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Immunology Flashcards

1
Q

Primary immune deficiency

A

inherited cause of immune compramise

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2
Q

Secondary immune deficiency

A

due to any other cause e.g. infection (HIV), malignancy, mmalnutrition, drugs (steroids)

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3
Q

Physiological immune deficiency

A
  • neonates
  • pregnancy
  • old age
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4
Q

Constitutive physical barriers of the immune system (3)

A
  1. commensal bacteria
  2. mucous surfaces
  3. epithelial barrier
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5
Q

Deficiency of epithelial barrier?

A

Burns - high risk of infection

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6
Q

Deficiency of mucosal barriers?

  • organs affected (2)
  • genetic risk factor
A

IgA deficiency

  • lungs, GI tracts - recurrent infections
  • caucasian population
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7
Q

Deficiency of commensal bacteria?

  • when
  • common infections (2)
A
  • after broad spectrum Abx
    1) candida albicans
    2) C.diff
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8
Q

Cells of innate immune system (7)

A
  1. Macrophages
  2. neutrophils
  3. eosinophils
  4. monocytes
  5. basophils
  6. NK cells
  7. dendritic cells
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9
Q

How the innate immune system works (7)

A
  1. Innate immune cells are produced in bone marrow, and circulate in blood to be able to migrate to tissues
  2. cytokines and chemokines detect site of infection and activate endothelium
  3. Toll-like and Mannose recpetors detect pathogen at infection site
  4. PAMPs recognise pathogen by responding to proteins on their bacterial sugars
  5. Fc receptors recognise immune complexes
  6. inflammatory chemokines and cytokines recruit phagocyte by
    a) increasing vascular permeability
    b) attracting phagocytes
  7. Oxidative and Non-oxidative killing of pathogen
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10
Q

Oxidative Killing

A

mediated by reactive oxygen species (superoxides and hydrogen peroxide) generated by action of the NADPH oxidase complex

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11
Q

Non-oxidative killing

A

mediated by bacteriocidal enzymes such as lysozyme

the lysosome and phagocyte come together to form a phagolysosome

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12
Q

Opsonisation

  • what
  • mediators
A

“making the pathogen tasty”
binding of pathogen and phagocyte in order to kill pathogen
facilitated by opsonin
mediated by antibodies, Fc receptors and acute phase proteins e.g. CRP

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13
Q

Common bacterial pathogens in recurrent infections? (2)

A
  1. staph aureus

2. mycobacteria

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14
Q

Common fungal pathogens in recurrent infections? (2)

A
  1. C.albicans

2. Aspergillus

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15
Q

Types of phagocyte deficiency (3)

A
  1. recruitment of phagocytes
  2. find & catch organism
  3. kill organism
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16
Q

Reticular Dysgenesis

  • what
  • inheritance pattern
  • enzyme mutation
  • lab findings
  • outcome
A
  • Severe form of Severe Combined Immunodeficiency (SCID)
  • failure of stem cells to differentiate down myeloid/lymphoid lineage leading to a complete absence of granulocytes
  • autosomal recessive
  • adenylate kinase 2 (AK2)
  • absolute deficiency in neutrophils, leukocytes, monocytes, platelets
  • fatal without BMT
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17
Q

Kostmann Syndrome

  • what
  • inheritance pattern
  • mutation
  • Nitroblue test of oxidative killing (NBT)
  • neutrophil count
  • leukocyte adhesion markers
A
  • severe congenital neutropenia
  • autosomal recessive
  • HAX1 protein
  • NBT neg
  • absent neutrophil count
  • leukocyte adhesion markers NORM
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18
Q

Cyclic Neutropenia

  • what
  • inheritance pattern
  • mutation
A
  • cyclic neutropenia every 4-6weeks
  • autosomal dominant
  • neutrophil elastase ELA-2
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19
Q

Leukocyte Adhesion Deficiency LAD1

  • what
  • mutation
  • presentation
  • lab findings
  • treatment
A
  • failure to express leukocyte adhesion markers therefore neutrophils are unable to get to site of infection
  • B-2 integrin subunit of CD18 in LAD1
  • Neonatal bacterial infection
  • HIGH neutrophil count
  • bone marrow transplant
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20
Q

