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infection and immunity > Unit 2: Advanced Concepts In Immunology > Flashcards

Unit 2: Advanced Concepts In Immunology Flashcards

1
Q

what is the function of interferons (type 1, a/b)?

A
  • makes cells more resistant to replication
  • enhances antigen presentation
  • increased degradation of viral mRNA
  • reduction of viral protein synthesis
  • increased antigen presentation
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2
Q

what is the function of virus neutralising antibody?

A

virus neutrilisation in extracellular fluid

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3
Q

what is the function of CD8+ killer T cells?

A

destruction of virus-infected cells during replication phase

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4
Q

how can viruses avoid virus neutrilising antibodies?

A
  • formation of syncytium
    continual transmission without ever going into extracellular fluid via viral fusion protein to surrounding uninfected cells
    = large multinucleated cells
  • genome integration into host (retrovirus)
  • malignant proliferation
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5
Q

Describe how Ebola uses antigen decoys to evade the immune system

A
  • decoy similar to structural protein, but soluble
  • secreted on mass to saturate antibody binding sites
  • v.particle released, but antibody already complexed
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6
Q

describe how CD8+ killer T cells cause infected cell death

A
  • detect MHCI presentation on infected cell
  • degranulate = release perforin + granzymes
  • FasL + TNF = cytotoxic cytokines act on death receptors
  • trigger caspase cascade = apoptosis
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7
Q

give some examples of immune-privileged sites

A
  • CNS
  • eyes
  • testes
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8
Q

what is recrudescence?

A

reactivation of latent infection to become fulminant again

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9
Q

what are some triggers for recrudescence?

A
  • stress (cortisol = immunosuppressive)
  • medication
  • lowered immunity
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10
Q

some bacterial capsules are made from components commonly found in the host - what is the advantage of this?

A

molecular mimicry - immune system evasion

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11
Q

how does a bacterial capsule interfere with the complement cascade?

A

inhibit correct binding of serum proteins (for activation of complement) via C3b pathway
inhibits phagocytosis

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12
Q

what do adhesin proteins A and M target as a phagocytosis evasion strategy?

A

Fc portion of IgG
interferes with IgG binding - binds Fc region instead of binding domain

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13
Q

how are some bacteria able to survive within a phagosome?

A
  • production of detoxifying components
  • catalase production
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14
Q

what is an AMP?

A

antimicrobial peptides
- multiple cysteine residues

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15
Q

how can bacteria evade AMPs?

A
  • presence of a capsule
  • LPS layer in G-ve (LPS binds to AMP, prevents binding with membrane target)
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16
Q

how can bacteria evade the action of lysozyme?

A

can alter the chemistry of peptidoglycan = deacetylation at O residue

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17
Q

what is horizontal gene transfer?

A

the ability to require genetic material from eg the environment
= genetic variation

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18
Q

what is phase variation?

A

the switching of protein expression in bacteria to an off phase (reversible)

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19
Q

what are the mechanisms of phase variation?

A
  • hypermutable sequences eg poly G-tracts
  • recombination
  • promotor inversions
  • epigenetic mechanisms eg methylation
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20
Q

what is the process which causes phase variation occurs via hypermutable sequences

A
  • tract length of G9 = full length transcription product (ON)
  • insertion mutation = G10/G11 = often early stop codon (gene OFF state)
  • more insertions (G12) = gene back to ON
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21
Q

what genes contribute to capsule synthesis via addition of sialic acid?

A
  • cssA
  • cssC
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22
Q

what are DAMPs?

A

damage-associated molecular patterns

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23
Q

give some examples of prokaryotic PAMPs

A
  • flagellin
  • peptidoglycan
  • LPS
  • bacterial DNA
  • lipoteichoic acid
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24
Q

give some examples of DAMPs

A
  • ATP (found in ECF after death)
  • mitochondrial DNA
  • heat shock proteins
  • IL-1a
    last two induced by dying cells = alert
25
Q

what are the 4 types of PRRs?

A
  1. vesicular
  2. membrane-associated
  3. cytoplasmic
  4. soluble
26
Q

how does the innate immune system detect viral infection?

A
  • the presence of dsRNA or DNA in cytoplasm
  • TLRs expressed on cell surface/ intracellular vesicles
  • cytoplasmic helicases detect v.nucleic acid (RIG-1…)
27
Q

what are the molecules which recognise bacteria (phagocytic cells)?

A
  • TLRs
  • NOD-like receptors
  • C-type lectins
  • complement C3 protein mannose-binding lectin C-reactive protein
28
Q

what are some important TLRs (extracellular) for bacteria recognition? what do they bind to?

A
  • TLR-2 = peptidoglycan + zymosan
  • TLR-4 = LPS + HSP60
  • TLR-5 = flagellin
  • TLR-9 = CpG DNA
29
Q

what are some NOD proteins (intracellular) for bacteria recognition? what do they bind to?

A
  • NOD1 = iE-DAP (from LPS)
  • NOD2 = MDP (from peptidoglycan)
30
Q

what are C-type lectins sensors for?

