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Immunology Flashcards

1
Q

What is a Type I hypersensitivity reaction?

A

Mechanism: IgE mediated

Clinical Symptoms: urticaria, angioedema, anaphylaxis, anaphylactic shock, bronchial asthma, rhinitis, eczema

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2
Q

What is a Type II hypersensitivity reaction?

A

Mechanism: IgG-mediated cytotoxic hypersensitivity (i.e. antibody mediated)

Clinical symptoms: Autoimmune haemolytic anaemia, thrombocytopenia, blood transfusion reactions; bullous pemphigoid

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3
Q

What is a Type III hypersensitivity reaction?

A

Mechanism: immune complex mediated hypersensitivity; Ag-Ab complexes deposit and induce complement / inflammatory/ neutrophil response
Clinical symptoms: Vasculitis, GN, Organ specific reactions; SLE

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4
Q

What is a Type IV hypersensitivity reaction?

A

Mechanism: T cell-mediated hypersensitivity
Th1 cells activate macrophages or Tc cells

Clinical symptoms: SJS; TEN; DRESS; fixed drug eruption; contact dermatitis; delayed urticaria; MS; Scabies; GVHD; TB skin reaction

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5
Q

What is the function of IL-1?

A

Central regulator of the inflammatory response
Proliferation of activated T cells, B cells
Produced by macrophages, dendritic cells

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6
Q

What is the function of IL-2?

A

Produced by T cells
Growth of activated T and B cells
Activation of NK cells

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7
Q

What is the function of IL-3?

A

Produced by T cells, macrophages
Mast cell growth
Growth and differentiation of haematopoetic precursors

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8
Q

What is the function of IL-4?

A

Produced by T and B cells, macrophages, mast cells and basophils
Activation of B cells to promote IgE switching
Differentiation of Th2 cells

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9
Q

What is the role of IL-5?

A

Produced by Th2 subset, mast cells
IgM, IgA production
Driver ofWCC differentiation to eosinophilic pathway
Activated B cell proliferation

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10
Q

What is the function of IL-6?

A

Produced by T cells, macrophages, monocytes
Production of acute phase proteins
Growth and differentiation of haemopoetic cells
FEVER

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11
Q

What is the role of IL-8?

A

Produced by T cells, monocytes and neutrophils

Activation of Neutrophils

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12
Q

What is the function of IL-10?

A

Produced by T and B cells, macrophages
Suppression of macrophage functions & Th1 cells
Activation of B cells

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13
Q

What is the function of IL-17?

A

Produced by CD4 T cells, ILC3, NK cells
Promotes inflammation by increasing production of pro inflammatory cytokines (IL-1, IL-6, TNF alpha, G-CSF, GM-CSF) by epithelial, endothelial & fibroblast cells

IL-17 Deficiency = Job Syndrome

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14
Q

What is the function of TNF alpha?

A

Produced by macrophages, lymphocytes, neutrophils, eosinophils, NK cells
Activates macrophages, granulocytes, cytotoxic cells and endothelium
Enhanced HLA class I expression
Stimulation of acute phase response
Anti-Tumor effects

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15
Q

What is the function of TNF beta?

A 
Produced by CD4 T cells
Acute phase proteins
Anti viral / anti parasite activity
Activation of phagocytes 
Induce pro inflammatory cytokines
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16
Q

General function of Tumor Necrosis Factor?

A

Transmembrane protein - can be cleaved and released to act as a cytokine
Principle mediator of response to gram negative bacteria

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17
Q

What is the function of IFN-alpha?

A

Produced by leukocytes

Antiviral; up-regulates MHC Class I

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18
Q

What is the role of IFN-gamma?

A

Antiviral macrophage activation
Enhance HLA class I and class II expression
Characterises Th1 cells
Suppression of Th2 cells
Antagonises IL-4 effect
Stimulation of macrophages and endothelium

Aberrant IFN-gamma expression is associated with a number of auto inflammatory and auto immune conditions e.g. MS

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19
Q

What is BAFF?