LAD2

A
  • rare
  • associated with
    a) growth restriction
    b) mental retardation
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21
Q

Chronic Granulomatous Disease

  • pathophysiology (5)
  • investigation
  • inheritance pattern
A
  1. deficiency in NADPH oxidase
  2. inability to generate oxygen free radical s
  3. excessive inflammation due to high neutrophil/macrophage recruitment
  4. granuloma formation
  5. lymphadenopathy + hepatosplenomegaly
  • Nitroblue test of oxidative killing (NBT) - abnormal
    Dihydrorhodamine test - abnormal
  • x-linked
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22
Q

IFN gamma receptor deficiency

  • what
  • cytokines involved
  • outcome
A
  • defect of interaction between macrophages and other cells (T cells)
  • IL12 & IFNgamma
  • susceptibility to mycobacterial infections, salmonella, TB and GBS
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23
Q

Common infections associated with chronic Granulomatous Disease (7)

A 
PLACESS
Pseudomonas
Listeria
Asperigillus
Candida
E coli
Staph aureus
Serratia
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24
Q

Inflammatory cytokines (4)

A

IL-1
IL-12
TNF
IL-6

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25
Q

Non-inflammatory cytokines (2)

A

IL-10

TGF-beta

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26
Q

Neutrophil

A

Polymorphonuclear cells capable of phagocytosing pathogens and killing by oxidative and non-oxidative mechanisms

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27
Q

NKC

A

Lymphocytes that express inhibitory receptors capable of recognising HLA class I molecules and have cytotoxic capacity

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28
Q

Dendritic Cell

A

Immature cells are adapted for pathogen recognition and uptake whilst mature cells are adapted for antigen presentation to prime T cells

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29
Q

Macrophage

A

Derived from monocytes and resident in peripheral tissues

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30
Q

Complement Classical Pathway

  • which proteins?
  • main protein and function
  • dependant on?
  • causes
A
  • C1, C2, C4
  • C1 provides binding site on Ab
  • immune response
  • formation of immune complexes Ab/antigen
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31
Q

MBL Pathway

  • which proteins
  • protein function
  • causes
A
  • MBL
  • MBL direct binding to microbial carbohydrates
  • links in classical pathway via C2, C4
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32
Q

Complement Alternative Pathway

  • which proteins?
  • protein function
  • factors involved
A
  • C3
  • C3 directly binds to bacterial cell wall
  • B, I , P
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33
Q

C3

A

Cleavage of this protein may be triggered via the classical, MBL or alternative pathways

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34
Q

C1

A

Binding of immune complexes to this protein triggers the classical pathway of complement activation

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35
Q

C9

A

Part of the final common pathway resulting in the generation of the membrane attack complex

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36
Q

MBL

A

Binds to microbial surface carbohydrates to activate the complement cascade in an immune complex independent manner

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37
Q

Classical pathway deficiency

  • common protein affected
  • association
  • why
  • test
A
  • C2
  • SLE
  • Classical pathway is repsonsible fro removing immune complexes, these build up in SLE in skin, joints, kidneys
  • CH50
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38
Q

MBL deficiency

  • common or rare?
  • significant when?
A
  • very common (30%)

- significant is another immune impairment present e.g. chemo/HIV

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39
Q

Alternative pathway deficiency

  • common factor involved
  • susceptible to infections caused by which microbes? (4)
  • test
A
  • Factor B
  • ENCAPSULATED bacteria
    1. N menigitides
    2. Strep pneumoniae
    3. H influenzae
    4. GBS
  • AP50
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40
Q

Terminal Pathway Deficiency

  • what
  • why
  • associations (2)
  • susceptible to infections? (4)
  • tests
A
  • lack of C3, 5, 6, 7, 8, 9 so severe susceptibility to bacterial infections
  • cannot form MAC to kill bacteria
    1. glomerulonephritis
      1. connective tissue disease
  • ENCAPSULATED bacteria
    1. N menigitides
    2. Strep pneumoniae
    3. H influenzae
    4. GBS
  • CH50 & AP50
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41
Q

Membranoproliferative nephritis and bacterial infections

A

C3 deficiency with presence of nephritic factor

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42
Q

Meningococcus meningitis with family history of sibling dying of same condition aged 6

