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I&I > Immunodefiency > Flashcards

Immunodefiency Flashcards

1
Q

What factors can cause immunodeficiency (adaptive and innate)

A

Innate - NP, PRR, complement, NK, splenectomy

Adaptive - antibody deficiency, b/t cell defects

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2
Q

NP defects

A

Adhesion problems
Production problems
Killing problem (respiratory burst enzymes)

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3
Q

Df. Of neutropenia

A

< 0.5 x 10^9 /L

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4
Q

Tx for neutropenia

A

G-CSF to stimulate NP production (rare)

Treat underlying septicaemia by giving antifungals or antibiotics (TAZocin)

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5
Q

Cause of Neutropenia

A

Myelodepression due to chemo (drugs), leukaemia

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6
Q

NP enzyme defects

A

Chronic granulomas disease

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7
Q

Classical sign of NP enzyme defect

A

Recurrent fungal and Staph infection
No respiratory burst formation
Granulomas due to activation of MPs (IFNgamma response due to NETOsis activation)
Susceptible to TB

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8
Q

NP adhesion defect (e.g. LFA1)

A 
No pus (pus normally produced due to NP apoptosis)
High serum NP because they can't get into the cell
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9
Q

Types of complement defects

A

C3 def.
Classical def. (C1qrsC4C2) defect
C5-C9 def.

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10
Q

What does C3 def affect in the complement pathway and bacteria killing?

A

Defect in pathogen opsonisation and further activation of the classical and alternative pathways (MBL not affected)
Seen in pyogenic infections

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11
Q

Classical defect will affect what part of the complement pathway

A

Defective clearance of apoptotic cells
Immunogenic compounds remain (antibody:antigen complex clearance)
Immune complex disease
SLE
Cannot activate c3 convertase causing downstream effect

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12
Q

C5-C9 deficiency cAuses what defect in the complement pathway

A

MAC complex formation defect and cannot result in cell lysis
Characterised by neisseria and gonorrhoea infections

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13
Q

NK deficiency makes patient susceptible to what types of infections

A

HSV (zoster,EBV, CMV)
NK cells normally target virally infected cells and cancer cell via MHCI presentation, which is commonly downregulated by virus

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14
Q

How does splenectomy impair immunity

A

Spleen is a secondary lymphoid organ that is essential in adaptive immune response
Many encapsulated bacteria can evade innate response but are eventually killed via adaptive immunity due to IgM/G opisonisation
If remove - more likely to have septicaemia caused by malaria and meningococci

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15
Q

T cell defect can cause

A

Lymphopenia

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16
Q

Lymphopenia can be caused by

A

Defect T/B cell production

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17
Q

How does T cell defect causes defective antibody response?

A 
T cell can stimulate B cell antibody production via TD Th2)
It can also help class switch of B cells in the GC (Tfh)
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18
Q

Genetic B cell defect is not seen until

A

Mothers passive immunity (antibody received through placenta and milk) IgG, wanes off after 6 months time

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19
Q

CD40L defect of B cells will have high IgG/A and low IgM

True or false

A 
False 
CD40L defect result in difficult of B cell class switch  therefore there will be high IgM in serum with low IgA/G
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20
Q

BTK defect results in

A

No B. Cells in the peripheral blood due to delayed development

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21
Q

What does antibody normally do in the sense of combating infections

A

Binds to toxins and neutralise them (GC dependent)

Binds to C3b which is present on the pathogen to mark for opsonisation

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22
Q

Hypersensitivity type I is mediated or characterised by

A

Presence of IgE

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23
Q

What is hypersensitivity

A

Body reacting to harmless objects due to loss of tolerance. Exaggerated inappropriate immune response which can be detrimental to host

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24
Q

Process of sensitisation

A

First exposure - (no allergic symptoms)
T dependent B cell activation to produce Ab against the object but no cross link (classswitch) had occur yet. However patient is sensitised due to production of Ab

Second exposure
Cross linking of IgE Ab onto FceRI on mast cell - facilitate degranulation when antigen bind and hence symptom shown

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25
Q

Symptoms of anaphylaxis

A

Tachycardia
Hypovolaemia
Bronchoconstriction
Systemic vasodilatation and oedema

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26
Q

Immediate Tx for anaphylaxis

A

Adrenaline (epipen)

Decrease vascular permeability by increasing vasoconstriction

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27
Q

Does all IgE+ results indicate allergy and why

A

No, you can have IgE but no symptoms and hence patient is sensitised but not allergic

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28
Q

Histamine irritates nerve ending is the body’s reAction to do what

A

Eliminate pathogen

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29
Q

Late phase release of inflammatory mediators

A

Leukotrienes, prostaglandins, 5-HT

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30
Q

Process of class switch recombination

A

B cell migrate to GC from LN

B cells receive signals from Th cells and cytokines in response to the antigen binding VDJ rearrangement on heavy chain