A 
B-cell-activating factor
Member of of the TNF family 
Cytokine that promotes B cell maturation, proliferation and survival 
Survival factor for B cells
Induced by interferon type 1 and type 2
Co-stimulates immune B cell responses
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20
Q

What is BLyS?

A

B lymphocyte stimulator
Soluble ligand of the TNF cytokine family
Role in B cell differentiation, homeostasis and selection
BLyS levels affect survival signals and selective apoptosis of auto-antibody producing B cells

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21
Q

What is VEGF?

A

Vascular Endothelial Growth Factor
Expressed on endothelial and non endothelial cells including tumor cells
Potent angiogenic factor

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22
Q

Investigations in Common Variable Immunodeficiency (CVID)

A

IgG low - one or both of IgA/IgM also decreased
B cell count nor
Impaired vaccination response
Low switched memory B cells

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23
Q

Investigations in X-linked (Bruton’s) Agammaglobulinaemia

A 
IgG levels - typically undetectable 
B-cell count - zero
No plasma cells or germinal centres in tissue biopsies
B-cell precursors present in the marrow
BTK expression in flow cytometry
Genetic analysis of BTK gene
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24
Q

Northern blotting is used for?

A

Detect RNA

SNOW - South - NOrth - West
DROP - DNA - RNA - Protein

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25
Q

Abacavir - HLA hypersensitivity

A

HLA-B*57:01

A derivative of abacavir binds to B57:01 within the cell - alters the repertoire of self peptides which can bind to B57:01. Presentation of altered self peptides to T cells = altered immune response

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26
Q

Carbamazepine - HLA hypersensitivity

A

HLAB*15:02

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27
Q

What is the role of the HLA / MHC in the immune response?

A

Presentation of antigens to T cells

Extracellular proteins (mainly bacteria) are processed through phagocytosis, phagolysomes onto MHC II = CD4+ T cells

Cytosine proteins made by the cell are processed via the golgi onto MHC I = CD8+ T cells (mainly viral response)

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28
Q

Distribution of HLA / MHC?

A

MHC I - present on membrane of all nucleated cells (except RBCs)

MHC II - present on APCs: dendritic cells, B cells and macrophages

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29
Q

What is the main purpose of somatic hypermutation in B cells?

A

Selection of high affinity B cells

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30
Q

Absence of B cells is characteristic of which primary disorder?

A

X-linked agammaglobulinaemia (XLA)

Immunoglobulins are produced by plasma cells, which themselves are the result of the development & differentiation of B cells

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31
Q

Which disease is caused by decreased apoptosis resulting in increased presentation of self antigen?

A

SLE

The mediators of SLE are autoantibodies and the immune complexes they form with antigens

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32
Q

Cancers related to Common Variable Immunodeficiency Disease (CVID)

A

Non-Hodgkins lymphomas

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33
Q

Cancer’s related to Hyper-IgE syndrome (Job’s syndrome)

A

Aggressive B cell lymphomas

May be linked to abnormalities in STAT3 / IL-21 dependent differentiation of B cells

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34
Q

Activation of classical complement pathway?

A

Binding of C1q in the C1 complex to the Fc portion of IgG or IgM immune complexes

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35
Q

Activation of the leptin complement pathway?

A

Mannose-binding lectin binding to sugar moieties on the surface of pathogens leading to the engagement of proteases (analogous to Cr1 and C1s of the classical pathway)

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36
Q

Activation of alternative complement pathway?

A

Does not require antibody or contact with a microbe to become activated. C3 is constantly autoactivated at a low level, a process that is rapidly amplified in the presence of a microbe / damaged host cell / lack of a complement regulatory protein

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37
Q

Goal of the 3 complement cascades?

