary immunodeficiency?

A

Common
Often subtle
Often involves more than one component of the immune system

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5
Q

What are the characteristics of a primary immunodeficiency?

A

Rare - 1:10000 live births

>200 primary immune deficiencies now described

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6
Q

What are some conditions associated with secondary immune deficiency?

A 
Physiological immune deficiency 
Infection
Treatment interventions 
Malignancy 
Biochemical and nutritional disorders
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7
Q

What cells and protetins are involved in the innate immune system?

A 
Marcophages 
Neutrophils 
Mast cells 
NK cells 
Complement proteins 
Acute phase protiens
Cytokines
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8
Q

What is the function of the innate immune system?

A

To recognise structures (PAMPs) that are unique to infectious organisms. Rapidly clear microorganisms, stimulate the adaptive immune response and buy time whilst the adaptive immune system is mobilized

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9
Q

What type of cells phagocytose?

A

Neutrophils

Monocytes/macrophages

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10
Q

What is the function of phagocytosis?

A

To initiate and amplify the inflammatory response
To scavenge for cellular and infectious debris
To ingest and kill microorganisms
To produce inflammatory molecules which regulate other components of the immune system
Resolution and repair

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11
Q

What are clinical features of phagocyte deficiencies?

A

Recurrent infections:
May affect common or unusual sites
Organisms:
Common bacteria such as staphylococcus aureus
Unusual bacteria: Burkholderia cepacia
Myobacteria: TB and atypical myobacteria
Fungi: Candida, aspergillus

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12
Q

What is the life cycle of a neutrophil?

A

Mobilisation of neutrophil and precursors in the bone marrow or within tissues
Upregulation of endothelial adhesion markers that allow neutrophil adhesion and migration into the tissues
Recognition of the organism
Phagocytosis and killing of organism
Activation of other components of the immune system

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13
Q

What can occur if there is a failure to produce neutrophils?

A

There is a failure of stem cells to differentiate along myeloid lineage. The primary defect results in reticular dysgensis and the decondary defect results after stem cell transplantation

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14
Q

What is reticular dysgenesis?

A

More severe form of inobrn SCID. Absence of neutrophils and other myeloid cells and almost complete deficiency of lymphocytes in peripheral blood and a lack of innate and adaptive immune responses leading to fatal septicemia within days after birth
The production of RBCs is not affected

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15
Q

What can occur if there is specific neutrophil maturation?

A

Kostmann syndrome: severe congenital neutropaenia

Cyclic neutropaenia - episodic neutropaenia every 4-6 weeks

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16
Q

What is Kostmann syndrome?

A

A rare autosomal recessive disorder that causes severe chronic neutropenia

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17
Q

What is severe chronic neutropenia?

A

The absolute neutrophil count is <200 microlitres whereas the normal is >3000 microlitres

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18
Q

What is the clinical presentation of Kostmann syndrome?

A 
Infections usually within 2 weeks of birth - recurrent bacterial infections, systemic or localised infection 
Fever
Irritability 
Oral ulceration 
Failure to thrive
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19
Q

What is the management of Kostmann syndrome?

A

Supportive treatment: Prophylactic antibiotics
Prophylactic antifungals
Mortality 70% in the first year of life without definitive treatment
Definitive treatment: Stem cell transplantation - defect is in neutrohphil precursor to the strategy is to replace all precursors with allogenic stem cells and start again
Granulocyte colony stimulation factor (G-CSF) :
Give specific growth factor to assist maturation of neutrophils

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20
Q

What is leukocye adhesion deficiceny?

A

A rare primary immunodeficiency that is caused by a genetic defect in leucocyte integrins (CD18)
This results in failure of neutrophil adhesion and transendothelial migration the clinical picture is characterized by marked leukocytosis and localized bacterial infections that are difficult to detect

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21
Q

What is direct recognition?

A

There are many different types of pathogen recognition receptors:
Toll like receptors
Scavenger receptors
Lectin receptors
These recognise microbial-specific structures:
Bacterial sugars
Lipopoplysaccharides
They exhibit genetic polymorphism - some are associated with increased susceptibility to bacterial infection but most do not cause significant disease

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22
Q

What is indirect regonition?

