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Cross reference - year 5 > Immunology > Flashcards

Immunology Flashcards

1
Q

how does lacterferrin stop bacteria?

A

starves bacteria of iron

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2
Q

what are the different innate immune cells?

A
  • polymorphonuclear cells (neutrophils, eosinophils, basophils)
  • monocytes and macrophages
  • dendritic cells
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3
Q

macrophage name in: kidney, neural tissue, connective tissue

A

kidney: mesangial cell
neural tissue: microglia
connective tissue: histiocyte

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4
Q

forms of oxidative killing

A
  • NADPH oxidase = forms ROS

- Myeloperoxidase = forms hydrochlorus acis (oxidant and anti-microbial)

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5
Q

what is the job of NK cells?

A

cytotoxic
kills altered self cells e.g. malignancy or virus-infected virus
regulates inflammation and promote DC function

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6
Q

following phagocytosis, DC will?

A

upregulate expression of HLA molecules
express co-stmulatory molecules
migrate via lymphatics to lymph nodes (mediated by CCR7)

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7
Q

what do CD4+ T cells (Helper T cells) do?

A

recognise peptides derived from extracellular proteins (presented on HLA class II = HLA-DR, DP, DQ)

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8
Q

what are the CD4 subsets?

A 
Th1
Th17
Treg
TFh
Th2
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9
Q

what do Th1 cells do?

A

help CD8 T cells and macrophages

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10
Q

what do Th17 cells do?

A

help neutrophil recruitment

enhance generation of auto-Abs

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11
Q

what do TFh cells do?

A

promote germinal centre reactions

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12
Q

what are Th2 cells?

A

helper T cells

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13
Q

what do CD8+ cytotoxic T cells do?

A 
recognise peptides derived from intracellular proteins 
HLA class 1 (A, B, C)
important in defence against viral infections and tumours
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14
Q

what are the features of the classical complement cascade?

A
  • activated by immune complexes
  • dependent on activation of immune response
  • C1, C2, C4
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15
Q

what are the features of the MBL pathway?

A

direct binding of MBL to microbial cell surface

C4, C2

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16
Q

what are the features of the alternative pathway?

A
  • directly triggered by binding of C3 to bacterial cell wall components
  • not reliant on acquired immune response
  • B, I, P factors
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17
Q

what is the amplification step of alternative pathway?

A

activation of C3 comvertase

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18
Q

what ligands and chemokine are important in directing DC trafficking to lymph nodes?

A

CCL19 and CCL21 are ligands for CCR7

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19
Q

what is reticular dysgenesis and the gene mutation?

A

AK2 mutation

failure of stem cells to differentiate along myeloid/lymphoid lineage

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20
Q

what is Kostmann syndrome and the mutation?

A

AR severe congenital neutropaenia

HCLS1-associated protein X-1

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21
Q

what is the mutation in cyclic neutropaenia?

A

neutrophil elastase

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22
Q

what is the problem in leukocyte adhesion deficiency?

A

deficiency of CD18

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23
Q

what is the colour change in Nitroblue tetrazolum test?

A

yellow to blue

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24
Q

what is the change seen in dihydrorhodamine (DHR) test?

A

becomes fluorescent

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25
Q

what is the phenotype on NK cell deficiencies?

A

increase risk of VIRAL infections

e.g. severe chicken pox, disseminated CMV

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26
Q

what is the most common complement deficiency and the phenotype?

A

C2

Phenotype: SLE, severe skin disease, increase risk of infection

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27
Q

what are nephritic factors?

A
  • autoAbs directed against components of complement pathway

- they stabilise C3 convertases (which break down C3) = C3 activation and consumption

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28
Q

what are nephritic factors associated with?

A

glomerulonephritis

partial lipodystrophy

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29
Q

what is C1q deficiency?

A
  • inherited complement deficiency
  • SLE in childhood
  • CH10 low, normal levels of C3 and C4
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30
Q

what is the phenotype of C7 deficiency?

A

meningococcus meningitis

FH of sibling dying young

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31
Q

what is basophillic stippling?

A

presence of aggregated ribosomal material

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32
Q

causes of basophillic stippling

A
  • beta-thalassaemia trait
  • lead poisoning
  • alcoholism
  • sideroblastic anaemia
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33
Q

causes of target cells?

A

3 H’s
Hepatic pathology
Hyposplenism
Haemoglobinopathies

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34
Q

what are howell jolly bodies? cause?

A

nuclear remnants visible within red blood cells

cause: hyposplenism

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35
Q

what are causes of hyposplenism?