A

Deposition of C3b on a target (opsonisation), which marks it for elimination
Also leads to the release of pro inflammatory anaphylatoxins (C3a and C5a) and assembly of the membrane attack complex (MAC)

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38
Q

Diseases associated with deficiencies in C3-C9

A

Pneumococcal & influenza - C3 deficiency

Neisserial infections - C5, C6, C7, C8 or C9 deficiency

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39
Q

3 stages of Tcell development

A
  1. Migration to thymus
  2. T cell receptor gene rearrangement
  3. Selection = learn to respond to MHC
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40
Q

Selection of T cells

A

Need to be useful: positive selection - choose T cells that can interact with MHC
Can’t be useless: death by neglect - ignore T cells that cannot interact with MHC
Can’t be harmful: negative selection - delete self reactive T cells
Turn harmful to useful: induce Treg cells from self reactive T cells

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41
Q

3 signal model of T cell activation

A

Signal 1: Ag peptides presented by MHC
Signal 2: co-stimulation (CD40 / 80 / 86)
Signal 3: Th subset preference (Th 1 / Th2 / Th17 / Treg)

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42
Q

What is the critical step in central T cell tolerance?

A

Negative selection

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43
Q

Role of AIRE?

A

AIRE is a transcription factor expressed in the medullary of the thymus
Is part of the mechanism which eliminates self reactive T cells - i.e. drives negative selection

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44
Q

Recurrent infection suggestive of a T cell immunodeficiency?

A

Intracellular organism infections

  • Fungi e.g. mucosal candida, pneumonitis
  • viruses e.g. CMV, VZV, HSV, Protozoa (CD8)
  • Listeria
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45
Q

Mechanism of Hereditary Angioedema

A

Due to deficiency (Type 1) / dysfunction (Type 2) of C1 esterase inhibitor - leads to increased levels of bradykinin (a potent vasodilatory peptide) and uncontrolled activation of the complement pathway (consumption of C4 through loss of C1r and C1s).

Due to mutations in the SERPING1 gene
Type one is more common

Treatment: Icatibant (bradykinin B2 receptor antagonist)

46
Q

Investigations for Hereditary angioedema

A

Suggestive history and physical findings
C4 level
C1 inhibitor level low or abnormal function
Genetic testing not usually required

47
Q

Role of conjugate vaccine attached to a carrier protein AND polysaccharide antigen?

A

Better efficacy due to better T cell response

Addition of the carrier protein to a polysaccharide vaccine makes a polysaccharide vaccine T cell dependent thus boosting the effect of the vaccine

48
Q

Role of IL-12?

A

Promotes formation of Th1 cells

49
Q

Role of Th1

A

Secretes IFN-gamma, TNF, lymphotoxin

Prevents intracellular organisms (e.g. mycobacteria, listeria, toxoplasma, leishmania)

50
Q

Role of IFN-gamma

A

Activates macrophages
Activates NK cells
Acts on B cells to stimulate Ab formation
Defence against intracellular pathogens (viruses & intracellular bacteria)

51
Q

Role of Th2?

A 
Differentiate in response to IL-4
Secrete IL-4, IL-5, IL-6, IL-10, IL-13
Activates B cells to make neutralising antibodies
Role in inducing ‘atopic’ type response
- IgE production by B cells (IL-4, 13)
- Eosinophils (IL-5)
Defence against helminths
52
Q

Role of Th17?

A

Differentiate in response to IL-1, IL-6, IL-23
Secrete IL-17 and IL-22
Defence against Candida, staphylococcus

53
Q

Role of Treg?

A

Secretes cytokines (Is-10, TGF-beta) with immunosuppressive properties

54
Q

Cardinal feature of the innate immune system?

A

Inflammation

55
Q

What is CRP?

A

Acute phase protein that binds to phospholipid in foreign pathogens or damaged host cells
Can promote the recognition and elimination of pathogens and enhance clearance of apoptotic and necrotic cells

56
Q

Diseases associated with lack of complement components

A

Classical pathway

  • C1q, C1r, C1s: SLE
  • C4: SLE, GN
  • C2: SLE, vasculitis, GN, recurrent pyogenic infections
  • C3: recurrent pyogenic infections, CN, immune complex diseases

Alternative pathway
- Properdin, factor D: Neisseria infections

Terminal components
- C5/6/7/8/9: disseminated Neisseria infections

57
Q

Examples of Live Attenuated Vaccines?