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31
Q

Type II hypersensitivity is classified as what type of disease and characterised by presence of what Ig

A

Cytotoxic autoimmune IgG
Autoimmune disease
E.g autoimmune haemolytic anaemia

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32
Q

What T cell subtype is responsible for allergy

A

Absence of germs - Th2

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33
Q

Killing of parasite is mediated by what cell and how

A

Eosinophils
Parasites are recog. By eosinophils and binds to IgE via FceRI - eosinophils will release toxic granules to kill parasites (ROS, MBP, ribonuclease,peroxidase)

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34
Q

Route of entry for surface bacteria

A

Anthropod vectors - direct access to blood steam
Wounds/punctures/trauma - exposure to environment allows access
Active infection/invasion

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35
Q

Arthropod vectors invasion example

A

Lyme disease (tick)
Typhus (louse)
Plague (flea)

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36
Q

Staph aureus normally is the cause of septic complications after major surgery, why

A

Surgery increase wounds and puncture therefore increase chances of exporesure to pathogen. Most dangerous Staphylococcus aureus is known for being drug resistant (MRS

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37
Q

Local spread of disease can be via

A

Bacteria secreting degrading enzymes

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38
Q

Cellulitis and necrotising factor is a feature of what type of infection spread

A

Local spread

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39
Q

Difference between necrotising fasciitis and cellulitis

A

Cellulitis spreads within surface tissue whilst necrotising fasciitis spreads into deeper subcutaneous tissues

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40
Q

How does TB spread and avoid immune activation

A

Trojan horse - exploit alveolar MP to travel in bloodstream to avoid immune detection and disseminate in blood

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41
Q

Can we cure TB

A

No but immune system will suppress

  • formation of granuloma
  • MP surrounds TB
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42
Q

DIC (disseminated intravascar coagulation) is the phenomenon of

A

Systemic Micro-thrombosis accompanied with severe bleeding which results in single or multiple organ failure

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43
Q

HSV1 and HSV2 latency area and which one deactivates more frequently

A

HSV1- in the DRG of trigeminal nerve
HSV2- sacral sensory nerves
HSV2 > HSV1 reactivatig frequency

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44
Q

What is herpes neonatrum

A

When babies contract heroes due to presence of virus in the vaginal tract
Local manifestation disseminated illness

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45
Q

How does bacteria control transcription

A

Alter sigma factor - change polymerase binding site

Regulatory proteins - directly block RNAP to regulon (groups of similar genes)

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46
Q

What is the sigma factor

A

Part of RNAP that binds to the promotor region of the gene that is upstream (determines what genes to transcribe and also known as a scanner

47
Q

Bacterial genome

A

Circular densely packed genome
Can have plasmid
Core and accessory genome

48
Q

Difference between core and accessory genome

A

Core genome is more conserved and more important in function and survival (house keeping
Accessory genome depends on strains and can show other properties such as antibiotic resistance

49
Q

Why do we need to control gene expression

A

Good housekeeping
Response to environment
Duplication of Effort (many metabolic pathway are redundant
Coordinate gene expression of related genes

50
Q

Ways of Changing gene expression in bacteria

A

1) structural change to DNA (mutation in promoters, programmed mutations, epigenetics change)
2) change accessibility of DNA by RNAP (change sigma factor or regulatory protein availability

51
Q

How is Treg generated

A

TTreg via medullary selection
PTreg when T cells in PNS respond to low levels of costimulation in a immunosuppressive rich environment (TGFb, IL10)
Or just switch on foxp3 to become regulators themselves

52
Q

Genome loading ways in envelopes and naked viruses

A

Enveloped - psi signal that is encoded in the newly made viral genome makes virus capsid pick up the newly made sequence
Naked - accumulation of genome made drives packaging into capsule

53
Q

Does genome loading require energy

A

No, spontaneous

54
Q

Pathogenesis of virus is determined by

A 
Viral release
(Not host viral interaction).
55
Q

Where does viral envelope come from

A

From host cell as they bud out of the cell (pick up each type of envelope)

56
Q

Group 7 virus is

A

DsDNA virus with RNA intermediate that uses RdDP

57
Q

When does the reverse transcription occur for group 6/7 viruses during the vital life cycle