A
  • absent spleen (therapeutic, trauma)

- poorly functioning spleen (IBD, coeliac, SCD, SLE)

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36
Q

what is the most common association of coeliac?

A

HLA-DQ2

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37
Q

what is the T cell response to gluten?

A
  1. peptides from gluten deaminated by TTG
  2. APCs take up deaminated gluten
  3. presented via HLA (DQ2/DQ8) to CD4 cells
  4. causes increase in IFN-gamma and IL-15
  5. cytokines promote activation of IELs
  6. IELs kill epithelial cells via KG2D receptor = gut damage
  7. Primed T cells can help B cells with Abs that recognise gliadin to undergo germinal centre reactions = memory cells and plasma cells
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38
Q

what is the most accurate anti-bodies to measure in coeliac?

A

anti-TTG

check if IgA deficient first

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39
Q

what are some other causes of villous atrophy?

A
  • Chron’s
  • GvHD
  • CVID
  • nutritional def
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40
Q

what are the IELs in Coeliac compared to most T cells?

A

gamma delta T-cells

most T cells are alpha-beta

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41
Q

what are other causes of increased IELs?

A

drugs
IgA def
post-infective malabsorption
giardiasis

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42
Q

what is the most dangerous side effect of coeliac?

A

multi-focal T cell lymphoma

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43
Q

what is X-linked SCID and mutation?

A

most common SCID
mutation: gamma cgain on Chr Xq13.1
inability to respond to cytokines = early arrest of T cells, NK cells, produce immature B cells

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44
Q

what is ADA deficiency?

A

16.5% of SCID
adenosine deaminase deficiency (needed by lymphocytes for cell metabolism)
failure of maturation along any lineages

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45
Q

features of DiGeorge

A

deletion of 22q11.2
CATCH features
normal B cells, low T cells

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46
Q

what are the features of Bare lymphocyte syndrome type 2?

A

deficiency of MHC II genes
low CD4
CD8/B cell normal
Low IgG and IgA

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47
Q

what does T lymphocytes deficiency lead to?

A

viral infections
fungal infections
some bacterial infections (especially intracellular e.g. TB, salmonella)

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48
Q

what is Bruton’s X-linked hypogammaglobulinaemia?

A

abnormal B cell tyrosine kinase deficiency

Pre-B cells cannot mature into mature B cells

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49
Q

what is the mutation in hyperIgM?

A

mutation in CD4 ligand gene

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50
Q

what is CVID?

A

unknown cause

low IgG, IgA, IgE, recurrent bacterial infecitons

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51
Q

typical phenotype of CVID

A

adult with bronchiectasis
recurrent sinusitis
atypical SLE

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52
Q

what are the features of antibody deficiency?

A

bacterial infection
toxins
some viral infections

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53
Q

what can protein electrophoresis show?

A

gamma peak (all the Abs)

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54
Q

name 2 mixed pattern diseases

A
  • ankylosing spondylitis

- psoriatic arthritis

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55
Q

what are 3 rare monogenic auto-immune diseases?

A
  • APS-1/APECED
  • ALPS
  • IPEX
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56
Q

regarding the inflammasome complex, what mutations cause increased inflamation?

A
  • gain of function mutation in cryopyrin = increased inflammation
  • loss of function mutation in pyrin-marenostrin = increased inflammation
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57
Q

what is the mutation in familial mediterranean fever?

A
  • mutation in MEFV gene

- this encodes pyrin-marenostrin (expressed by netrophils)

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58
Q

association of FMF

A

AA amyloidosis

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59
Q

treatement of FMF

A

colchine
anakinra (IL1R antagonist)
etanercept (TNF-alpha inhibitor)

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60
Q

what is the cause of APECED? Associations?

A

defect in AIRE

associated with AI conditions, candidiasis

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61
Q

what is the cause of IPEX? symptoms?

A

mutation in FoxP3

  • immune dysregulation
  • polyendocrinopathy (DM, hypothyroid)
  • enteropatht
  • dermatitis
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62
Q

what is the mutation in ALPS?

A

mutation in Fas pathway

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63
Q

what is mutation in Chron’s disease?

A

IBD1 on Chr 16 = encodes NOD2

NOD 2 expressed in cytoplasm of myeloid cells, is a microbial sensor

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64
Q

genetic association of Ankykosing Spondylitis and treatment?

A

HLA-B27

Tx: Anti-TNFa, anti-IL17

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65
Q

HLA association of Goodpastures

A

HLA-DR15

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66
Q

HLA association of Graves

A

HLA-DR3

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67
Q

HLA association of SLE

A

HLA-DR3

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68
Q

HLA association of T1DM

A

HLA-DR3/DR4

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69
Q

HLA association of RA

A

HLA-DR4

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70
Q

what is the function of PTPN22? what happens if he is mutated?