A

Opsonins - molecules that act as binding enhancers for the process of phagocytosis, these include complement C3b, IgG antibody and C-reactive protein
Phagocytes express Fc receptors which allow the binding of antibodies that are also bound to an antigen.
Phagocytes also express complement receptor 1 (CRI) which binds to complement fragments which are also bound to antigens

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23
Q

What can occur from defects in recognition?

A

Defect in opsonin receptors may cause defective phagocytosis however significant redundancy means that this generally does not cause significant disease
Any defect of complement or antibody will also result in decreased efficieny of opsonisation = functional defect of phagocytosis

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24
Q

What can occur from failure of oxidative killing mechanisms?

A

Chronic granulomatous disease
Absent respiratory burst - deficiency of the intracellular killing mechanism of phagocytes. The commonest form is deficiency of p47phox component NADPH oxidase which is x-linked
An inibility to generate oxygen free radicals (ROS/RNS)
Impaired killing of intracellular micro-organisms

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25
Q

What are some characteristic of failure of oxidative killing mechanisms

A

Inability to clear organisms
Excessive inflammation - failure to degrade chemoattractants and antigens
persisten accumulation of neutrophils, activated macrophages and lymphocytes
Granuloma formation

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26
Q

What are features of chronic granulomatous disease?

A 
Recurrent deep bacterial infections - especially staphylococcus, aspergillus, pseudomonascepacia 
Mycobacteria, atypical mycobacteria 
Recurrent fungal infections 
Failure to thrive 
Lymphadenopathy and hepatosplenomegaly 
Granuloma formation
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27
Q

What are laboratory investigations of granulomatous disease?

A

NBT test - feed patient neutrophils source of E coli
Add dye that is sensitive to hydrogen peroxide
If hydrogen peroxide is produced by neutrophils then the dye changes colour

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28
Q

What is the treatment for chronic granulomatous disease?

A

Supportive treatment - prophylactic antibiotics
Prophylactic antifungals
Definitive treatmen - stem cell transplantation, gene therapy

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29
Q

How do some intracellular organisms hide from the immune system?

A

By locating within cells - salmonella, chlamydia, rickettsia
Some will even hide within the immune cells - mycobacteria species
Therefore specific strategies are needed to clear infections

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30
Q

What happens when there is an infection with mycobacteria (TB)?

A

Activated IL-12: IFNgamma network
Infected macrophages are stimulated to produce IL-12
IL-12 induces TH1 cells to secrete gamma interferon
Then gamma interferon feeds back to macrophages and neutrophils to stimulate the production of tumour necrosis factor alpha
This activates NADHP oxidase which stimulates the oxidative pathway

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31
Q

What happens if there is a defect in this pathway?

A

May cause increased susceptibility to mycobacterial infections

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32
Q

What infections occur if there is a gamma interferon receptor deficiency or IL-12 deficiency?

A

A mycobacterial infection such as TB or an atypical mycobacteria

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33
Q

What infection occurs if there is an IL-12 receptor deficiency?

A

Salmonella

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34
Q

How can you investigate phagocyte function?

A

FBC and differentiation from mobilisation from bone marrow
Presence of pus and expression of neutrohpil adhesion molecules from migration to site of infection
Find and catch the bug
Chemotactic assays - chemotaxis
Phagocytosis assays - formation of phagolysosome
NBT test of oxidative killing

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35
Q

How can phagocyte deficiencies be treated?

A

Aggressive management of infection by prophylaxis - septrin, itraconazole - anti-fungal
Oral/intravenous antibiotics
Surgical draning of abscesses
Definitive therapy - bone marrow transplantation, specific treatment for CGS - gamma interferon therapy, gene therapy

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36
Q

What is the function of the adaptive immune system?

A

Responds sepcifically to an antigen
It is responsive to an unlimited number of molecules
Specificity - able to discriminate between very small differences in molecular structure
Memeory - able to recall previous encounters with an antigen and respond more effectively than on the first occasion

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37
Q

What is the primary lymphoid tissue?