A

Group 6 - RT during entry

Group 7 - RT during exit

58
Q

Most group 3/5 viruses encode for a RdDP, why

A

Humans uses DdDP system hence they often code for their own machinery

59
Q

Human translational system is ____-dependent

A

Cap-dependent

60
Q

4 steps of viral assembly

A

Attachment
Replication
Assembly
Release

61
Q

Receptor entrance ways (4 dif ways

A

1) one virus target only one receptor
2) multiple viruses can target one receptor (e.g. ICAM-1 is targeted by 91 serotype of rhinovirus
3) anyreceptor in the body will allow entry (HSV, Ebola- often cause multiple organ infection
4) every receptor must be bound to before entry - ensure specificity and chronic infection - HCV

62
Q

VECHS methods

A

Total host cell shut down

Subtle control of host cell machinery

63
Q

Mechanism of VECHS

A

1) Hijack CAP-dependent translation system
2) attack polyadenylation signals
3) cap stealing

64
Q

How do viruses hijack the cap system (or inactivate it)

A

1) cleave elF-4G via viral protease 2A which prevents eIF-4E activation (cap)
2) dephosphorylation of eIF-4E - can’t bind to eIF-4G
3) dephosphorylation eIF4bp can bind to and inactivate eIF-4E

65
Q

How do viruses utilises the machinery when the cap pathway is inactivated

A

They have IRES (internal ribosome entry site) at 5’ end which allows ribosome to directly bind and initiate translation

66
Q

How do virus attack the poly A tail to mess up initiation of translation

A

nsP3 (eIF4G binding protein) of the virus (part of transcript) displaces Pab1p (poly A tail binding protein) due to higher affinity and allow rotaRNA to bind to nsP3 and hijack the translation system

67
Q

Cap stealing of the virus is utilised by flu, how does it work

A

The virus chop of the first 20bp of mRNA transcript (contains cap) which is later glued in front of the virus RNA

68
Q

Picovirus structure

A

Long 5’ UTR (600-1200 nt) - contains clover leaf structure (IRES) - important in translation, virulence and encapsulation

Genome encore for a single polyprotein
Short 3’ UTR (50-100nt) - necessary for antistrand synthesis

69
Q

Ig classes

A

IgM/G/D/E/A

70
Q

IgM characteristics

A

900kDa, pentamer form in blood, first Ab secreted in response to infection
Low affinity, does not travel efficiently in tissue
Activate complement but poor toxin and viral neutralisation

71
Q

IgG properties

A

Smallest Ab, present everywhere in serum (highest concentration), can transfer to foetus via placenta
Opsonin, activate NK cell for ADCC, neutralise viral proteins and form immune complexes
Cause type II/III hypersensitivity

72
Q

IgDproperties

A

A marker for mature B cells along with IgM
We don’t know why it’s there
Membrane Bound

73
Q

IgE properties

A

Related to type I sensitivity
Binds to FceRI on mast cells/eosinophils/basophils
In serum and plasma
High affinity

74
Q

IgA properties

A

High concentration/main in mucosal surfaces
Can transfer to babies via breast milk
165 KDA
Secreted as dimer or monomer (dimer in mucosal system)
Does not activate complement
Antiviral capacity

75
Q

How is IgA secreted to the mucosal durfaces

A

Via plgR - captures IgA and transport it to the surface

76
Q

Complement activating Ig

A

IgG/M

77
Q

Neutralisation Ig

A

IgA/G

78
Q

NK cell sensitisation Ig

A

IgG

79
Q

Function of Ab (TAICON)

A

Type I-III hypersensitivity
ADCC (Ab-dependent cellular cytotoxicity)
Immune complexes formation - complement activation
Neutralisation - prevent viral entry/bacteria adherence to cell/toxin binding to host cell
Opsonisation - IgG mainly with C3B

80
Q

How is B cell attracted to LN for maturation

A

Express. CCR7 which sense chemokines secreted by follicular cells (CCL21/19)

81
Q

How does super antigen work

A

Binds to Vb region of TCR and bypass specificity to activate random CD4 T cells

82
Q

Constitutive proteasome is what dependent

A

Threorinine dependent

83
Q

What stimulates constitutive proteasome to become immunoproteasome

A

IFNGamma

Causes change in beta 1,2,5 subunit

84
Q

Intracellular signal transduction for TCR and BCR is via

A

TCR - CD3 complex

BCR- CD79/CD21

85
Q

Tdt (terminal deoxynucleotidyltransferase function)

A

Important for adding 1-3 random nucleotides at junction sites during VDJ recombination to increase diversity

86
Q

Alleic exclusion is the process whereby

A

Alleic exclusion is the process whereby further chromosomal rearrangement is prevented once a functional combination has occurred from one chromosome

87
Q

Why does baby respond poorly to capsid polysaccharide derived chromosome? And how do you bypass this?