A

C9 deficiency

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43
Q

Severe childhood onset SLE with normal levels of C3 and C4

A

C1q deficiency

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44
Q

Recurrent infections when receiving chemotherapy but previously well

A

MBL deficiency

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45
Q

Characteristics of the adaptive immune system (4)

A
  1. wide repertoire of antigen receptors
  2. specificity
  3. clonal expansion
  4. immunological memory
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46
Q

Primary lymphoid tissues (2)

A
  1. Bone marrow

2. Thymus

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47
Q

Secondary lymphoid tissue (3)

A

1, Lymph nodes

  1. MALT
  2. Spleen
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48
Q

Where does B cell maturation occur?

A

Bone marrow

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49
Q

Where does T cell maturation occur?

A

Thymus

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50
Q

T Cell Maturation (5)

A
  1. arise from haemopoetic stem cells
  2. exported as immature cells to the THYMUS
  3. Mature T lymphocytes leave thymus and enter circulation
  4. Reside in secondary lymphoid tissue
  5. T cell receptor interacts with HLA molecule on APC
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51
Q

Which HLA Class do CD4+ T cells interact with?

A

Class II

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52
Q

Which HLA Class so CD8+ T cells interact with?

A

Class I

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53
Q

Three types of T Cell tolerance ?

A
  1. Low affinity for HLA - to avoid inadequate reactivity
  2. Intermediate affinity for HLA - positive selection for 10% cells
  3. High affinity for HLA - to avoid autoreactivity
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54
Q

CD4+ T Cell subsets (5)

A
  1. Th1
  2. Th17
  3. Treg
  4. TFh
  5. Th2
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55
Q

Th1 (2)

A
  1. Help CD8 T cells and macrophages

2. Subset of cells that express CD4 and secrete IFN gamma and IL-2

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56
Q

Th17

A

Help neutrophil recruitment

Enhance generation autoantibodies

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57
Q

Treg (2)

A
  1. Regulate IL-10/TGF beta expressing

2. Subset of lymphocytes that express Foxp3 and CD25

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58
Q

TFh (2)

A
  1. Support the germinal centre on the lymph node
  2. Play an important role in promoting germinal centre reactions and differentiation of B cells into IgG and IgA secreting plasma cells
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59
Q

Th2

A

T helper cells

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60
Q

CD8+ T cells (5)

A
  1. cytotoxic T cells
  2. recognise HLA Class I peptides
  3. kill cells directly
  4. produce cytokines INFgamma and TNFalpha
  5. important defence against viral infections & tumours
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61
Q

CD8+ T Cells

A

Express receptors that recognise peptides usually derived from intracellular proteins and expressed on HLA class I molecules

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62
Q

Antigen encounter in germinal centre of LN (4)

A
  1. CD4+ T cell is primed by dendritic cell
  2. CD4+ T cell helps IgM B cell differentiation
  3. B cell proliferation
  4. Isotype switching to IgG, IgE, IgA
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63
Q

What area of the immunoglobulin recognises the antigen?

A

Fab antigen binding region on both the heavy and light chain

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64
Q

What is the effector area of the immunoglobulin?

A

Fc region of the heavy chain

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65
Q

Antibody function (3)

A
  1. identification of toxins and pathogens - Fab
  2. Interaction with other immune cells to remove pathogens - Fc
  3. Defence against bacteria
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66
Q

B Cell Memory (4)

A
  1. reduced time between antigen exposure and antibody production
  2. increased titre of antibody produced
  3. IgG antibodies dominate
  4. can be independant of CD4+ T cells
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67
Q

Pre B Cells

A

Exist within the bone marrow and develop from haematopoietic stem cells

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68
Q

IgA

A

Divalent antibody present within mucous which helps provide a constitutive barrier to infection

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69
Q

IgG secreting plasma cells

A

Cell dependent on the presence of CD4 T cell help for generation

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70
Q

IgM secreting plasma cells

A

Are generated rapidly following antigen recognition and are not dependent on CD4 T cell help

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71
Q

Common infections in Lymphocyte deficiencies

  • bacterial (2)
  • fungal (2)
  • viral
  • malignancy
A 
Bacterial 1) mycoplasma
2) salmonella
Fungal 1) Pneumocystis
2) Crytosporidium
Viral - CMV
Early malignancy
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72
Q

Age of presentation of SCID and WHY?

