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Defence > Def1 > Flashcards

Def1 Flashcards

1
Q

What are the functions of the IIS? (4)

A

Reacts to microbes/injured cells
First line of defence
Rapid (maximal response within hrs)
Prevents/controls + sometimes eliminates pathogens

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2
Q

How do we eliminate pathogens which have evolved to escape/resist the IIS? (1)

A

Via the adaptive immune systems

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3
Q

Name 3 components of the IIS (3)

A 
Barriers (phys, chem, microbiology)
Effector cells (NKs, PMNs, macrophages)
Soluble molecules (complement effector proteins + CKs)
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4
Q

Examples of physical barriers (3)

A

Skin

Mucosa of GI/resp tract

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5
Q

What do physical barriers do? (4)

A

Prevent entry of pathogen
Mucus coats pathogen + prevents adherence to epithelium
Pathogens are expelled by movements of cilia

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6
Q

What chemical barriers are there to infection? (2)

A

Antimicrobial enzymes e.g. lysozyme (tears, saliva)

Antimicrobial peptides e.g. defensins + cathelicidins

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7
Q

What are defensins + cathelicidins? (2)

A

Antimicrobial peptides which damage the bacteria cell membrane + kill the bacteria
Produced by PMNs, NK cells, CTLs, epithelial cells

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8
Q

What is meant by the microbiological barrier? (1)

A

Normal flora (= non-pathogenic bacteria) competes with pathogens + keeps levels low

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9
Q

What can antibiotic treatment do to normal flora? (3)

A

Can kill it
Replaced with pathogenic organisms
E.g. C.difficile in antibiotic-associated colitis

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10
Q

Barrier defects (3)

A

Wounds, bites can lead to loss of integrity which predisposes to infection
In CF there is defective mucus production + inhibition of ciliary movements which leads to frequent lung infections

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11
Q

What are the effector cells of the IIS? (4)

A 
NK cells (lymphoid lineage)
PMNs, macrophages, DCs (myeloid lineage)
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12
Q

What are the 3 roles of NK cells? (3)

A

Kill viral-infected cells
Kill malignantly-transformed cells
Express cytotoxic enzyme (lyse target cells)

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13
Q

Characteristics of NK cells (3)

A

Kill malignant tumour cells without prior activation
Contain peforins (pores in target cells)
+ granzymes A-C (cytolytic enzymes)

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14
Q

What receptors do NK cells have + what do they do? (4)

A

Inhibitory + activating receptors
Outcome of NK cell interactions determined by integration of signals from inhib + activ Rs
InhibitoryRs recognise ligands on healthy cells
ActivatingRs recognise infected/injured cells

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15
Q

How do NKs interact with healthy cells? (3)

A

All healthy nucleated autologous cells have MHC class I
InhibitoryRs recognise MHCI + block signals from activatingRs
Do not attack healthy cells

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16
Q

Why do NK cells attack/kill infected/tumour cells? (4)

A

Viral-infected cells + malignant tumours downregulate MHCI
So inhibitroyRs are not ligated by MHCI + do not block signals from activatingRs
NK cells attack/kill these cells

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17
Q

Which motifs do the different NK receptors contain + where are they found? (4)

A 
InhibitoryR = ITIM (immunoreceptor tyrosine-based inhibitory motif) - found in cytoplasmic tail of receptor
ActivatingR = ITAM - most often found in cytosolic portion of  adaptor molecules (not in receptor)
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18
Q

How do inhibitoryRs block signalling of activatingRs? (2)

A

By engaging phosphatases that block signalling pathways triggered by activatingRs

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19
Q

How do NK cells kill target cells? (2)

A

Perforins form pore in target cell + allow delivery of granzymes
Granzymes induce apoptosis by activating caspases
(B can trigger mitochondrial apoptotic pathway)

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20
Q

How can NK cells activate macrophages to destroy phagocytosed microbes? (1)

A

Via production of IFN-γ

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21
Q

NK cell defects (4)

A
  • As part of broader immuno-deficiencies e.g. Chediak-Highashi
  • Complete absence of circulating NK cells
  • Norm numbers but functional NK deficiencies
    Patients have fatal viral infections (e.g. herpesvirus)
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22
Q

What are phagocytes? (3)

A

Identify, ingest, destroy pathogens (‘cell-eating’)
PMNs, macrophages, DCs
Belong to IIS

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23
Q

What are the roles of phagocytes? (3)

A

Protection from pathogens
Disposal of apoptotic cells
Processing + presentation of Ags (APCs in adaptive immunity)

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24
Q

Steps of phagocytosis (4)