A

PTPN22 suppresses T cell activation

if mutated = fail to control T cell activation

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71
Q

what does CTLA4 do?

A

controls T cell activation

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72
Q

difference between a T2SR and a T3SR

A

T2: antibody reacts with cellular antigen
T3: antibody reacts with soluble antigen to form immune complex

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73
Q

what is the autoantigen in pemphigus vulgaris?

A

auto-antigen against epidermal cadherin

74
Q

what are the autoantigens in SLE and RA (T3R)?

A

SLE: DNA, histones, RNP
RA: Fc region of IgG

75
Q

what does sensitisation show?

A

shows risk of allergic disorder but does not define allergic disease

76
Q

how do helminths/allergens/venoms trigger immune response?

A

cause functional change which is recognised

causes Th2 response

77
Q

what are the 3 different responses to allergens?

A
  1. Th2/Th9/ILC2 cells
  2. Follicular Th2 cells
  3. mast cell
78
Q

what is the process of Th2/Th9 and ILC2 cells response to allergens?

A
  1. release of IL4, IL5, IL13
  2. eosinophils and basophils activated
  3. expulsion of parasites and allergens
79
Q

what is follicular Th2 response to allergens?

A
  1. IL4 released

2. causes B cells to produce IgE and IgG4

80
Q

what is the mast cell response to allergen?

A
  1. cross-linking of IgE
  2. histamine/leukotrienes released
  3. expulsion
    (also responsible for symptoms of asthma, eczema and hayfever)
81
Q

what is the difference between oral exposure and skin/resp exposure?

A

oral exposure = immune tolerance

skin/resp exposure = IgE sensitsation

82
Q

what is a positive skin prick test ?

A

wheal >3mm compared to negative control

83
Q

what is the most frequent organ involved in anaphylaxis?

84
Q

what are the 4 mechanisms of anaphylaxis?

A

IgE
IgG
Complement
Pharmacological

85
Q

what cells and mediators are involved in IgE anaphylaxis and an example?

A

mast cells/basophils
histamine and PAF
e.g. food

86
Q

what cells and mediators are involved in IgG anaphylaxis and an example?

A

macrophages/neutrophils
histamine and PAF
e.g. biologicals and blood

87
Q

what cells and mediators are involved in complement anaphylaxis and an example?

A

mast cells/macrophages
PAF, histamines
e.g. dialysis and PEG

88
Q

what cells and mediators are involved in pharmacological anaphylaxis and an example?

A

mast cells
leukotrienes and histamines
e.g. NSAIDs

89
Q

what is the influence of IM adrenaline on the different receptors?

A
  • alpha 1: peripheral vasoconstriction
  • beta 1: increase HR, contraction and BP
  • beta 2: relaxes SM, decrease inflammatory mediators
90
Q

what are the different IgE mediated food allergy syndromes?

A
  • food associated exercise induced anaphylaxis (within 4-6 hrs)
  • delayed food induced anaphylaxis to beef, pork, lamb
  • oral allergy syndrome
91
Q

what is the MOA of delayed food induced anaphylaxis?

A

IgE antibody to alpha 1, 3 galactose in gut bacteria

induced by tick bites

92
Q

what are the reactions in oral allergy syndrome?

A

pollen cross reacts to stone fruits/veg/nuts

93
Q

what chromosome is HLA expressed on?

94
Q

where are HLA class 1 and II expressed?

A

1: A, B, C = ALL cells
2: DR, DQ, DP = APC, upregulated in stress

95
Q

what are the most immunogenic HLA?

96
Q

what is important to remember about APCs involved in activating T cells?

A

combo of both DONOR and RECIPIENT APCs

97
Q

what are the histological features of T-cell mediated rejection?

A
  • lymphocytic interstitial infiltration
  • ruptured tubular BM
  • tubilitis
98
Q

what are the histological features of AB-mediated rejection?

A

presence of inflammatory cells within capillaries of kidney = capillaritis
= graft fibrosis

99
Q

what are the different T cell immunosuppressants?

A
  • calcineurin inhibitors e.g. tacrolimus/cyclosporine
  • cell cycle inhibitors e.g. mycofenolate mofetil, azathioprine
  • targeting TCR e.g. Anti-CD3 Ab (OKT3), anti-thymocyte
  • Alemtuzimab (anti-CD52 Ab)
  • Daclizumab (anti-CD25 Ab)
100
Q

what is the MoA of targeting TCR?