A

> 3/12

Prior to this protected by maternal IgG that CAN cross placenta

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73
Q

Most common form of SCID?
Mutation?
Pathogenesis (4)

A

X-linked
IL-2 receptor
1. IL-2 receptor shared by numerous interleukins
2. Inability to respond to cytokines
3. T Cell and NK cell development is arrested
4. Formation of immature B cells

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74
Q

Di George syndrome

  • what
  • symptoms
  • chromosomal abnormality
  • laboratory findings
A 
- developmental defect of pharyngeal pouch 
C- cardiac abnormalities
A- abnormal facies
T - thymic aplasia
C- cleft palate
H - hypocalcemia 
22 - 22q11.2 deletion 
- reduced numbers of T cells due to thymic immaturity
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75
Q

Most common type of Bare Lymphocyte Syndrome?

76
Q

Regulatory proteins involved in BLS? (2)

A
  1. Regulatory Factor X

2. Class II transactivator

77
Q

BLS Type I

A

defect in expression of MHC Class I therefore profound deficiency in CD8+ T Cells

78
Q

BLS Type II

A

defect in expression of MHC Class II therefore profound deficiency in CD4+ T Cells

79
Q

Association with BLS?

A

Sclerosing cholangitis

80
Q

Severe recurrent infections from 3 months,CD4 and CD8 T cells absent, B cell present, IgM present, IgA and IgG absent

A

X-linked SCID

81
Q

Young adult with chronic infection with Mycobacterium marinum

A

IFN gamma receptor deficiency

82
Q

Recurrent infections in childhood, abnormal facial features, congenital heart disease, normal B cells, low T cells, low IgA and IgG

A

Di George syndrome

83
Q

6 month baby with two recent serious bacterial infections. T cells present – but only CD8+ population. B cells present. IgM present but IgG absent

A

Bare Lymphocyte Syndrome Type II

84
Q

Bruton’s hypogammaglobulinaemia

  • inheritance pattern
  • defect
  • lab finding
A

X-linked
B cell tyrosine kinase
Lack of mature B cells

85
Q

Selective IgA Deficiency

  • who
  • what infections? (2)
  • 70%?
A
  • caucasian
  • resp and GI
  • asymptomatic
86
Q

Hyper-IgM Syndrome

  • what (2)
  • mutations (4)
  • lab findings
  • who
  • common infection
A
  • disruption in T/B Cell communication
  • failure of antibody class swtichinh
    1. CD40 Ligand
    2. CD40
    3. AICDA
    4. CD154
  • HIGH IgM, abesent IgG/IgE/IgA
  • boys
  • pneumocystis carinii
87
Q

Common variable immune deficiency

  • what
  • presentation (3)
  • lab findings
A
  • defect in B cell differentiation of unknown cause
    1. failure to thrive
    2. recurrent infections
    3. autoimmune & granulomatous diseasae
  • LOW IgG/IgE/IgA
88
Q

Adult with bronchiectasis, recurrent sinusitis and development of atypical SLE

A

Common variable immune deficiency

89
Q

Recurrent bacterial infections in a child, episode of pneumocystis pneumonia, high IgM, absent IgA and IgG

A

X-linked hyper-IgM syndrome due to CD40 ligand mutation

90
Q

1 year old boy. Recurrent bacterial infections. CD4 and CD8 T cells present. B cells absent, IgG, IgA, IgM absent

A

Bruton’s hypergammaglobulinaemia

91
Q

Recurrent respiratory tract infections, absent IgA, normal IgM and IgG

A

IgA deficiency

92
Q

Type I hypersensitivity reaction

  • immunoglobulin
  • process (6)
  • how long?
  • symptoms (7)
A
  • IgE
    1. crosslinking of IgE on mast cells
    2. degranulation of mast cells
    3. release of histamine
    4. recruitment of neutrophils
    5. increased blood vessel permeability
    6. inflammation
  • within minutes, up to 2 hours
    1. angioedema
    2. urticaria
    3. rhinoconjunctivits
    4. wheeze
    5. diarrhoea
    6. vomiting
    7. anaphylaxis
93
Q

