Immunology Flashcards

1
Q

HLA class I

  1. Presents to
  2. Main subtypes
A
  1. CD8+ T cells

2. Groups A, B and C

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2
Q

HLA class II

  1. Presents to
  2. Main subtypes
A
  1. CD4+ T cells

2. Groups DR, DQ, DP

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3
Q

Most important subtypes for HLA matching

A

HLA A, B and DR

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4
Q

Screen for HLA type using which technique?

A

PCR-based DNA sequence analysis

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5
Q

Screen for anti-HLA antibodies using which three techniques?

A
  1. Cytotoxicity assays
  2. Flow cytometry
  3. Solid phase assays
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6
Q

Anti-CD52 (suppresses T cell response, used for pre-transplant induction)

A

Alemtuzumab

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7
Q

Anti-CD25 (suppresses T cell response, used for pre-transplant induction)

A

Basiliximab

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8
Q

Baseline immunosuppressants used post-transplant to reduce rejection

A

Calcineurin inhibitors, mycophenolate mofetil and azathioprine

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9
Q

Anti-CD20 (destroys B cells)

A

Rituximab

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10
Q

Treatment of episodes of acute rejection:

  • cellular?
  • antibody-mediated?
A

Cellular: steroids, ATG, OKT3

Antibody-mediated: IVIG, plasma exchange, anti-C5 (Eculizumab), anti-CD20 (Rituximab)

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11
Q

Eliminate host immune system before haematopoietic stem cell transplant using?

A

Cyclophosphomide

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12
Q

GVHD prophylaxis

A

Methotrexate / cyclosporin

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13
Q

Treat acute GVHD with?

A

Corticosteroids

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14
Q

Kaposi’s sarcoma associated virus

A

HHV8

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15
Q

Live vaccines

A
MMR
Chickenpox
Yellow fever
Typhoid
BCG
Polio (oral sabin)
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16
Q

CD45 RO T cells

A

Memory T cells

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17
Q

CD45 RA T cells

A

Naive T cells

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18
Q

Central memory T cells found in lymph nodes and tonsils

A

More CD4, CCR7+ve and CD62L+ve (allow entry via high endothelial venules), produce IL2

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19
Q

Effector memory T cells founds in liver, lungs and gut

A

More CD8, CCR7-ve, CD62L-ve, produce perforin and IFN-gamma

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20
Q

T helper cell response

  • Th1
  • Th2
A
Th1 = cell mediated, involves cytokines IL-2, IFN-gamma, TNF
Th2 = antibody mediated, involves cytokines IL-4, IL-5, IL-6
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21
Q

Pavalizumab

A

Monoclonal antibody for RSV

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22
Q

Adjuvant which provides slow-release antigen to help prime immune response. Activates Gr1+ cells to produce IL-4 –> helps prime naive B cells. Stimulates monocytes into DCs (primes adaptive response).

A

ALUM

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23
Q

Unmethylated motif with 2 purines at 5’ end and 2 pyrimidines at 3’ end - acts as an immunostimulatory adjuvant. Activates TLRs (PRRs) on APCs stimulating expression of costimulatory molecules.

A

CpG

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24
Q

Water-in-oil emulsion containing mycobacterial cell wall components. Mainly for animals, painful for humans.

A

Complete Freund’s adjuvant

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25
Q

Experimental - multimeric antigen with adjuvant built in

A

ISCOMS

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26
Q

Passive vaccine HNIG

A

Hep A and measles

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27
Q

Encapsulated bacteria

A
Streptococcus pneumoniae
Group B Strep.
Haemophilus influenzae
Neisseria meningitidies (meningococcus)
Klebsiella
Salmonella typhi
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28
Q

Test for classical pathway deficiency

A

CH50

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29
Q

Test for alternative pathway deficiency

A

AP50

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30
Q

Type I hypersensitivity reaction

A

Immediate IgE-mediated

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31
Q

Type II hypersensitivity

A

Antibody reacts with cellular antigen

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32
Q

Type III hypersensitivity

A

Antibody reacts with soluble antigen to form an immune complex

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33
Q

Type IV hypersensitivity

A

Delayed type hypersensitivity - T cell mediated

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34
Q

Diseases associated with ANA

A

SLE, Sjogren’s syndrome, systemic sclerosis, dermatomyositis, polymyositis

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35
Q

Rheumatoid arthritis antibody

A

Anti-CCP

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36
Q

Crescentic nephritis

A

Goodpasture’s disease

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37
Q

What is rheumatoid factor?

A

IgM anti-IgG

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38
Q

C1 esterase deficiency

A

Hereditary angioedema

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39
Q

Smooth linear deposition of antibody along GBM

A

Goodpasture’s disease

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40
Q

“Lumpy-bumpy” pattern of antibody complex deposition in basement membrane

A

SLE

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41
Q

Causes of high ESR

A

Myeloma, SLE and Sjogrens

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42
Q

Low complement indicates?

A

Severe disease activity

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43
Q

What type of reaction is dermatomyositis?

A

Type III (perivascular CD4 T cells and B cells)

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44
Q

What type of reaction is polymyositis?