A 
BCG
MMR
Oral rotavirus 
Oral polio
Yellow fever
Oral typhoid
Varicella
58
Q

Contraindications to yellow fever vaccine?

A

Anaphylaxis to previous dose
Anaphylaxis to eggs
HIV withCD4 count <200
Thymus disorder e.g. myasthenia gravies, thymoma, thymectomy, DiGeorge syndrome
Haematopoetic stem cell transplant recipients
Pregnant women
Breastfeeding infant <9 months old

59
Q

Most important event in complement dependent cytotoxicity

A

Formation of membrane attack complex

60
Q

Paracetamol hypersensitivity

A

A weak inhibitor of COX1
The majority of suspected paracetamol reactions occur in conjunction with NSAID intolerance and relate to the pharmacological action of COX1 inhibition

REMEMBER: cyclooxygenase inhibition blocks the conversion of arachidonic acid to prostaglandins and thromboxane resulting in a therapeutic anti-inflammatory effect

61
Q

What is haemophagocytic lymphohistiocytosis (HLH)?

A

Syndrome of excessive inflammation and tissue destruction due to abnormal immune activation
NK cells and / or cytotoxic lymphocytes fail to eliminate activated macrophages

62
Q

Immunologic changes that occur in allergen immunotherapy?

A
  1. Decreases in mast cells and basophil activity and degranulation
  2. Changes in allergen-specific antibody isotypes
  3. Generation of allergen-specific regulatoryT and B cells
  4. Decrease in tissue mast cells and eosinophils
63
Q

Highest association with fatal anaphylaxis

A

Poorly controlled asthma

Other risk factors for death:
Patient age
Concurrent use of ACEi and/or Beta Blockers
Dose of allergen

64
Q

What is an auto inflammatory syndrome?

A

Autosomal dominant inherited disorders
Distinguished by absence of a defined adaptive immune response
Prototype = hereditary periodic fever syndromes; share a common involvement of certain specific cytokines e.g. IL-1 beta and TNF

Canakinumab: anti IL-1 beta

65
Q

Most important costimulatory signal in naive T cells?

A

CD28 - binds to B7-1 and B7-2 (CD80/86) on the APC

66
Q

Action of CTLA-4 on T cells ?

A

Inhibits activation of T cells

67
Q

Indications for allergy desensitisation

A

IgE mediated disease
Sensitisation is relevant for the symptoms
Symptoms are of sufficient severity and duration
Availability of a standardised high-quality allergen extract of the specific allergen intended to be used for immunotherapy

68
Q

Contraindications for allergy desensitisation

A 
Malignant disease
Autoimmune disease
Current therapy with beta blockers
Asthma patients with FEV1<70% under treatment or uncontrolled asthma
Pregnancy 
Acute infection e.g. influenza
69
Q

Indications for drug desensitisation

A

No alternative/ alternative inferior (e.g. syphillus in pregnancy)
No history of anaphylaxis to medication

70
Q

Mechanism of calcineurin inhibitors

A

Ciclosporin and Tacrolimus form complexes with cytoplasmic immunophilims (cyclophilin and FKBP-12 respectively) which block the action of calcenurin in activates cells. This prevents production of IL-2 (which normally stimulate T cell proliferation and differentiation)

AE: hypertension, nephrotoxicity, gum hyper trophy

71
Q

Mechanism of Azathioprine

A

Metabolised to

  1. 6-mercaptopurine: inhibits de novo purine synthesis
  2. Thioguanine: anti proliferative effect on mitotically active lymphocyte populations; inhibits CTL/NK cells; induces apoptosis of T cells via Rac1 gene
72
Q