Anaphylaxis

A

a severe, systemic allergic reaction

94
Q

Types of anaphylaxis

A
  1. IgE mediated e.g. peanut, penicillin, bites
  2. Non-IgE mediated e.g. NSAIDs, IV contrast
    - both result in mast cell degranulation
95
Q

Management of Anaphylaxis (8)

A 
ABCDE
100% O2
elevate legs
IM Adrenaline 500mcg
Inhaled bronchodilators 
IC Hydrocortisone 100mg
IV Chlorphenamine 10mg
IV Fluids
96
Q

Type I Hypersensitivity Reactions (5)

A
  1. Atopic dermatitis
  2. Food allergy
  3. Oral allergy syndrome
  4. Allergic rhinitis
  5. Acute urticaria
97
Q

Type IV Hypersensitivity

  • onset
  • mediated
A

Delayed hypersensitivity

  • 24-48 hours
  • T Cell mediated
98
Q

Examples of Type IV Hypersensitivity (4)

A
  1. T1DM
  2. Multiple sclerosis
  3. RA
  4. Crohn’s disease
99
Q

Type II Hypersensitivity

  • mediated by
  • results in
A
  • IgM IgG

- IgG/IgM reacts with self antigen and results in tissue damage, receptor blockade/activation

100
Q

Type III Hypersensitivity

  • mediated by
  • pathphysiology
  • association
  • examples (4)
A
  • IgG/IgM
  • immune complex mediated damage
  • underlying Hep C
    1. SLE
    2. Mixed essential cryoglobinaemia
    3. Serum sickness
    4. Polyarteritis Nodosa
101
Q

Serum Sickness

  • what
  • pathophysiology (4)
  • type of hypersensitivity reaction
  • Abx
  • Symptoms (7)
  • Onset
A
  • reaction to proteins in antiserum
    1. formation of immune complexes
    2. that activate complement and
    3. infiltrate vessels causing inflammation
    4. small vessel vasculitis
  • Type III
    Sx
    rashes
    urticaria
    arthralgia
    lymphadenopathy
    fever
    malaise
    confusion
  • 7-12 days
102
Q

Sjogren’s Syndrome

  • what
  • who (2)
  • symptoms (3)
  • test
A
  • chronic autoimmune disease against exocrine glands
  • M>F >40years
    1. dry eyes- xerostomia
    2. keratoconjunctivitis sicca
    3. parotid or salivary gland enlargement
  • Schirmer test
103
Q

IPEX Syndrome

  • what
  • who (2)
  • symptoms 4)
A 
I - immmune dysregulation 
P - polyendocrinopathy
E - enteropathy 
X - X-linked
- male children
104
Q

Human immunoglobulin therapy

  • use
  • where from?
  • which diseases? (4)
A
  • post exposure prophylaxis
  • screened human donors
    1. Tetanus
    2. Rabies
    3. Varicella zoster
    4. Primary antibody deficiencies
105
Q

Anti T Cell monoclonal antibodies

  • use (3)
  • examples (3)
A
  1. during active transplant rejection
  2. prevention of rejection
  3. RA if anti-TNF have failed
  4. Muromonab-CD3
  5. Basiliximab
  6. Abatacept
106
Q

Use of recombinant cytokines (2)

- examples (3)

A
  1. boost immune response to cancer
  2. boost immune response to specific pathogens

IFN alpha
IFN beta
IFN gamma

107
Q

Uses of IFNalpha (3)

A
  1. Hep C
  2. Karposi’s sarcoma
  3. CML
108
Q

Uses of IFNbeta

A

relapsing MS

109
Q

Uses of IFNgamma

A

chronic granulomatous disease

110
Q

Ipilimubab

  • what
  • mechanism
  • example of use
A
  • immune booster
  • blocks CTLA4 to allow T cell activation
  • melanoma
111
Q

Pembrolizumab

  • what
  • mechanism
  • example of use
A
  • immune booster
  • blocks PD-1 to allow T cell activation
  • melanoma
112
Q

uses of corticosteroids (5)