A

Baby’s have immature marginal zone, where the M2 T cells develop and hence they don’t respond to CP vaccines well - bypass by conjugating to peptide TK activate immune response via TD

88
Q

Ways of NP killing

A

1) phagosome activation
- respiratory burst
- granules secretion
2) netosis
3) NO production from iNOS

89
Q

Assembly of NADPH oxidase on phagolysosome membrane is activated when what binds

A

When p47/67 bind and assemble to the p21/91 complex

90
Q

Process of respiratory Burst

A

NADPH oxidase convert 02 to superoxide anions (O2-)
O2- can be converted to H2O2 via SOD (superoxide dismutase)
H2O2 can be further converted to HOCl (bleach ) by MPO (myeloperoxidase)

All of which can act on microbe and impair microorganism and cause death

91
Q

Granules inNP

A

1) azurophilic granules - contains antimicrobial proteins

2) specific granules

92
Q

Avidity and affinity definition

A

Affinity - defines the FIT between a receptor and it’s ligand (how well it binds)

Avidity - determined by how many numbers of receptors engaged with the ligand (if too high -> may produce dif magnitude of signal or different signals

93
Q

Cytotoxic T cells contains what to kill virally infected/cancer cells

A

Contains granules which consist of granzyme B and perforin

94
Q

How does Tc kill

A

Via FAS ligand binding or granzyme B induced apoptosis by inducing granules into cells

95
Q

Th1 production stimulate by

A

IL12

96
Q

Peripheral tolerance mechanisms

A

Ignorance
Anergy
Deletion
Immune regulation

97
Q

How does ignorance work in peripheral tolerance

A

Naive T cells have strict circulation pattern through blood and secondary lymphoid tissues and they don’t enter nonlymphoid tissues unless activated
Low concentration also be insufficient to activate T cells

98
Q

Immune privilege mechanism

A

Some tissues such as eyes brains and testes are isolated and inaccessible to lymphocytes
They also express immunosuppressants to prevent activation

99
Q

T cell checkpoint involves

A

PD1 receptor and CTLA4 on T cells

100
Q

How does T cell checkpoint work

A

When T cell receive signal 1 and 2, they also transport CTLA4 to the cell surface. CTLA4 binds to B7 at higher affinity to prevent overstimulation of T cells. Tissue at inflammation site also express PD1 ligand which binds to PD1 on T cell to send negative signals to T cell to dampen response

101
Q

Mechanism of Treg

A

1) express Il2 receptor (CD25) to take up IL2, prevent T cell use for division
2) express CTLA4 which binds to B7 and rip B7 off APCs cells so T cell don’t get signal 2 for activation
3) secrete immunosuppressive molecules (IDO) - breakdown tryptophan so T cells cannot proliferate
4) release soluble mediators (immunosuppressants) - adenosine, TGFb, IL10/35
5) directly kill cell by pumping cAMP into cells

102
Q

Genetic risk of Rhematois arthritis

A

MHCII genes

PTPN22

103
Q

5 ways in which autoantibodies can cause autoimmune disease

A

1) complement dependent cell lysis of target cell
2) opsonisation
3) formation of immune complexes
4) blockade of receptor for physiological ligand
5) stimulation of cell surface receptors

104
Q

Systemic autoimmune disease

A

SLE (systemic lupus erythematous)
Rheumatoid arthritis
Scleroderma

105
Q

Multiple sclerosis causes

A

T cell cause damage to neurones which result in demyelination

106
Q

SLE causes

A

Loss of B cell tolerance

Autoantibodies form precipitate which leads to inflammation in vascualture

107
Q

Evasion strategies of bacteria

A

Elicit minimum response - mycobacterium
Destroy host molecules - IgA1 protease by neisseria
Intracellular lifestyle - listeria (O chain that disrupt phagosomal membrane)
Superantigen - activated immune response
Antigenic variation - programmed mutation
Molecular mimicry

108
Q

CCR7 expressed by Immature B cells responds to what chemokine to migrate to LN

A

CCL19/21

109
Q

B cells can undergo somatic hyper mutation and class switch recombination after being activated, what is the process

A

The activated B cells in the LN can migrate into the dark zone where they undergo somatic hypermutation (point mutation induced by AID which change affinity of Fab region) - coined centroblast. They move to the light zone and become centrocyte and then undergo selection in the light zone by follicular DC and Th cells which presents the orignial antigen. The centroblasts outcompete each other and the one with the highest affinity will be selected. Selected cell will undergo class switch recombination (RAG) and further proliferate and form memory B or long live plasma cells

110
Q

What is calnexins role in MHC processing

A

Stabilises the MHCI heavy chain until a peptide is delivered

111
Q

Attenuated vaccine example

A

BCG, MMR, OPV

112
Q

I activated vaccine example

A

Pertussis, IPV (polio)

113
Q

Recombinant protein vaccine

A

HBV

I&I (1 decks)

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