Mechanism of glucocorticoids

A 
Bind to glucocorticoid receptor - translate to nucleus- alters transcription and intercepts secondary messengers 
Inhibits synthesis / release of
- cytokines (IL-1, TNF, IL-2, IFN-gamma)
- prostaglandins, leukotrienes
- plasminogen activator 
Non selective
73
Q

Presentation of Takayasu’s arteritis

A 
Young women <40 years
Limb claudication
Decreased brachial artery pulse
Differential limb SBP >10mmHg
Subclavian artery or aortic bruit
Abnormal angiogram

Gold standard for diagnosis = angiogram (beading, stenosis, aneurysms)

74
Q

Mechanism of mycophenolate

A

Converted to mycophenolic acid, which selectively suppresses lymphocyte proliferation and antibody formation by inhibition of inosine monophosphate dehydrogenase
Depletion of guanosine nucleotides (required for de novo purine synthesis in lymphocytes) results
= G1 arrest

75
Q

Mechanism of methotrexate

A

Inhibits dihydrofolate reductase = essential for DNA synthesis

76
Q

Mechanism of Cyclophosphamide

A

Alkylating agent - alters DNA
Cell cycle inhibitor
Cytotoxic effects on lymphocytes = Lymphocytopenia (B>T cells)

77
Q

Mechanism of abnormal phagocytise cell function in chronic granulomatous disease?

A

Failure to produce reactive oxygen intermediates

CGD: Diverse group of hereditary diseases in which certain cells of the immune system have difficulty forming the reactive oxygen compounds to kill certain ingested pathogens.
Phagocytes require the enzyme ‘phagocyte NADPH oxidase’ to produce reactive oxygen species to destroy ingested bacteria

78
Q

Role of transforming growth factor (TGF) beta?

A

Immunosuppressive cytokine

Implicated in Treg function

79
Q

Cell type playing the predominant role in the early inflammatory phase of an IgE mediated allergic response?

A

Mast cells involved in early inflammatory phase

Eosinophils involved in late inflammatory phase

80
Q

What interaction will lead to septic shock in gram negative sepsis?

A

Binding of Toll Like Receptor 4 to bacterial lipopolysaccharides

81
Q

Variation in which cell surface molecule is capable of conferring the greatest resistance to HIV infection?

A

Chemokine receptor CCR5

82
Q

Clinical features of chronic granulomatous disease?r

A

Recurrent infections with coagulase negative bacteria and fungi
Staphylococcus infection of the skin
Purulent dermatitis
Aspergillus pneumonia

83
Q

What NOD-like receptor is responsible for the acute inflammation seen in gout?

A

NALP3
Urate crystals and calcium pyrophosphate dehydrate (CPPD) activates the NALP3 inflammation. Caspase 1 is activated and IL-1 beta is released causin inflammation and pain

84
Q

Severe Combined Immune Deficiency

A

Features produced by the loss of expansion of Lymphoid Progenitor Cells (‘alymphocytosis’)

85
Q

What cell surface molecule is least important in the regulation of NK cell function?

A

MHC class II on the target cell

86
Q

What is a T dependent antigen?

A

Antigens that do not directly stimulate the production of antibody without the help of T cells
E.g. Proteins

87
Q

What is a T independent antigen?

A

Antigens which can directly stimulate the B cells to produce antibodies without T cell help
E.g. polysaccharides, dextran, lipopolysaccarides, peptidoglycans

88
Q

Which immunoglobulin binds with low affinity and high avidity when exposed to antigen?

A

IgM
Affinity- overall strength of the bond between antibody and antigen
Avidity - overall strength of the interaction between antibody and antigen
IgM is a pentameter therefore has the highest avidity

89
Q

Treatment of hereditary angioedema

A

C1-inhibitor concentrate

Danazol

90
Q

3 cardinal features of Autoimmune Polyendocrine Syndrome Type 1?