A
  1. auto-immune
  2. allergic disorders
  3. auto-inflammatory disorders
  4. transplantation
  5. malignant disease
113
Q

Mechanism of corticosteroids (4)

A
  1. inhibits phospholipase A2
  2. Reduces prostaglandin synthesis
  3. Inhibits phagocyte migration and function
  4. Inhibits lymphocyte function and promotes apoptosis
114
Q

Side effects of corticosteroids (10)

A 
C - cataracts
U - ulcers
S - skin; bruising, thinning, striae
H - hypertension, hirsuitism, hyperglycemia
I - infection
N - necrosis of femoral head
G - glaucoma
O - obesity, osteoporosis
I - immunosuppression 
D - diabetes
115
Q

Anti-proliferative agents

  • target
  • cells affected
  • examples (3)
  • side effects (4)
A
  • inhibit DNA synthesis
  • rapid turnover
    1. Cyclophosphamide
    2. Mycophenolate mofetil
    3. Azathioprine
  1. Bone marrow suppression
  2. infection
  3. malignancy
  4. teratogenicity
116
Q

Cyclophosphamide

  • mechanism of action
  • uses (2)
A
  • alkylates guanine base of DNA
    1. multi-system connective tissue disease
    2. vasculitis with end-organ damage
117
Q

Azathioprine

  • mechanism of action
  • uses (3)
  • side effect
A
  • blocks de novo purine synthesis
    1. auto-immune disease
    2. auto-inflammatory disease
    3. transplantation
  • hepatotoxicity
118
Q

Myclophenolate mofetil

  • mechanism of action
  • uses (3)
  • side effects (2)
A
  • blocks de novo nucleotide synthesis
    1. Autoimmune disease
    2. vasculitis
    3. transplantation
  1. bone marrow suppression
  2. herpes
119
Q

Plasmapharesis

  • what
  • uses (3)
A
  • removal of pathogenic antibody by treating patients own plasma and then reinfusing
  • type II antibody mediated hypersensitivity reactions
    1. Goodpasture’s
    2. Myasthenia Gravis
120
Q

Inhibitors of Cell signalling

  • mechanism (2)
  • examples (3)
A
  • inhibits calcineurin
  • therefore downregulates IL-2 expression
  1. Tacrolimus
  2. Ciclosporin
  3. Sirolimus
121
Q

Side effects of Ciclosporin (6)

A
  1. gingical hypertrophy
  2. DM
  3. nephrotoxicity
  4. neurotoxicity
  5. hypertension
  6. dysmorphism
122
Q

Rituximab

  • mechanism of action
  • result
  • use
A

Anti-CD20
Decreases B cells
Lymphoma

123
Q

Methotrexate

  • mechanism of action
  • result
  • uses (3)
  • side effects (2)
A
  • inhibitis dihydrofolate reductase DHFR
  • decreases DNA synthesis
    1. RA
    2. psoriasis
    3. Crohn’s
  1. teratotoxicity
  2. hepatotoxicity
124
Q

Basiliximab

  • mechanism of action
  • result
  • use
A

Anti-CD25
Inhibits T cell proliferation
Prophylaxis for allograft rejection

125
Q

Abatacept

  • mechanism of action
  • result
  • use
A

CTLA4-Ig fusion protein
Reduces T cell activation
RA

126
Q

Natalizumab

  • mechanism of action
  • result
  • use (2)
A

Antibody to alpha4 subunit
Inhibits T cell migration
1. relapsing-remitting MS
2. Crohn’s

127
Q

Efalizumab

  • mechanism of action
  • result
  • use
A

Antibody to CD11a
Inhibits T cell migration
Psoriasis

128
Q

Tocilizumab

  • mechanism of action
  • result
  • use
A

Antibody to IL-6
Reduces macrophage, T cell and B cell activation
RA

129
Q

Alemtuzumab

  • mechanism of action
  • result
  • use
A

Antibody to CD52
Lymphocyte depletion
CLL

130
Q

Anti-cytokines

  • what
  • examples (5)
  • uses (4)
A

TNF-alpha

  1. Infliximab
  2. Adalimumab
  3. Certolizumab
  4. Golimumab
  5. Etanercept

Uses

  1. RA
  2. AS
  3. Psoriasis
  4. IBD
131
Q

Denosumab

  • mechanism of action
  • result
  • use
A

RANK ligand inhibitor
inhibits RANK mediated osteoclast differentiation
OA

132
Q

Three stages of Transplant rejection

A
  1. Recognition
  2. Activation
  3. Effector function
133
Q

Most relevant proteins in transplant recognition

A
  1. ABO blood antigens

2. HLA coded by chromosome 6 on MHC

134
Q

Where are ABO antigens expressed?