A

Phagocyte mobilisation (chemotaxis)
Recognition + attachment
Engulfment
Digestion (pathogen destruction)

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25
Q

Phagocyte defects (6)

A 
Quantitative or qualitative
Chediak-Higashi syndrome
Chronic granulomatous disease
LADs (leucocyte adhesion defects)
Phagocytosed microbes can't be killed -> recurrent infections
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26
Q

What is chronic granulomatous disease? (2)

A

Mutation in NADPH component

Defect in oxidation

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27
Q

What is Chediak-Higashi syndrome? (4)

A

Defective phagosome-lysosome fusion
Rare genetic disease caused by defective LYST gene (lysosomal trafficking regulator)
Neutrophils have defective phagocytosis
Repetitive, severe infections

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28
Q

What are LADs due to? (2)

A

Defect in beta-chain integrins

Defective neutrophil chemotaxis

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29
Q

TLR roles + locations (4)

A

TLRs recognise pathgoens
Present on phagocytes, mucosal epithelial cells, endothelial cells
Cell surface TLRs = detect extracellular pathogens
Intracellular TLRs = detect microbial nucleic acids

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30
Q

Defects in TLRs (5)

A

Humans lacking TLRs have not been identified
Polymorphism in TLR genes predisposes to:
- bacterial infections
- asthma
- autoimmunity

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31
Q

What is an Ab? (4)

A

Tetramic protein
2 identical light chains + 2 identical heavy chains
Variable region (Fab)
Constant region (Fc)

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32
Q

What is the variable region responsible for? (4)

A

Within variable region are 3 CDRs (complementarity determining regions)
CDRs recognise + bind Ag
CDR3 is most variable region
Other parts of variable region just form framework - allow CDRs to face Ag

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33
Q

How do we have specific Abs to bind specific Ags? (4)

A

Body randomly generates over 100mil diff. B-cells making different random Igs
During infection, by chance, 1/several naive B-cells will happen to have surface Ig which binds foreign Ag from pathogen
These B-cells are activated + begin to multiply -> clonal selection
Some become memory cells, some become plasma cells (mass produce Abs)

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34
Q

What else does B-cell activation need in order to occur and why? (3)

A

Direct involvement of Th1 + cks produced by Th1

Check that autoAbs are not being generated

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35
Q

Are immunoglobulin genes inherited? (2)

A

No complete Ig gene is inherited only gene segments

Many diff. Ig sequences can be generated by rearrangement of these segments

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36
Q

What does the germline kappa light chain gene consist of? (3)

A

1 constant segment
35 variable segments
5 joining segments

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37
Q

Why is the unrearranged gene not functional? (1)

A

Promoter + enhancer regions are not close enough together

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38
Q

How many different variable region structures can rearrangement of the kappa light chain produce? (1)

A

175 (= 35 x 5)

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39
Q

How is the VJ junction formed? (5)

A

Endonuclease binding sites after each V segment + before each J segment
Enzymes cuts randomly at one V + one J
Free ends are then ligated together
V, J + C now form a functional gene
RAG recombinases cut + remove intervening DNA

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40
Q

How is further junctional variation achieved with the kappa light chain? (3)

A

TdT randomly adds a few nucleotides to the free ends before they are ligated together
Creates most variable region of Ab (CDR3)
x10 more variation (>1750 possible different structures

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41
Q

What is the importance of TdT? (3)

A

Generation of Ig + TCR diversity
Leukaemia marker (mature lymphoblast don’t make TdT)
Useful enzymes in gen. engineering/recombinant DNA work

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42
Q

Which gene segments encode which components of the kappa light chain? (3)

A

C segment codes for constant region
V segment codes for maj or variable region
VJ codes for the most hypervariable region (CDR3)

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43
Q

How is the lambda light chain generated? (2)

A

Same principle to kappa light chain

Slightly more complex, but similar number of possible structures

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44
Q

What does the germline heavy chain gene consist of? (4)

A

1 constant segment
45 variable segments
6 joining segments
20 diversity segments

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45
Q

How many different variable region structures can rearrangement of the heavy chain produce? (1)

A

5,400 (= 45 x 6 x 20)

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46
Q

How is the heavy chain rearranged? (3)

A

Same process as light chain but one V segment joins with one D segment + one J segment
Endonuclease + TdT can add further variation to both VD + DJ junctions
x10 more variation at each junction therefore 540,00 possible different structures

47
Q

Diversity generated by rearrangement of kappa light chain + heavy chain gene segments ()

A

1750 x 540,000 = 945mil

48
Q

Why can B-cells not make 2 different heavy chain proteins despite there being 2 different heavy chain alleles? (3)