A
  1. Chronic mucocutaneous candidiasis
  2. Autoimmune hypo parathyroidism
  3. Autoimmune Addison’s disease + other autoimmune manifestations
91
Q

IPEX

A 
Lack of foxP3 means no Treg cells = global overactivity of immune function 
Immune dysfunction
Polyendocrinopathy
Enteropathy
X-Linked
92
Q

Primary IgA deficiency

A

Most common primary immune disorder
High incidence of atopy and food allergy
Associated with IBD, RA, SLE, Sjogrens, ITP
Patients at increased risk of transfusion reactions due to presence of Anti-IgA antibodies
Ix: absent IgA, normal B cell count
Rx: NOT IVIG, antibiotics for acute episodes

93
Q

The polymeric Ig receptor (PIgG) transports predominately which class of immunoglobulin into the mucosal lumen?

A

IgA

94
Q

Cross reacting foods in patients with latex allergy?

A

Banana, avocado, kiwi, chestnut

Papaya, fig, potato, tomato

95
Q

Clinical manifestations is CVID

A 
Recurrent sinopulmonary infections
Chronic diarrhoea, malabsorption 
Skin infections 
Autoimmunity e.g. ITP, RA, thyroid disease, vitiligo
Neoplasia (400x risk of NHL)
Food allergies
Bronchiectasis and respiratory failure
96
Q

Ciclosporin: adverse effects

A

Nephrotoxicity
Hypertension
Neurotoxicity: tremor, headache, confusion, seizures, coma, psychosis
HUS

97
Q

Mycophenolate: adverse effects

A

D / N / V / abdominal pain
Abnormal LFTs
Leucopenia, neutropenia, anaemia, thrombocytopenia, pancytopenia

98
Q

Mechanism of Sirolimus

A

mTOR inhibitor
Following entry into the cytoplasm, sirolimus binds to the FK binding protein to modulate the activity of mTOR - inhibits IL-2 = cell cycle arrest in G1-S phase
Also blocks the response of T and B cell activation by cytokines, which prevents cell cycle progression and proliferation
AE: hyperlipidemia via inhibition of lipoprotein lipase

99
Q

Cyclophosphamide toxicity

A 
Infertility secondary to gonadal toxicity 
Malignancy 
Bladder toxicity 
Myelosuppression 
Herpes Zoster
Major infection
100
Q

Mycophenolate toxicity

A 
GI upset
Leukopenia
Thrombocytopenia 
Anaemia
Infection 
Malignancy
101
Q

Low serum complement level systemic diseases

A 
SLE
Sub acute bacterial endocarditis 
Visceral abscess
Shunt nephritis
Cryoglobulinaemia
Acute post infectious GN
MPGN
102
Q

Normal serum complement level systemic diseases

A 
Polyarteritis nodosa
Hypersensitivity vasculitis 
Wagner’s
HSP
Goodpasture Syndrome
IgA nephropathy
RPGN
Anti GBM disease
Immune complex disease
103
Q

Mechanism for hypokalemia in a patient who develops metabolic alkalosis secondary to vomiting?

A

Increased intracellular exchange of potassium for hydrogen

Metabolic alkalosis causes K movement into cells

104
Q

GATA2 deficiency

A

Syndrome of monocytopenia and mycobacterial diseased
Characterised by late childhood/ adult onset of disseminated nontuberculosis disease or disseminated fungal disease
Monocytopenia, NK cell cytopenia, B cell lymphopenia

105
Q

CD 40 ligand is primarily expressed on?

A

Activated CD4+ T helper cells

106
Q

HLA-A3 association

A

Haemochromatosis

107
Q

HLA-B5

A

Bechet’s disease

108
Q

HLA-DQ2/DQ8

A

Coeliac disease

109
Q

HLA-DR2

A

Narcolepsy

Good pastures

110
Q

HLA-DR3

A

Dermatitis herpetiformis
Sjogrens
Primary biliary cirrhosis

111
Q

HLA-DR4

A

T1DM

RA

BPT Written (16 decks)

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