A

Anti-CD3 Ab (OKT3), anti-thymocyte globulin

= apoptosis of T cells

101
Q

what is the MoA of alemtuzimab?

A

anti-CD52 Ab

= lysis of T cells

102
Q

what is the MoA of Daclizumab?

A

anti-CD25Ab

= targets cytokine signals

103
Q

name 2 types of B cell immunosuppression

A
  • BAFF inhibitors

- Proteasome inhibitors e.g. bortezemib

104
Q

what is the MoA of BAFF inhibitors?

A

target cytokines that promote B cell activation

105
Q

what is the MoA of proteasome inhibitors?

A

e.g. bortezemib

= blocks production of Ab by plasma cell

106
Q

induction transplant immunosuppressive regimen

A

OKT3.ATG
anti-CD52
anti-CD25

107
Q

baseline transplant immunosuppressive regimen

A

calcineurin inhibitor

mycophenolate +/- steroids

108
Q

what is GvHD prophylaxis?

A

methotrexate

cyclosporine

109
Q

what are the neutralising Ab in HIV?

A

Anti-gp120

anti-gp41

110
Q

what are the non-neutralising Ab in HIV?

A

anti-pp24gagIgG

111
Q

what are the 2 error prone steps in HIV replication?

A
  1. reverse transcriptase (RNA to DNA)

2. transcription of DNA into RNA copies

112
Q

what is the life cycle of HIV?

A
  1. attachment and entry
  2. reverse transcription and DNA synthesis
  3. integration
  4. viral transcription
  5. viral protein synthesis
  6. assembly of virus, release of virus
  7. maturation
113
Q

what is the screening vs confirmatory test for HIV?

A

HIV Ab ELISA = screening test

HIV Ab Western blot = confirmatory test

114
Q

what is the HIV ART therapy?

A

2 x NRTI + 1 NNRTI/boosted PI

115
Q

what do NNRTI/NRTI end in?

116
Q

what do PIs end in?

117
Q

what is the target of the flu vaccine?

A

Ab against HA

118
Q

what are the live vaccines

A 
MMR
BCG
Yellow fever
typhoid
polio (sabin)
119
Q

what are the toxoid (inactivated toxin) vaccines?

A

diptheria

tetanus

120
Q

what are the component/subunit vaccines?

A

Hep B
HPV
Influenza

121
Q

what are the conjugate vaccines?

A

HiB
Meningococcus
Pnemococcus

122
Q

what is the role of an adjuvant?

A

increase immune response

mimic action of a PAMP

123
Q

how does CAR-T therapy work?

A

chimeric receptors

can influence both B and T cells

124
Q

what diseases is CAR-T therapy being used in?

A

ALL and NHL

125
Q

what are CTLA4 and CD28?

A
  • both expressed on T cells
  • both regulate same antigens on APCs (CD80, CD86)
    CD28 = stimulatory signal
    CTL4 = inhibitory signal
126
Q

what is the MoA of ipilimumab?

A

Ab spcific to CTLA4 = blocks it

interactions occur through CD28 = stimulatory = more T cells

127
Q

ipilimumab indication

A

advanced melanoma

128
Q

what is the MoA of pembrolizumab/nivolumab?

A

Ab specific to PD1

129
Q

pembrolizumab/nivolumab indication

A

advanced melanoma

130
Q

what can IFN alpha be used to treat?

A 
hep B
Hep C
Kaposi sarcoma
CML
MM
131
Q

what can IFN beta be used to treat?

A

Behcet’s

132
Q

how do corticosteroids decrease inflammation?

A

corticosteroids inhibit phospholipase A2
block arachidonic acid and prostaglandin formation
= decrease inflammation

133
Q

effect of corticosteroids on lymphocyte function?

A
  • lymphopaenia
  • blocks cytokine gene expression
  • decrease Ab production
  • promotes apoptosis
134
Q

what are the different anti-proliferative agents?

A

inhibit DNA synthesis

  • cyclophosphamide
  • mycophenolate
  • aziothioprine
  • methotrexate
135
Q

MoA of cyclophosphamide

SE

A

alkylate G base of DNA

SEs: haemorrhagic cystitis

136
Q

MoA of azathiorpine and a caution

A

metabolised to 6-mercatopurine
blocked de novo purine synthesis
Check TPMT

137
Q

MoA of mycophenolate

SE

A

block de novo nucleotide synthesis
prevents T cell > B cell
SE: PML (JC virus)

138
Q

MoA of calcineurin inhibitors

monitor what?