A

Allelic exclusion
As soon as one allele successfully rearranges + starts making heavy chain protein, the gene rearrangement process for heavy chains is switched off
(Same in light chains but 4 alleles - 2 kappa, 2 lambda)

49
Q

What light chains do we see in a normal immune response? (2)

A

Mixture of kappa + lambda light chains

As polyclonal B-cells are produced

50
Q

If patient’s B-cells are only making one kind of chain, what is this diagnostic of + why? (3)

A

Leukaemia
Malignancy is clonal - one cell multiples out of control + its progeny will only make one kind of chain
This is light chain restriction

51
Q

What other process resembles rearrangement of Ig genes? (2)

A

Rearrangement of TCR-alpha + TCR-beta

52
Q

Where are perforin + granzymes delivered to + why is this important? (2)

A

Delivered at site of contact b/w NK + target cell

Prevents killing of neighbouring healthy cells

53
Q

Primary lymphoid organs (2)

A

Thymus + BM

54
Q

Secondary lymphoid organs (3)

A

Spleen, lymph nodes, Peyer’s patches

55
Q

What are the phases of the humoral immune response? (4)

A

Resting IgM/IgD mature B-cell
Meets Ag + is activated
Requires help of Th1 + Th1 cytokines to prevent generation of autoAbs
Clonal expansion occurs

56
Q

What can occur as a result of clonal expansion? (4)

A

Plasma cells (mass produce Abs)
Memory cells
Affinity maturation
Isotype switching

57
Q

How is Ig expressed during B-cell maturation? (3)

A

Functional Ig is first expressed as membrane IgM
Membrane IgM acts as B-cell receptor (along with IgD)
Ag recognition by membrane IgM -> activation of signalling pathways -> B-cell activation

58
Q

What are the signalling pathway of B-cell activation (3)

A

sIgM acts as B-cell receptor in similar way to GF receptor
Does not have intrinsic tyrosine kinase activity
But associates with SRC family of tyrosine kinases e.g. LYN/FYN

59
Q

What are the 2 main forms of Abs + how are they related? (3)

A

Membrane bound on B-cell surface
Secreted (circ, tissues, mucosa)
Membrane bound Ig recognises Ag -> B-cell activated -> begins to secrete soluble IgM (humoral immune response)

60
Q

How is secreted Ig produced? (1)

A

By differential splicing

61
Q

Differential splicing to generate membrane-bound + secreted Ig (5)

A

Cµ is coded for by 4 exons which need to be transcribed + then spliced
2 alt versions of exon 4
Differential splicing gives 2 diff mRNAs coding for proteins with diff. C-terminal ends
VDJ complex does not change
Signal sequence determines whether is it secreted protein (via GA + endosomes etc) or membrane specific Ig

62
Q

Structural difference b/w secreted + membrane forms of Ig (2)

A

Membrane forms have cytoplasmic tail + transmembrane region for embedding
Secreted forms have no transmembrane region

63
Q

What is the importance of secreted Igs? (5)

A

Circulate in blood
Access various sites to deal with pathogens
Effector functions:
- neutralise microbes/toxins (block adherence/entry)
- opsonisation of microbes to enhance phagocytosis (Fc receptors on phagocytes)
- activation of complement (pathogen killing)

64
Q

How do different classes of Ig work? (5)

A

Work best at diff. sites e.g. IgG (circulating blood), IgA (specifically for secretion)
Work best agains different pathogens e.g. IgE is particularly effective against parasites
Bind to extracellular microbes/toxins
- neutralisation, opsonisation, complement activation

65
Q

What is class/isotype switching? (4)

A

B-cell capability of producing Abs of different classes without changing Ag specificity
Different Fc regions
No change in light chain
Requires signals from T helper cells

66
Q

Which classes can IgM switch to?

A

IgM can switch to IgG, IgA + IgE

67
Q

Which classes can IgG switch to?