A

Thymus and bone marrow

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38
Q

What is the secondary lymphoid tissue?

A

Lymph nodes and spleen

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39
Q

What is the life of a T lymphocyte?

A

Arise from a haematopoetic stem cell in bone marrow
Exported as immature cells to the thymus, where they undergo selection (only 10% of cells survive)
Mature T lymphocytes enter the circulation and reside in lymph nodes and secondary lymphoid follicles

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40
Q

What are CD8 T cells?

A

Cytotoxic cells that kill infected cells
Virus cells DNA will be expressed on the surface of the cell and form a complex with an MHC class 1 receptor.
Cytotoxic T-lymphocytes can recognise MHC complexes and kill the cell

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41
Q

What is TH1 cell’s primary function?

A

To secrete interferon gamma, this links TH1 cells to macrophages. Once the macrophages receive interferon gamma signals, they will become super killer cells and produce NADHP oxidase to kill intracellullar pathogens and viruses

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42
Q

What do CD4+ lymphocytes produce?

A

Costimulatory signals which is necessary for the activation of CD8+ T lymphocytes and naive B cells
Influences phagocyte function
Prooduces cytokines
Regulates lymphocytes and phagocytes
Recognises peptides presented on MHC Class 2 molecules

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43
Q

Where are B lymphocytes produced?

A

Arise from haemopoetic stem cells in the bone marrow. Mature B lymphocytes are found mainly in bone marrow, lymphoid tissue or the spleen

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44
Q

What is the function of B lymphocytes?

A

Antibody production

Antigen presentation

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45
Q

What is immunoglobulin class switching?

A

IgM can switch to other types of antibodies. This is controlled and helped by CD4+ T cells. TH2 cells secrete cytokines that influence what antibody is made

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46
Q

How are B cells activated?

A

Encounters with antigens occurs at lymph nodes. If provided with appropriate co-stimulatory signals from T cells then the antigen-activated B cells will rapidly proliferate, this is helped by TH1 cells
They will undergo highly complex genetic rearrangements to generate B cells that express antibodies with different Ig heavy chain constant regions
They can then further differentiate into long-lived memory cells and plasma cells which produce antibodies

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47
Q

What are the functions of antibodies?

A

Identify pathogens
Recruit other components of the immune response to remove pathogens such as the complement, phagocytes and NK cells
Neutralisation of toxins
Particularly important in the defence against bacteria of all kinds

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48
Q

What can happen if the haemopoetic stem cells are defective?

A 
Failure to produce: 
Neutrophils 
Lymphocytes 
Monocytes/macrophages 
Platelets
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49
Q

What can happen as a results of failure to produce lymphocytes?

A

Severe combined immunodeficiency

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50
Q

What is the clinical phenotype of SCID?

A 
Unwell by age 3 
Persistent diarrhoea
Failure to thrive
Infections of all types 
Unusual skin disease: graft vs host disease: colonosiation of infants empty bone marrow by maternal lymphocytes 
Family history of early infant death
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51
Q

What are some known causes of SCID?

A

Deficiency of cytokine receptors
Deficiency of signalling molceules
Metabolic defects
Defective receptor rearrangements
Presence of different lymphocyte subsets (T, B, NK) depends on exact mutations
If you cannot form a functional antigen binding site on the T cell because you cannot shuffle the alpha and beta chains to create a functional receptor then the T cell will not work properly

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52
Q

What is the commonest form of SCID?

A

X - linked SCID

45% of all SCID

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53
Q

What is the problem in x-linked SCID?

A

A mutation of a component of the IL-2 receptor which is shared by many other cytokine receptors. This results in the inability to respond to cytokines, failure of T cell and NK development and production of immature B cells

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54
Q

What is the phenotype of X-linked SCID?

A

Very low or absent T cells as IL-2 is needed for T cell development
Normal or increased B cells but they are abnormal
Poorly developed lymphoid tissue and thymus - to maintain their size the secondary lymphoid tissues require T cells and therefore in X-linked SCID they will shirnk

55
Q

What is the prophylactic treatment of SCID?

