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Trinity Term 1 > Immunology II > Flashcards

Immunology II Flashcards

1
Q

Describe some features of adaptive immune systems

A
  • immense Diversity
  • alterations in repertoire
  • memory
  • TCR and BCR (jawed vertebrates)
  • VLR (jawless fish)
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2
Q

Describe the immense diversity of adaptive immune systems

A

– alteration of genomic sequence
- “Anticipatory Repertoires”

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3
Q

Describe repertoire alterations in adaptive immunity

A

cell proliferation and clonal distribution of receptors according to circumstance

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4
Q

Describe adaptive immune receptors

A
  • antibodies
  • T cell receptors
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5
Q

Describe antibodies

A
  • duplicated heterodimer (heavy and light chains
  • two forms
  • secreted by B cells
  • membrane bound (B cell receptor)
  • recognise diverse products (e.g. protein or carbohydrate)
  • epitopes can be linear or conformational
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6
Q

Describe T cell receptors (TCR)

A
  • always membrane-bound heterodimer
  • TCRab and TCRgd
  • TCRab recognise linear peptide in context of a
    presentation complex called MHC
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7
Q

MHC

A

major histocompatibility complex

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8
Q

Adaptive immunity stimuli

A
  • antigen or immunogen
  • epitope
  • antigenic or immunogenic molecules
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9
Q

Describe antigens and immunogens

A

a molecule seen by the adaptive immune syste

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10
Q

Describe epitopes

A

the specific part of the antigen involved in recognition

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11
Q

Describe antigenic or immunogenic molecules

A

molecule capable of stimulating a specific adaptive response

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12
Q

Describe anticipatory repertoire generation

A
  • rearrangement with junctional modification
  • four chains, two heterodimeric pairs
  • TCRab and TCRgd
  • conserved organisation of TCR loci (multiple V regions, [D], J and C regions)
  • up to 10^15 different TCRVb rearrangements in humans
  • we only express ~108 different TCR at any time
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13
Q

Describe T cell receptor rearrangement

A
  • TCRalpha or TCRgamma with TCRbeta and TCRdelta D
    region inserts between the V-J junction
  • nucleotide modification
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14
Q

D region

A

Diversity region

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15
Q

CDR3 region

A

complementary determining region 3

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16
Q

The RAG complex

A
  • initiates rearrangement
  • Recombination Activation Gene
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17
Q

RSS=

A

Recombination signal sequence

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18
Q

Describe the action of the RAG Complex

A
  • RAG1/2 binds RSS
  • synapsis of RAG complices
  • cleavage of RSSs
  • Ku70:Ku80 binds 5’-phorphorylated DNA ends at signal and coding joints
  • DNA-PK:Artemis opens hairpin
  • TdT processes DNA ends and adds N-nucleotides
  • stands are paired
  • exonuclease removes unpaired nucleotides
  • gaps filled by DNA synthesis
  • DNA ligase IV:XRCC4 ligates DNA ends
  • forms coding joint
  • creates junctional diversity
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19
Q

TdT

A

terminal deoxynucleotidyl transferase

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20
Q

What is the importance of extreme diversity in the adaptive immune response?

A

avoidance of self-reactivity

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21
Q

Describe the avoidance of self-reactivity

A
  • clonal distribution of the receptor
  • selective removal of self-reactive cells
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22
Q

The rarity of successful cells means that success depends upon:

A

– self-renewal andrapid replication in the face of challenge
- evolution of the lymphocyte (T cell and B cell)
- specialised selective sites (e.g. Thymus for T cells)

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23
Q

Describe thymic T cell development

A
  • an ordered process
  • TCRbeta, gamma and delta at DN3 Allelic exclusion at DN4
  • RAG on in late DN2
  • RAG off in DN4
  • RAG on in early DP
  • RAG off in SP
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24
Q