A

IgG can switch to IgA + IgE

68
Q

Why is class switching important? (2)

A

Ability to perform different effector functions

Can deal better with pathogens

69
Q

How does class switching occur? (4)

A

First Ig made is always IgM
Cell needs mechanisms to keep Ab specificity (coded for by rearranged VDJ) but add diff. C regions = diff. classes
Minor + major mechanisms

70
Q

What is the minor mechanism of class switching? (2)

A

IgD only

By differential splicing

71
Q

What is the major mechanisms of class switching? (2)

A

All other classes

By DNA rearrangement

72
Q

Class switching by differential splicing (3)

A

Cµ + Cδ are transcribed as part of single precursor RNA
Differential splicing removes Cµ exons so Cδ are now used
Original VDJ now joined to Cδ producing IgD

73
Q

Class switching by further DNA arrangement (4)

A

There are alternative constant regions further downstream
Endonuclease recognition site (switch region) before each CH segment
Cute before Cµ + alternative C segment
Original VDJ region now transcribed along new C region

74
Q

How are T helper cells involved in class switching? (5)

A 
CD40L on T-cell interacts with CD40 on B-cells
Cytokines produced by T-cell:
- IFN-γ = switch to IgG1/3
- IL-4 = switch to IgE
- TGF-β = switch to IgA
75
Q

What is affinity maturation? (3)

A

Process that leads to increased affinity of Abs for Ags
Abs produced in early immune response have lower affinity for Ag
Production of high affinity Abs later in immune response/in secondary immune response

76
Q

How does affinity maturation occur? (5)

A

Somatic mutation of Ig genes
Selection of B-cells that produce Abs with highest affinity
Requires signals from T helper cells
B-cells with high affinity Ag receptors are selected to survive
B-cells with low affinity Ag receptor may fail to survive

77
Q

Why might B-cells with low affinity Ag receptors not survive? (3)

A

B-cells encounter Ag on follicular DCs (in germinal centres)

Higher affinity Ag receptors will preferentially recognise Ag on FDCs, interact with TFH cells + are selected to survive

78
Q

Why does high affinity sub-clone outgrow the original clone? (2)

A

Higher affinity gives stronger cell signalling

Faster replication

79
Q

What is an Ag? (2)

A

Any molecule that can bind specifically to an Ab

Can be proteins/carbs/lipids capable of binding BCRs, TCRs

80
Q

What Ag does HIV express on its cell surface? (1)

A

gp120

81
Q

What is an epitope? (1)

A

Portion of Ag which specifically interacts with Ab

+ generates adaptive immune response

82
Q

What do infections/vaccinations usually induce? (2)

A

Polyclonal B- + T-cell responses

83
Q

How do B-cell recognise Ags? (2)

A

Surface receptors interact with Ag + begin to proliferate

When released become secreted Abs

84
Q

Can T-cells recognise native Ags? (2)

A

No
No activation -> no proliferation -> no ck release
Ags must be processed by APCs + presented in the context of MHC

85
Q

Viable APCs vs fixed APCs (dead but preserved structure) (3)

A

Viable APC allows proliferation of T-cells in response to native Ag whilst fixed cells do not
However if Ag is digested then even fixed cells will cause proliferation
Act of presentation doesn’t require viable cells

86
Q

Exogenous antigens

A

COME BACK TO THIS

87
Q

Endogenous antigens

A

COME BACK TO THIS

88
Q

What is hypersensitivity? (3)

A

An exaggerated or inappropriate event
Can result in tissue damage
Type I - IV

89
Q

Examples of HS type I ()

A

Pollen, animal hair, HDM, latex, medicine (penicillin), insect bites, foods (peanuts), moulds

90
Q

Using pollen as an example, describe a typical HS type I event ()

A

FIRST EXPOSURE
SENSITISATION PHASE
- B-lymphocytes recognise Ag, internalise it + present to Th2 cells
- Th2 cells secrete CKs e.g. IL-4 = important in inducing B cells to switch class + become IgE producing cells
EFFECTOR PHASE
- IgE produced diffuses throughout body
- IgE comes into contact with mast cells
- IgE binds to mast cells by Fc region (as mast cells have Fc receptors)
SECOND EXPOSURE
- Mast cells with Ab attached to them
- Pollen enters + binds to Ag binding sites of Abs
- Pollen can link 2 Abs together (cross linking)
- This causes rel. of histamine from mast cell histamine granules
- Late-phase reaction happens
- Mast cell generate other cytokines + encourage Th cells to produce cytokines as well
- Allergic reaction is prolonged

91
Q

What %pop suffer from IgE mediated allergic diseases? (1)

A

15%

92
Q

What is another example of a type I HS reaction? (1)

A

Allergic asthma -> inflamm. response to allergen sensitise the airways

93
Q

Examples of type II HS reaction (3)

A

Myasthenia gravis
Rhesus isoimmunisation/HDN
Grave’s disease
(MA + GD are sometime classified as type V)

94
Q

What happens in healthy non-MA individuals? (2)

A

Nerve impulses trigger rel. of Ach from nerve endings

Binds to Ach receptors on muscle cells triggering contraction

95
Q

What happens in MA individuals? (2)