A

Avoid infections:
Prophylactic antibiotics and antifungals
No live attenuated vaccines
Aggressive treatment of existing infections
Antibody replacement - intreavenous immunoglobulin

56
Q

What is the definitive treatment of SCID?

A

Stem cells transplant from HLA identical sibling if possible
Stem cell transplant from other sibling or parent or from matched unrelated donor

57
Q

What is DiGeorge syndrome?

A

A complex developmental disorder caused by a chrosomal deletion at 22q11
This results in:
Failure of thymic develpoment
Congenital heart defects
Cleft palate
Hypocalcaemia secondary to hypoparathyodism
Developmental delay
Psychiactric disorders: OCD, schizophrenia

58
Q

How is DiGeorge syndrome diagnosed?

A

Absent of decreased numbers of T cells
Normal or increased B cells but low IgG, IgA and IgE. Poor antibody response to specific pathogens
Normal NK

59
Q

How is DiGeorge syndrome managed?

A

Correct metabolic/cardiac abnormalities
Prophylactic antibiotics
Early and aggressive treatment of infection
Immunoglobulin replacement

60
Q

What can cause disorders of T cell effector function?

A

Cytokine production
Ctyotoxicity
T-B cell communication

61
Q

What is the process when there is an infection with mycobacteria?

A

IL-12: IFNgamma network
Infected macrophages stimulated to produce IL-12
IL-12 induces T cells to secrete IFNgamma
IFNgamma then feeds back to macrophages and neutrophils to produce TNF which in turn activates NADHP oxidase

62
Q

What can occur where there is deficiencies in IL-12, IL-12 receptors, IFNgamma and IFNgamma receptors?

A

TB
Atypical mycobacteria
BCG infection after vaccination
Deep fungal infections e.g. aspergillus

63
Q

What is bare lymphocyte syndrome?

A

Mutations that affects the MHC production or antigen processing and presentation by MHC molecules. Type of SCID but has normal T cells numbers

64
Q

What is autoimmune lymphoproliferative syndrome (ALPS)?

A

Rare genetic disorder of immune system that affects children and adults.
High numbers of WBC accumulate in lymph nodes, liver and spleen causing enlargement. Can cause:
anaemia, thrombocytopenia and neutrophenia

65
Q

What are some clinical features of T cell deficiencies?

A

Recurrent infections: viral, fungal, bacterial, mycobacteria
Opportunistic infections
Malignancies at young age
Autoimmune disease

66
Q

How are T cell deficiencies investigated?

A

Total WBC count
Quantilation of lymphocyte subpopulations
Serum immunoglobulins
Functional tests of T cell activation and proliferation
HIV test

67
Q

What is the presentation of antibody deficiencies?

A

Recurrent bacterial infections: recurrent upper and lower resp tract infections
Recurrent GI infections
Often common organisms
Viral infections less common but may occur

68
Q

What is Bruton’s X-linked hypogammaglobulinaemia?

A

No circulating B cells
No plasma cells
No circulating antibodies after first 6 months

69
Q

What is selective IgA deficiency?

A

2/3rd are asymtomatic

1/3rd have recurrent resp tract infections

70
Q

What is common variable immune deficiency?

A

Low IgG, IgA and IgE
Recurrent bacterial infections
Often associated with autoimmune disease

71
Q

How are B cell deficiencies investigated?

A

Total WCC
Serum/urine immunoglobulins
Quantilation of B and T cell lymphocytes
Measure IgG antibodies against tetanus, haemophilus influenzae B and S. pneumoniae

72
Q

How are B cell deficiencies managed?

A

Aggressive treatment of infection
Immunoglobulin replacement: derived from pooled plasma from thousands of donors
Contains IgG antibodies to a wide variety of common organisms
Stem cell transplant

73
Q

What is type 1: immediate hypersensitivity?