A

foreign carbohydrates

31
Q

what does TLR-4 associate with in order to work?

A

CD14 (marker of macrophages)

32
Q

what are the two TLR-2 heterodimers? what does this allow for?

A

triacylated lipopeptides
diacylated lipopeptides - detects PAMPs of g+ve bacteria + yeast

33
Q

what do keratinocytes express in response to infection? what are they adapted to recognising?

A
  • influx of B-defensins + cathelicidin = anti-microbial
  • expression of IL-1a + IL-8
    g+ve bacteria and yeast
34
Q

what do enterocytes express in response to infection? what are they adapted to recognising?

A
  • influx of B-defensins + cathelicidin
  • internal production of DAMPs + chemokines
  • expression of IL-1a + IL-8
  • have TLR-4 and TLR-5
  • g-ve bacteria
35
Q

what are b-defensins? what is their function?

A
  • small cationic peptides
  • different anti-microbial properties
  • disrupt microbial membrane and/or interfere with intracellular functions
36
Q

what are the b-defensin genes in humans and what are their functions?

A
  • HBD1 = expressed by human keratinocytes
  • HBD2-4 = inducible in keratinocytes by PAMPs and pro-inflammatory cytokines
37
Q

what is CAMP?

A

cathelicidin antimicrobial peptide

38
Q

what mediates the inflammatory response and what are does this cause?

A
  • IL-1b, IL-6, TNF-a
  • vasodilation
  • increased capillary permeability
  • influx of white blood cells
39
Q

how does the innate immune response influence T cell activation?

A
  • PRRs induce cytokine expression = influence of T cell differentiation
  • PRRs induce different cytokine profiles = influence CD4 T cell differentiation
40
Q

what are the subsets of B cells and what are their generic population size within the spleen?

A
  • B-1 cells (a+b = PRIMITIVE) = 2%, <1%
  • B-2 cells (marginal zone, follicular = GENERAL) = 15%, >70%
  • regulatory B cells = 1%
41
Q

where in the body would you find primitive B cells?

A

pleura and peritoneum

42
Q

what is central tolerance to B cells?

A

recognition to self-protein = cell death
- IgM first expressed on immature B cells, if encounter target antigen that can crosslink their sIgM = programmed death = no longer in repertoire

43
Q

what two signals are required for B cell activation?

A
  • B cell receptor binding (antibody)
  • T cell help = TD antigens (thymus-dependent)
44
Q

describe the antibody response against a virus

A
  • B cell virus binding through v.coat protein
  • particle internalised and degraded
  • peptides presented to T cell = B cell activation
  • B cell produces antibody to v.coat protein
45
Q

describe the antibody response against a bacterial component

A
  • B cell binds b.polysaccharide epitope
  • antigen internalised and processed
  • peptides from protein presented to T cell
  • antibody produced against polysaccharide antigen
46
Q

what signals are required to activate T-independent antigens?

A

only binding to receptor, second signal can be delivered by antigen
ONLY produces IgM - no class switching without T cell help

47
Q

what type of cells produce antibodies?

A

plasma cells

48
Q

which T cell subset is involved in B cell activation?

A

CD4 Th2

49
Q

what processes generate high affinity Ig’s?

A
  • somatic mutation = in V region of activated B cells = increased affinity
  • class (isotype) switching = requires cell-cell contact and cytokine production)
50
Q

what is the function of regulatory B (Breg) cells?

A
  • immunosuppressive - immunological tolerance
  • produce IL-10, IL-35 + TGF-B
  • suppression of immunopathology via prevention of pathogenic T cell expansion
51
Q

where is the complementary determinant region on antibodies?

A

found in variable region

52
Q

what is the function of these T cells and what pathogens do they target?:
- CD8 cytotoxic T cell
- CD4 Th1 cell
- CD4 Th2 cell
- CD4 Th17 cell
- CD4 regulatory T cells

A
  • kill infected cells; viruses + some intracellular bacteria
  • activate infected macrophages + help B cell antibody production; macrophage-vesicle microbes + extracellular bacteria
  • help B cell antibody production (switch to IgE); helminths
  • increase neutrophil response; extracellular bacteria
  • T cell response suppression; N/A
53
Q

what is the function of CTLA-4? what would happen if cells didn’t have this?

A
  • upregulated after activation = negative proliferation signal (not expressed when inactivated)
  • cells would keep proliferating (bad)
54
Q

what APC activates naive T lymphocytes (the best)?

A

dendritic cells

55
Q

what is the co-stimulatory molecule on T cells?

A

CD28

56
Q

which cytokines are responsible for the differentiation of naive T cells into Th17?

A

IL-6 and TGF-B - act via RORyT = key transcription factor

57
Q

what is the primary mediator of macrophage activation to kill intracellular pathogens?

A

IFN-y

58
Q

what is the primary mediator of B cell activation and class switching?

A

IL-4

infection and immunity (8 decks)

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