A

AutoAbs to Ach receptors block the AchRs at postsynaptic NMJ

Muscle contraction is diminished

96
Q

What happens in Rhesus isoimmunisation? (4)

A

RhD -ve mother, RhD +ve father, likely to be RhD +ve foetus
During delivery of 1st infant (when embryonic chorion breaks) the mother is sensitised
Foetal RBCs enter maternal circ + mother produces anti-D and develops immune response
If 2nd child is RhD +ve then cross of RBCs across placenta will result in haemolysis of foetal RBCs in placental circ

97
Q

What is Grave’s disease? (4)

A

Autoimmune thryoid disease
Circulating autoAbs to TSH receptor on thyroid follicle cells triggering cells to release thyroid hormones
Abs stop pit. from producing TSH but autoAbs continue to trigger rel of thyroid hormones
Goitre + exopthalmos (abnormal protrusion of eyeballs)

98
Q

What is type III HS? (3)

A

Target is soluble circulating Ag
Ag can be own tissue/foreign material
E.g. SLE

99
Q

What is SLE? (6)

A

Patients make autoAb directed against several self molecules e.g. DNA + nuclear ribonucleoproteins
Immune complexes form + the Abs in the complexes can fix complement -> tissue injury
Glomerulonephritis
B-cell activation abnormal in patients with SLE
High no. of B-cells with increased sensitivity to stimulatory cytokines
Changes in T-cell function
Problems with phagocytic cells (immune complexes can’t be cleared)

100
Q

What is type IV delayed HS? (2)

A

T-cell mediated

E.g. Mantoux test

101
Q

What happens in the Mantoux test? (5)

A

Patient is injected with extract of mycobacterial Ag in skin
Macrophages present Ag
T helper cells activated + rel cytokines which activate macrophages to rel cytokines
Firm red swelling of skin
Strong reaction with latent TB

102
Q

What is coeliac disease? (9)

A

Type IV HS
Affects small intestine
Gluten intolerance
Patients have IgA anti-gliadin, anti-endomysium + anti-reticulin Abs
T-cells present in intestine
Villous atrophy -> malabsorption
High number of B-cells producing Abs on site
Deposition of complement components in intestinal mucosa
Increased IL levles

103
Q

Other IV disorders (2)

A

IBDs - ulcerative colitis (Th2 may be involved) + Crohn’s disease (Th1 may be involved

104
Q

Psoraisis (5)

A 
Type IV HS
Chronic skin disease
2% Caucasians
Red plaque covered by silvery skin scales
Relapsing remitting
High numbers of CD4+ in skin
105
Q

What is autoimmunity? (2)

A

An acquired immune reactivity to self-Ags

Autoimmune disease occurs when autoimmune response causes tissue damage

106
Q

How common are autoimmune disease? (1)

A

~3.5% pop

107
Q

Which factors contribute to development of autoimmune disease? (6)

A
  • Age + gender
  • Genetics (HLA gene associated with some autoimmune diseases
  • Infections (association b/w EBV + SLE)
  • Specific autoAgs
  • Drugs (e.g. procainamide for ventricular arrhythmia - develop SLE)
  • Immunodeficiency (may allow persistant infections/ inflammation resulting in autoimmunity )
108
Q

Why does age + gender contribute to autoimmune disease? (2)

A

AutoAbs more common in older people

SLE + GD are more common in women

109
Q

Why do specific autoAgs contribute to autoimmune disease? (2)

A

Highly conserved proteins often = targets for autoimmune response
Abs to human shock proteins are sometimes seen in autoimmune disease

110
Q

What happens in complement immunodeficiency? (2)

A

E.g. C1q inhibitor deficiency leads to hereditary angioedema -> continuous complement activation
C3 deficiency -> infection

111
Q

What is Chediak-Higashi syndrome? (3)

A

Rare disease in which LYST gene is defective
Failure of phagolysosome formation + lysosome degranulation
Neutrophils have defective phagocytosis

112
Q

B-cell immunodeficiencies (3)

A

Severe combined immunodeficiency syndrome (lack of dev of SCs into B-cells + T-cells)
Hyper IgM syndrome
(increased IgM, little or no IgG)
Common variable immunodeficiency (IgG/IgA deficiency)
- mainly cos of B-cells being unable to mature into plasma cells

113
Q

What might cause a T-cell immunodeficiency? (2)

A

Lack of thymus

DiGeorge syndrome = incomplete dev. of thymus

114
Q

What might cause a secondary immunodeficiency? (4)

A

HIV
Malnutrition
Tumours (cancerous cells can rel. immunosuppresive factors)
Therapy using cytotoxic drugs + irradiation

Defence (1 decks)

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