A

An IgE-mediated antibody response to external antigens (allergens)

74
Q

What type of conditions are characterized by type 1 immediate hypersensitivity?

A 
Asthma
Hayfever
Urticaria
Angioedema
Atopic eczema
Food allergy
Drug allergy and anaphylaxis
Allergic rhinitis
75
Q

What are some types of allergens?

A 
House dust mite 
Pollen and animal dander
Food
Drugs 
Latex 
Bee and wasp venom
76
Q

What is the hygiene hypothesis?

A

Improved sanitation and decreased incidence of infectious disease has resulted in a world that is too clean
Changes in microbial stimuli influences the maturation of the immune response resulting in increased predisposition to allergic conditions during childhood

77
Q

What are some generic features of type 1 allergic disease?

A

Occurs quickly after exposure to antigen
Responses are sterotyped
May be associated with more than one organ system
Presentation is influenced by site of contact
Threshold for reactions may be influenced by cofactors such as exercise, alcohol and infection

78
Q

What are some specific features of type 1 allergic disease?

A 
Asthma
Urticaria
Angioedema
Allergic rhinitis (hayfever)
Allergic conjunctivitis
Diarrhoea and vomiting
Anaphylaxis
79
Q

What occurs during sensitisation of Type 1 hypersensitivity

A

Allergen presented to naive T cells by dendrites or macrophages
Naive T helper cell binds to antigen and costimulatory molecule and naive T cell turns into TH2.
TH2 cells release IL-4 which induces B cells to undero class switching - changing from IgM to IgE that are specific to the allergen
TH2 also release IL-5 which stimulates production and activation of eosinophils
IgE will bind to Fc receptors on the mast cells

80
Q

What interlukins (cytokines) help change the CD4+ into a TH2 cell?

A

IL-4
IL-5
IL-10

81
Q

What occurs during secondary exposure in type 1 hypersensitivity?

A

The primed mast cells that have IgE bound to their Fc receptors will recognise that allergen and cross link to it, causing the mast cell to degranulate releasing pro-inflammatory molecules, this includes histamine

82
Q

What chemicals do mast cells contain and what occurs when they degranulocyte?

A 
Histamine, tryptase and heparin
leukotrines and prostaglandins 
Proinflammatory cytokines including IL-4 and TNFalpha 
They increase blood flow
Contract smooth muscle
Increase vascular permeability
Increase secretions at mucosal surfaces 
Important in defence against parasites and wound healing
83
Q

What is extrinsic asthma?

A

A response to an external allergen
IgE mediated
Triggers: house dust, mite, grass pollen, animal dander
Associated with other allergic disease

84
Q

What haappens clinically when an allergic reaction ocurs in the lung?

A

There is a release of histamine and other inflammatory mediators

85
Q

What does hisatmine and other inflammatory mediators in the lung cause?

A

Muscle spasm - bronchoconstriction and wheeze
Mucosal inflammation - mucosal oedema and increases secretions - sputum production
Inflammatory cell infiltrate - infiltration of lymphocytes and eosinophils into bronchioles - clinical manifestation - yellow sputum

86
Q

What are other names for urticaria?

A 
Hives
Wheals
Nettle rash
Blisters
Lesions appear within an hour
87
Q

What is angioedema?

A

Self-limiting, localised swelling of subcutaneous tissues or membranes
Non-pitting oedema
Not itchy unless associated with urticaria

88
Q

What are the clinical features of anaphylaxis?

A

Feeling of impending doom, loss of consciousness or death
Conjunctival infection, rhinorrhea, angiodema
Flushing urticaria
Wheeze, bronchoconstriction
Itch of palms
Laryngeal obstruction
Hypotension, cardiac arrythmias, myocardial infarct
Oral itching, vomiting, diarrhoea, abdo pain

89
Q

Why are allergies diagnosed?

A

To identify causitive agents - pinpoint specific allergens and target measures to reduce exposure and encourage lifestyle modification
Determine risk of future severe reaction
Determien appropriateness of therapy

90
Q

How can allergies be diagnosed?