A
  1. RBCs

2. endothelial lining of blood vessels in transplanted organ

135
Q

Where is HLA Class I expressed?

A

A, B, C

ALL cells

136
Q

Where is HLA Class II expressed?

A

DR, DQ, DP

expressed by APCs and cells under stress

137
Q

What’s special about HLA?

A

Highly polymorphic as there are hundreds of alleles for each locus so any two people are unlikely to have the same two alleles

138
Q

Where is most of the variability in HLA?

A

peptide groove

139
Q

Maximum number of HLA mismatches allowed in transplantation?

140
Q

Direct recognition?

A

Donor APC presents antigen and/or MHC to recipient T cells

Acute rejection

141
Q

Indirect recognition?

A

Recipient APC presents donor antigen to recipient T cells

Chronic rejection

142
Q

Phases of transplant rejection (3)

A

Phase 1 - recognition of foreign antigens
Phase 2 - T cell activation
Phase 3 - effector phase

143
Q

Effector phase of rejection (5)

A
  1. T cells proliferate
  2. T cells produce cytokines
  3. Activate CD8+ cells
  4. Provide help for antibody production
  5. Recruit phagocytic cells
144
Q

What type of hypersensitivity reaction is rejection?

145
Q

Symptoms of rejection

  1. general
  2. kidney
  3. liver
  4. lung
A
  1. fever, tenderness
  2. rise in creatinine, fluid rentention, HTN
  3. deranged LFTs, coagulopathy
  4. breathlessness, pulmonary infiltrate
146
Q

How to investigate transplant rejection?

A

Biopsy - check for acute cellular reaction

  • infiltration of cells
  • tubular function
147
Q

Time scale of acute rejection?

- pathology

A

weeks - months

cellular infiltrate

148
Q

Time scale of chronic rejection?

- pathology

A

months - years

fibrosis & vasculopathy

149
Q

Prevention of rejection (3)

A
  1. AB/HLA matching
  2. Screening for anti-HLA antibodies
  3. Immunosuppression
150
Q

screening for HLA antibodies? (3)

A
  1. cytotoxicity assays
  2. flow cytometry
  3. solid phase assays
151
Q

HLA matching is very important in…? (2)

A
  1. Kidney

2. BMT

152
Q

Graft versus host disease?

  • onset
  • symptoms
A

donor cells attacks hosts
days-weeks
rash, D&V, bloody stool, jaundice

153
Q

Treatment of antibody-mediate damage? (2)

A
  1. Plasma exchange

2. IVIg

154
Q

Common opportunistic infections post-transplant? (3)

A
  1. CMV
  2. BK virus
  3. pneumocystis carini
155
Q

Post-transplantation’s malignancies? (2)

A
  1. Karposi’s sarcoma

2. EBV

156
Q

What kind of virus is HIV?

A

RNA retrovirus

157
Q

HIV Lifecycle (7)

A
  1. Targets CD4+ T helper cells
  2. Reverse transcription & DNA synthesis
  3. Integration (viral DNA + host DNA)
  4. viral transcription
  5. viral protein synthesis
  6. assembly of virus & release of virus
  7. maturation
158
Q

HIV-1 co-receptors used to enter target cells? (2)

A

CCR5

CXCR4

159
Q

Transmission of HIV (3)

A
  1. Sexual - mucosal surfaces contain dendritic cells
  2. Vertical - mother to child through birth or via breast milk
  3. Blood - transfusion, sharing needles
160
Q

Where does HIV bind to?