A

prevent T cell signalling
blocks IL2 production so prevents proliferation
monitor BP and renal function

139
Q

PDE4 inhibitors and indications

A

prevent activation of TFs

indication: psoriasis and psoriatic arthritis

140
Q

effect of anti-thymocyte globulin

A

T cell depletion

141
Q

MoA of Basiliximab

A

Ab against CD25 (IL-2 receptor)

decrease T cell proliferation

142
Q

MoA of abatacept

A

CTLA-4-Ig fusion protein

decrease T cell activation

143
Q

MoA of Natalizumab

A

antibody against alpha-4 integrin

inhibit leukocyte migration

144
Q

indication of Natalizumab

145
Q

what is the MoA of Tocilizumab

A

decrease activation of macrophages/ T cells/ B cells

146
Q

indications of Tocilizumab

A

Castleman’s disease (IL6 producing tumour)

RA

147
Q

MoA of Etanercept

A

TNF-alpha antagonist

inhibits TNF alpha and beta

148
Q

Etanercept indications

A

RA

Ankylosing spondylitis

149
Q

MoA of Ustekinumab

A

inhibition of IL12 and IL123 (binds p40 subunit)

150
Q

Ustekinumab indication

A

psoraisis

Chron’s

151
Q

MoA of Secukinumab

A

Ab to IL17A

152
Q

indication of Secukinumab

A

psoraisis

AS

153
Q

what is osteoprotegrin?

A

binds RANKL

regulated osteoclast resorption = natural decoy

154
Q

what is a big risk of biological therapy?

A

auto-immunity

155
Q

what antibodies are found in T1DM

A

anti-GAD

anti-IA2

156
Q

histology of T1DM

A

CD8 T cell infiltration of pancreas

157
Q

genetic associations of RA

A

HLA DR4
HLA DR1
PAD 2 and PAD 4 polymorphism

158
Q

what does PAD2 and PAD4 do?

A

increase citrullination = more citrullinated peptides

159
Q

what strange things can cause increased citrinullation and so RA?

A

smoking

gum infection with porphyromonas gingivalis

160
Q

what can be seen in the joint in RA?

A

inflamed synovium = pannus

161
Q

what is ANA?

A

Ab that bind to nuclear proeins

162
Q

what is lupus nephritis? pattern detection?

A

immune complex deposition

granular “lumpy bumpy” pattern

163
Q

2 subtypes of ANA

A

dsDNA

extractable nuclear antigen (ENAs)

164
Q

different types of ENAs

A

ribonucleoprotein (Ro, La, Sm, U1RNP)

enzymes

165
Q

what provides a homogenous staining ?

166
Q

what is dsDNA found in?

A

specific for SLE

high titres = severe disease

167
Q

what provides a speckled pattern?

A

Extractable nuclear antigens (Ribonucleoproteins)

168
Q

Ribonucleoproteins associated with SLE

A

Ro
La
Sm
U1RNP

169
Q

Ribonucleoproteins associated with Sjogren’s

170
Q

antibodies in dermatomyositis

A

anti-Jo

anti-Mi2

171
Q

what is the pathophysiology of systemic sclerosis

A

inflammation with Th2 and Th17

cytokines –> fibroblasts –> fibrosis

172
Q

distinct features of CREST (limited)

A
  • skin involvement does not progress beyond forearms

- pulmonary HTN not fibrosis

173
Q

Abs in diffuse vs limited (CREST)

A

diffuse = Scl70 (anti-topoisoerase)

limited (CREST) = anti-centrometere

174
Q

antibodies in polymyositis

A

anti-signal recognition peptide Ab

175
Q

what are the small vessel (ANCA) associated diseases?

A

microscopic polyangiitis
granulomatosis with polyangiitis
Churg Strauss

176
Q

what are the small vessel (immune complex) associated diseases?

A

anti-GBM
IgA
cyroglobuinaemia

177
Q

cANCA

A
  • cytoplasmic fluorescence
  • Abs to enzyme proteinase 3
  • Wegner’s
178
Q

pANCA

A
  • perinuclear staining pattern
  • Ab to myeloperoxidase
  • microscopic polyangiitis and Churg Strauss
179
Q

what is the problem in X-linked agammaglobulinaemia?

A

failure of pre-B cells to mature in bone marrow

180
Q

describe what the PADI enzymes do

A

arginine to cirtrulline (deamination)

181
Q

what is the treatment for RA

A

1st: methotrexate
2nd: Rituximab, abatacept, tocilizumab

Cross reference - year 5 (22 decks)

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