A

Skin prick tests
Quantitate specific IgE to putative allergen
Challenge test
During an acute anaphylactic episode: serum mast cell tryptase levels

91
Q

How are IgE mediated allergic disorders managed?

A 
Block mast cell activation
Prevent effects of mast cell activation
Anti-inflammaotry agents
Management of anaphylaxis
Immunotherapy
92
Q

How is mast cell activation blocked?

A

Mast cell stabilisers - sodium cromoglycate, stabilises the mast cell membranes and prevents the release of inflammatory mediators such as histamine from mast cells
Topical spray for prophylaxis

93
Q

How are the effects of mast cell activation prevented?

A

Anti-histamines - H1 receptor antagonists that blocks the biological effects of histamines
Leukotrine receptor antagonists

94
Q

What is type 2 hypersensitivity?

A

Direct cell killing thats main feature is antibody binding to cell surface antigens
Antibody binding to cell-surface antigen results in activation of complement - cell lysis, opsonisation, anti-body mediated phagocytosis

95
Q

What are the effects of complement activation?

A

Chemotaxis
Solubilization of immune complexes
Direct killing of bacteria
Opsonisation which enhances phagoytosis by macrophage and neutrophils

96
Q

What is the classical pathway of complement activation?

A

IgM and IgG trigger the classical pathway that leads to the cleavage of C3 into C3a and C3b, C3b can then move downstream into many different functions

97
Q

What does the activation of complement result in/

A

The formation of membrane attack complexes that can punch holes in bacterial cell membranes and directly kill encapsulated bacteria

98
Q

What complement proteins are important in chemotaxis?

A

C3a and C5a are very important in chemotaxis, they are released after activation and increase the permeability of blood vessels and increase traffic of cells to sites of infection

99
Q

What is an immune complex?

A

Antigen + antibody complexes
Fragments of complexes can disssolve the immune complexes that triggered them switching off the process of complement activation

100
Q

What is central tolerance?

A

Developing immune cells that are self-reactive are destroyed whereas immune cells that aren’t are allowed to survive
Some self-reactive cells can escape causing an autoimmune disease

101
Q

Where does central tolerance occur?

A

In the primary lymphoid organs

Thymus in T cells and bone marrow for B cells

102
Q

What happens to self-reactive B cells in type 2 hypersensitivity?

A

The B cells start to produce IgM or with the help from CD4+ T cells produce IgG which will bind to antigens on self cells

103
Q

What are the types of antigens present on cells in type 2 hypersensitivity?

A

Intrinsic - normally made by host

Extrinsic - antigen from an infection or drugs such as pencilin that gets attached to the host cell

104
Q

What is an antigen-antibody complex?

A

When the antibody binds to the antigen

This usually happens in infection but it causes problems when it occurs on host tissues

105
Q

What is the complement system?

A

A series of small proteins that work in an enzymatic cascade to fight infection

106
Q

How is the complement system activated?

A

C1 will bind to the Fc portion of IgG or IgM and will iniate the complement cascade

107
Q

What do C3a, C4a and C5a act as?

A

Chemotactic factors - attract neutrophils which will then degranulate releasing peroxidase, myeloperoxidase and proteinase 3 which are oxygen radicals that will cause tissue damage

108
Q

What is good pastures syndrome?

A

Antibodies bind to intrinsic antigens on collagen of the basement membrane of the glomeruli in the kidneys or the alveoli in the lungs

109
Q

What forms the membrane attack complex?

A

C5b + C6 + C7 + C8 + C9

110
Q

How does the MAC attack the cell?

A

It inserts itself into the cell membrane punching a hole - creating a channel to allow fluids and molecules to flow into the cell causing cell lysis

111
Q

What is a direct coomb’s test?

A

The red cells are separated from the plasma and then reacted with coomb’s reagent - an antibody against human antibodies
If the cells agglutinate it suggests that there are antigens present on the cell

112
Q

How can the complement system perform type 2 hypersensitivity?