A

gp120- intial binding

gp41 - conformational change

161
Q

Immune response to HIV-1 (3)

A
  1. Innate
  2. Adaptive
  3. Aquired
162
Q

Innate response to HIV (4)

A
  1. Non-specific activation of macrophages, NK cells, complement
  2. stimulation of dendritic cells by TLR
  3. release of chemokines & cytokines
  4. inflammation
163
Q

Adaptive response to HIV

  • neutralising antibodies (2)
  • non-neutralising antibodies (1)
A

neutralising 1. anti-gp120 2. anti-gp41

non-neutralising 1. anti-p24 gag IgG

164
Q

Acquired response to HIV

  • which cells?
  • chemokines (3)
  • how?
A

CD8+ Tcells
MIP-1a, MIP-1b, RANTES
prevent HIV entry into CD4+ T cells

165
Q

How does HIV-1 damage the immune response? (5)

A
  1. Infected CD4+ T cells are killed by CD8+ T cells
  2. Infected CD4+ T cells are anergised
  3. CD4+ T cells are unable to prime CD8+ T cells so T cell cell memory is lost
  4. Infected monocytes or dendritic cells are killed by the virus
  5. quasispecies are produced as reverse transcriptase is error-prone
166
Q

Development from HIV-1 to AIDS?

A

8-10 years

167
Q

Prediction of disease progression?

A

viral load

168
Q

Rapid progressors - development from HIV-1 to AIDS

169
Q

Long-term non-progressors?

A

stable CD4+ counts and no symptoms after 10 years

170
Q

AIDS CD4+ T cell count?

171
Q

Screening test fro HIV?

A

anti-HIV antibody detected by ELISA

172
Q

Confirmation test by HIV?

A

Anti-HIV antibody detected by Western Blot

173
Q

How long is the incubation period to seroconvert?

174
Q

HIV treatment?

A

HAART - highly active anti-retroviral therapy

= 2 non-nucelotide reverse transcriptase inhibitors + protease inhibitor

175
Q

Limitations of HAART? (5)

A
  1. doesn’t eradicate latent HIV-1
  2. fails to restore T cell responses
  3. high pill burden
  4. toxicities
  5. adherence
176
Q

HAART during pregnancy?

A

Zidovudine - reduces transmission to newborn from 26% to 8%

177
Q

8 week vaccinations (7)

A
  1. Diphtheria
  2. Tetanus
  3. Whooping cough
  4. Polio
  5. H.influenzae B
  6. Pneumococcal
  7. Rotavirus
178
Q

1 year vaccinations (4)

A
  1. H.influenzae B
  2. Men C
  3. Pneumococcal
  4. MMR
179
Q

best vaccine?

A

activate both B and T cell memory

180
Q

Antigen presenting cells (4)

A
  1. Macrophages
  2. B lymphocyte
  3. Langerhans cells
  4. Dendritic cell
181
Q

Cell mediated response

  • t cell
  • cytokines involved (3)
A

Th1 Cell

IL-2, IFN-gamma, TNF

182
Q

Humoral response

  • t cell
  • cytokines involved (3)
A

Th2 cell

IL-4, IL-5, IL-6

183
Q

T Memory cells

a) central memory cells
- where
- express
- produce
b) effector memory cells
- where
- express
- produce

A

a) central memory cells
- LNs and tonsils
- CCR7+ CD62L-
- IL-2

b) effector memory cells
- liver, lungs, gut
- CCR7- CD62 low
- IFN-gamma, perforin

184
Q

Live vaccine

  • advantages (2)
  • disadvantages (2)
  • examples (3)
A 
Ads 1) lifelong immunity
2) cross-reaction against different strains
Disads 1) reversion to virulence
2) careful in ID patients 
Examples - polio, MMR, BCG
185
Q

Inactivated vaccine

  • advantages (4)
  • disadvantages (2)
  • examples (3)
A 
Ads -1) easy storgae
2) cheaper
3) safe in ID patients
4) no reversion to virulence
Disadvs 1) repeated boosters required
2) shorter immunity

Examples - Diphtheria, tetanus, Hep B

186
Q

Adjuvants used in vaccines?

  • why
  • example
A

acts as a depot to increase immune response by slow release of the antigen without altering its specificity
- ALUM, CpG

Pathology (7 decks)

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