A

Type IV (CD8 T cells kill myofibres via perforin / granzymes)

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45
Q

Associated with ANCA and chronic Hep B

A

Polyarteritis nodosa

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46
Q

Small vessel vasculitis (ANCA associated)

A

Microscopic polyangiitis
Granulomatosis with polyangiitis (Wegener’s)
Eosinophilic granulomatosis with polyangitis (Churg-Strauss)

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47
Q

Small vessel vasculitis (immune complex associated)

A

Goodpasture’s disease
IgA nephropathy (Berger’s)
Cryoglobulinaemia

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48
Q

Haematuria a couple of days after URTI

A

Berger’s IgA nephropathy

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49
Q

Haematuria a few weeks after URTI

A

Post-streptococcal glomerulonephritis

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50
Q

c-ANCA

A

Wegener’s granulomatosis with polyangiitis

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51
Q

p-ANCA

A

Churg-Strauss (eGPA) and microscopic polyangiitis

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52
Q

Acute transplant rejection is:

  1. Mediated by what cell type?
  2. Treated how?
A
  1. T cells

2. Corticosteroids

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53
Q

Treatment of antibody-mediated rejection

A

IVIG and plasmapharesis

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54
Q

Order of importance of HLA types in transplant rejection

A

HLA DR > B > A

55
Q

Drug blocking DNA synthesis, especially of T cells

A

Mycophenolate mofetil

56
Q

Causes a transient increase in neutrophil count

A

Prednisolone

57
Q

Anti-TNF alpha

A

Infliximab and Adalimumab

58
Q

Side effect is gingival hypertrophy

A

Ciclosporin

59
Q

Test to confirm anaphylaxis

A

Mast cell tryptase levels (peak 1-2 hours, normalised by 6 hours)

60
Q

Causes of IgE-mediated mast cell degranulation–> anaphylaxis

A

Peanut, penicillin, wasp or bee venom, latex

61
Q

Causes of non-IgE-mediated mast cell degranulation –> anaphylaxis

A

Aspirin and NSAIDs, IV contrast media, opioid analgesics, exercise

62
Q

Cause of drug-induced angioedema

A

ACE inhibitors

63
Q

Inactivated vaccines

A
Hep A
Rabies
Whole cell ertussis
Influenza
Polio (salk)
64
Q

Component vaccines

A

Hep B (HbS)
HPV (capsid)
Influenza (haemagglutinin, neuraminidase)

65
Q

Conjugate vaccines

A

Tetanus (exotoxin)

HiB

66
Q

Toxoid vaccines

A

Diptheria

Tetanus

67
Q

Preferred host target of HIV

A

CD4+ T cells

68
Q

HIV: attachment inhibitor

A

Maraviroc

69
Q

HIV: fusion inhibitor

A

Enfuvirtide

70
Q

HIV: nucleoside reverse transcription inhibitor

A

Zidovudine (aka azidothymidine)

71
Q

HIV: non-nucleoside reverse transcription inhibitor

A

Efavirenz

72
Q

HIV: integrase inhibitor

A

Raltegravir

73
Q

HIV: protease inhibitor

A

Saquinavir

74
Q

Th1 CD4+ T cells produce

A

IL-2, IFN-gamma and lymphotoxin

75
Q

Th2 CD4+ T cells produce

A

IL-4, IL-5 and IL-10

76
Q

Th17 cells secrete

A

IL-17 and IL-22

77
Q

T reg cells express and secrete

A

Express CD25 and FoxP3

Secrete IL-10

78
Q

Tr1 cells secrete

A

IL-10 and TGF beta

79
Q

Ankylosing spondylitis HLA association

A

HLA B27

80
Q

Goodpasture’s syndrome HLA association

A

HLA DR15 / DR2

81
Q

Graves disease HLA association

A

HLA DR3

82
Q

SLE HLA association

A

HLA DR3

83
Q

T1DM HLA association

A

HLA DR3 / DR4

84
Q

Rheumatoid arthritis HLA association

A

HLA DR4

85
Q

Antiphospholipid syndrome Ab

A

Anti-cardiolipin
Anti-beta2 glycoprotein
Lupus anticoagulant

86
Q

Autoimmune hepatitis Ab

A

Anti-smooth muscle antibody
Anti-LKM-1
Anti-SLA (soluble liver antigen)

87
Q

AIHA Ab

A

Anti-Rh blood group antigen

88
Q

Autoimmune thrombocytopenic purpura Ab

A

Anti-glycoprotein IIb-IIIa

Anti Ib-IX antibody

89
Q

Churg-Strauss syndrome (eGPA) Ab

A

p-ANCA

90
Q

Coeliac disease Abs

A

Anti-TTG IgA

Anti-Endomysial IgA

91
Q

Antibody causing congenital heart block in mothers with SLE

A

Anti-Ro antibody

92
Q

Dermatitis herpetiformis Ab

A

Anti-endomysial IgA

93
Q

Dermatomyositis Ab

A

Anti-Jo-1 (t-RNA synthetase)