A

IgG antibodies coat cells that are bound by C3b. They opsonise the cell - making it a target for phagocytosis
The cell will then move to the spleen where it meets a macrophage. The macrophage will either bind to the Fc region of the IgG or the C3b complement fragment and will engulf it

113
Q

What is antibody-dependent cell-mediated cytotoxicity?

A

The bound antigen-antibody complex is recognised by NK cells which will bind to the Fc region of the antibody releasing its granules causing apoptosis of the cells

114
Q

What is a non-cytotoxic type 2 hypersensitivity?

A

Antibody-mediated cellular dysfunction

115
Q

What is antibody-mediated cellular dysfunction?

A

When an antibody binds to the antigen it can change the way the cell functions

116
Q

What is a clinical presentation of type 2 hypersensitivity?

A

Immune haemolytic anaemia

117
Q

How can type 2 hypersensitivity be managed?

A

Plasmapheresis - removal of pathogenic antibody

Immunosuppresion - rebound antibody production limits the efficacy of plasmapheresis

118
Q

What is type 3 hypersensitivity?

A

Antigen-antibody complexes deposit in blood vessel walls causing inflammation and tissue damage

119
Q

What are type 3 hypersensitivity reactions mediated by?

A

Immune complexes - antigen-antibody complexes

120
Q

What happens when a B cell becomes cross linked?

A

2 IgM antibodies expressed on the surface of the B cell bind to an antigen where it will be taken into the cell. The B cell will then express a MHC 2 receptor which is presents to the T helper cells along will complementary molecules causing the T helper cell to release cytokines resulting in class switching

121
Q

What is the class switching in type 3 hypersensitivity?

A

IgM to IgG

122
Q

What is an example of a type 3 hypersensitivity reaction?

A

Systemic lupus erythematosus - DNA is released from a damaged cell and a dysfunctional B cell will recognize this self antigen and attack it

123
Q

What are small immune complexes and what do they do?

A

They are less immunogenic - they are less attractive to macrophages and so won’t be removed from the blood stream and will therefore make its way into the basement membrane of cells. Here they will activate the complement system

124
Q

What is an anaphylatoxin?

A

Complement proteins (C3a + C4a + C5a) which increase vascular permeability allowing fluid to leak out causing odema. Neutrophils are then attracted to the site and will degranulate causing more tissue damage

125
Q

Where does lupus cause problems?

A

Kidneys - glomerulonephritis

Joints - arthritis

126
Q

What is a clinical type of local type 3 hypersensitivity?

A

Famers lung - inhaled fungal particles are deposited in the lungs and stimulate antibody formation. The antibodies form immune complexes with antigens resulting in complement activation, causing inflammation and the recruitment of other leukocytes

127
Q

What is acute hypersensitivy pneumonitis?

A

Adaptive immune response generated creating IgG binding to bird antigens forming complexes that get deposited in the alveoli. This drives complement and neutrophil activation and inflammation. This creates chronic inflammation in the alveoli of the lungs

128
Q

What are the clinical symptoms or acute hypersensitivity pneumonitis?

A

Wheeze - bronchoconstriction, inflammation of terminal bronchioles and alveoli
Breathlessness - airways become swollen due to inflammation, decreased gas transfer
Malaise, pyrexia - production of a particular cytokine that sends signals to the hypothalamus and drives fever

129
Q

What is the management of type 3 hypersensitivity?

A

Avoidance
Decrease inflammation - corticosteroids
Decrease production of antibodies - immunosuppression

130
Q

What are diseases associated with delayed type 4 hypersensitivity reactions?

A

Autoimmune - type 1 diabetes, psoriasis, rheumatoid arthritis
Non-autoimmune - contact dermatitis, TB, leprosy, sarcoidosis, cellular rejections of solid organ transplant

131
Q

What drives type 4 hypersensitivity?

A

CD4+ T cells

CD8+ cytotoxic T cells

132
Q

Where are T cells produced?

A

The thymus

133
Q

What do T cells start off as?

A

Naive cells because their T cell receptor hasn’t yet bound to the antigen

134
Q

Where do dentritic cells go with an antigen?

A

To the lymph node

Respiratory (24 decks)

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