DN

A

double negative

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25
Describe memory in T cells
- thymic selection - response - memory
26
Describe antibodies (imunoglobulins) as functional molecules
multiple antigen binding sites
27
Describe the Antibody Classes
have different numbers of units in the mature structure
28
List some antibodies
- IgG/IgE - IgM - IgA
29
Describe soluble antibody morphology
- two effective domains - antigen binding Fab fragment (two in each unit) - Fc region recruits other molecules (complement), or is bound by cells expressing the Fc-receptor
30
Describe the mechanisms of antibody activity
- block function (bind to important molecules on the pathogen) - agglutinate (stick pathogens together) - activate Complement - opsonise (Fc recognised by receptors on cells)
31
Describe the main T cell types
- TCRalphabeta and TCRgammadelta - TCRalphabeta divided into two subsets based upon co-receptor expression, type of MHC presenting the peptide and cytokine production
32
Describe CD4+ cells
- restricted to MHC class II - TH1, TH2, TH3, TH17 and T-reg cells
33
TH
T helper
34
Describe CD8+ cells
- restricted to MHC class I - TC1 and TC2 cells
35
TC
T cytotoxic
36
CD=
- Cluster of Differentiation - A term for cell surface molecules
37
Describe the relationship between TH and TC cells
distinct and overlapping functions
38
Describe CD4 cells
- help B cells make antibody (Th2 via IL4) - help macrophages become activated (Th1 via IFNg)
39
What drives Th0 cell proliferation?
- initial stimulus - IL-2 and IL4
40
Describe TH1
- active macrophage - IL-2 and IFNgamma
41
Describe TH2
- helper B cell - IL-4, Il-5, IL-6 and IL-10
42
Describe TH3
- helper B cell (IgA) - TGFbeta, IL-4, IL-10
43
Describe TH17
- neutrophil recruitment - IL17
44
Describe T-regs
- down-regulate T cell responses - IL-10
45
Delineate the two antigen presentation pathways
MHC class I pathway MHC class II pathway
46
Describe the MHC class I pathway
- samples the cytoplasm - endogenous - CD8+
47
Describe the MHC class II pathway
- samples the extracellular compartment - exogenous - CD4+
48
Describe the mechanics of the MHC class I pathway
- partly folded MHC class I alpha chains bind to calnexin until Beta2-microglobulin binds - MHC class I a:beta2m complex is released from calnexin, binds to a complex of chaperone proteins and binds to TAP - cytosolic proteins and DRiPs are degraded to peptide fragments by the proteasome - TAP delivers peptides to the ER - peptide binds the MHC class I molecule and completes its folding - MHC class I molecule is released from the TAP complex and exported to the cell membrane
49
What are the chaperone proteins involved in MHC class I antigen presentation
calreticulin, Erp57
50
How is TAP bound in the MHC class I antigen presentation pathway
tapesin
51
DRiPs
defective ribosomal products
52
Describe the mechanics of the MHC class II antigen presentation pathway
- Ii forms a complex with MHC class II molecule, blocking the binding of peptides and misfolded proteins - Ii is cleaved in an acidified endosome, leaving a short peptide fragment, CLIP, still bound to the MHC class II molecule - endocytosed antigens are degraded to peptides in endoscopes, but the CLIP peptide blocks the binding of peptides to MHC class II molecules - HLA-DM binds to the MHC class II molecule, releasing CLIP and allowing other peptides to bind - the MHC class II molecule then travels to the cell surface
53
Ii
invariant chain
54
CD4+ T cells
- restricted to peptides in MHC class II - only respond to some cell types and use soluble mediators to affect the local area
55
CD8+ T cells
- restricted to peptides in MHC class I - “recognise” any cytoplasmically infected cell - major cytotoxic function
56
MHC class I is
constitutively expressed by most cells in the body
57
MHC class II is
constitutively expressed on restricted set of cells (professional APCs)
58
pAPCs
professional antigen presenting cells
59
Describe pAPCs
- constitutively express MHC class I and MHC class II - dendritic cells - macrophages - B cells
60
Describe dendritic cells
- the innate cell that drives the adaptive immune response - the only cell to stimulate naïve T cells - after presentation and activation of lymphocytes, they undergo apoptosis
61
Describe macrophages
active scavengers, activity increased by interaction with CD4+ T cells
62
Describe B cells
Interactions with CD4+ T cells needed for efficient maturation and antibody production
63
Describe the immature dendritic cell
- in most tissues - take up and processes antigens
64
Describe the mature dendritic cells
- do not take up microbes - migrate to the lymphoid organs - present antigens to naive T cells
65
Describe dendritic cell maturation
- pathogen uptake - PRR activation - MHC I + II high - TCR:MHC (signal 1) - costimulatory molecules such as CD80/86 (signal 2) - cytokine production (signal 3) to drive TH0 cell differentiation
66
NK helps to create
active macrophage on exposure of TH1 to IFNgamma
67
PMN mast cell helps to create
helper B cell on exposure to IL4 of TH2
68
Describe immunology memory
- population of specific cells is larger - easier to activate - migration patterns differ
69
Why are memory cells easier to activate?
- transcriptional profile - signalling status - surface molecules - earlier commitment to effector status
70
Why do memory cell migration patterns differ?
- less focussed on lymph nodes - migration through tissues - chemokine receptors - adhesion molecules
71
How does a vaccine work?
- antigens from the pathogen stimulate T and B cells and induce memory
72
Describe the role of the adjuvant in vaccines
- carrier - immunostimulatory components - stimulate PRRs
73
Describe the types of vaccine
- live vaccines - dead vaccines - vectored vaccines
74
Describe live vaccines
- attenuated pathogen - related pathogen
75
Give examples of live vaccines
- Sabin polio - Bacillus Calmette-Guerin vaccine - attenuated form of Mycobacterium bovis, to protect against M. bovis and M. tuberculosis
76
Describe dead vaccines
- need adjuvant - whole killed pathogen - sub-unit
77
Describe vectored vaccines
Sub-unit delivery using a live carrier or DNA
78
Give examples of dead vaccines
- Salk polio - Influenza - tetanus toxoid

Trinity Term 1 (38 decks)

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