94
Q

Diffuse cutaneous scleroderma Ab

A

Anti-Scl70 (anti-topoisomerase)
RNA pol I, II, III
Fibrillarin (nucleolar pattern)

95
Q

Goodpasture’s syndrome Ab

A

Anti-GBM

96
Q

Graves disease Ab

A

Anti-TSH receptor antibody (stimulatory)

97
Q

Hashimoto’s thyroiditis Ab

A

Anti-thyroglobulin

Anti-thyroperoxidase

98
Q

Limited cutaneous scleroderma (CREST) Ab

A

Anti-centromere

99
Q

Microscopic polyangiitis Ab

A

p-ANCA

100
Q

Mixed connective tissue disease Ab

A

Anti-U1RNP (speckled pattern)

101
Q

Myasthenia gravis Ab

A

Anti-ACh receptor

102
Q

Pernicious anaemia Ab

A

Anti-gastric parietal cell (90%)

Anti-intrinsic factor (50%)

103
Q

Polymyositis Ab

A

Anti-Jo-1 (t-RNA synthetase)

104
Q

Primary biliary cirrhosis Ab

A

AMA

105
Q

Rheumatoid arthritis Ab

A
Anti-CCP
Rheumatoid factor (less specific)
106
Q

Sjogren’s syndrome Ab

A

Anti-Ro
Anti-La (speckled pattern)
60-70% Rh factor positive

107
Q

SLE Ab

A

Anti-dsDNA

Histones, Ro, La, Sm, U1RNP (speckled)

108
Q

T1DM Ab

A

Anti-GAD

Pancreatic beta cells

109
Q

Wegener’s granulomatosis (GPA) Ab

A

c-ANCA

110
Q

Polyarteritis nodosa Ab

A

ANCA

also associated with chronic Hep. B

111
Q

Give check point inhibitors e.g. CTLA4 to treat what?

A

Melanoma

112
Q

Anti CD28 (rheumatoid arthritis)

A

Abatacept

113
Q

Anti alpha 4 integrin (MS)

A

Natalizumab

114
Q

Anti IL-6 R (RhA)

A

Tocilizumab

115
Q

Autosomal recessive form of severe SCID presenting at a few days old. Failure of production of neutrophils, lymphocytes, monocytes/macrophages, and platelets. Failure of stem cells to differentiate along myeloid or lymphoid lineage.

A

Reticular dysgenesis

116
Q

Mutation in AK2

A

Reticular dysgenesis

117
Q

Specific failure of neutrophil maturation. Autosomal recessive severe congenital neutropenia. HAX1 mutation.

A

Kostmann syndrome

118
Q

ELA-2 neutrophil elastase mutation. Autosomal dominant episodic neutrophenia every 4-6 weeks. Failure of neutrophil maturation.

A

Cyclic neutropenia

119
Q

CD18 deficiency. Neutrophilia. No pus.

A

Leukocyte adhesion deficiency

120
Q

Absent respiratory burst due to deficiency of component of NADPH oxidase. X-linked. NBT test abnormal. Normal neutrophil count. Excessive inflammation and granuloma formation. Lymphadenopathy and hepatosplenomegaly.

A

Chronic granulomatous disease

121
Q

Treatment of chronic granulomatous disease

A

Interferon gamma therapy

122
Q

IL-12 and INF-gamma deficiency leads to what?

A

Inability to form granulomas. Susceptible to mycobacteria and salmonella.

123
Q

Deficiency in early classical pathway (C1/2/4) leads to what?

A

Increased susceptibility to infection and increased load of self-antigens (SLE)

124
Q

Factor B/I/P deficiency leads to?

A

Recurrent infections with encapsulated bacteria

125
Q

MBL deficiency leads to?

A

Only causes problems if there is a concurrent cause of immune impairment

126
Q

Any defect in complement pathway leading to problem with MAC causes?

A

Increased infections with encapsulated bacteria:
Neisseria meningitidis
Strep. pneumoniae
Haemophilus influenzae

127
Q

Mutation of gamma chain of IL-2 receptor

A

X-linked SCID (v. low T cells, normal B cells)

128
Q

DiGeorge CATCH-22

A
Cardiac abnormalities
Abnormal facies
Thymic aplasia (low T cells and IgG/IgA)
Cleft palate
Hypocalcaemia / hypoparathyroidism
22q11 microdeletion
129
Q

Absent MHC class II –> profound deficiency of CD4+ T cells and IgG/IgA

A

Bare lymphocyte syndrome

130
Q

Immune deficiency associated with sclerosing cholangitis

A

Bare lymphocyte syndrome

131
Q

Btk gene mutation. No circulating immunoglobulin after 3 months.

A

Bruton’s X-linked hypogammaglobulinaemia

132
Q

Mutation in CD40 ligand gene causes T cell defect and IgM only

A

HyperIgM syndrome

133
Q

Low IgG, IgA and IgE due to mutation of MHC III (aberrant class switching)

A

Common variable immune deficiency, presents in adulthood

134
Q

Low IgM, raised IgA and IgE

A

Wiskott-Aldrich Syndrome