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Immunology > Memory and Tolerance > Flashcards

Memory and Tolerance Flashcards

1
Q

Characteristics of immunological memory?

A

Secondary response - greater and more rapid, plus higher affinity

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2
Q

Stages of immunological memory?

A

Expansion of clonal cells (with specific antigen receptor genes)
Enhanced migration and restimulation
Survival of clones

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3
Q

Memory B cells?

A

All immunoglobins on membrane, plus complement receptors
Found in bone marrow, lymph node and spleen
High ICAM-1 for adhesion and migration
B cells have already proliferated but not differentiated to plasma cells - still need CD4 Ths

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4
Q

Effector T cells in memory?

A

CD4
Produce survival factors and cytokines, plus have surface proteins for adhesion, chemokines and activation markers
Assist B and CTLs, plus macrophages

CD8
May form killer cells

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5
Q

Pathways for memory T cell generation?

A

A. Divergent pathway, like B cells - T cell diverge to effector cells (with Ag) or memory cells

B. Linear Development
Naive cell – effector with Ag – loss of Ag = memory cell

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6
Q

Maintaining memory T cells?

A

Mediated by IL15 and IL17 cytokines driving homeostatic proliferation, capable of maintaining populations for decades

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7
Q

AICD?

A

Activation induced cell death - manner in which activated T cells are fated for death to avoid inflammation

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8
Q

Basis of vaccination?

A

Generating memory responses (hallmark of adaptive immunity) in absence of serious illness

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9
Q

What is required for a vaccine?

A

Antigens

Infection signal to stimulate immune system (often provided by adjuvant if only antigen is given)

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10
Q

Types of vaccine?

A 
Live attenuated
Killed/inactivated
Protein subunit
Recombinant viral-vectored
Virus-like particles
Nucleic acid-based
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11
Q

Live attenuated vaccines?

A
  1. related, less harmful pathogen

2. attenuated pathogen i.e. weakened - better

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12
Q

Killed/inactivated infection?

A

e.g. polio vaccine
Lower risk of disease - may need boosters
Cultivation of pathogen, inactivator e.g. irradiation added

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13
Q

Protein subunit vaccines?

A

Purified/recombinant agents to mimic antigen, picking those that are best for stimulating the immune system
Need a booster

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14
Q

Recombinant viral-vectored vaccines?

A

Viruses engineered to express pathogen antigens in vivo - safe, widely used

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15
Q

Virus like particles?

A

Non-infectious particles mimic the pathogen - very effective, can be engineered with multiple antigens to mimic mutations

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16
Q

Nucleic acid based?

A

Can encode the antigens, delivered to cells via carrier, cells then express the antigens

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17
Q

How can vaccines be improved?

A

Use of adjuvants to stimulate the immune system, e.g. oil/water emulsions, aluminium based TLR liganeds, liposomes
Can cause issues like septic shock, autoimmunity

MHCs
Not all antigens invoke an immune response - multivalent vaccines with many epitopes target all MHCs

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18
Q

Where do vaccines fail?

A

Where we lack natural immunity e.g. malaria, HIV, TB

These are also latent, so vaccines will not always induce a response

19
Q

Why do we lack vaccines?

A

Lack of understanding of pathogen life cycles
May not know the antigens
Antigens may vary e.g. mutators
Lack of good lab models as natural versions hard to find
Transport, storage and costs
Research gaps - neglect tropical diseases (more with climate change)

20
Q

Vaccine hesitancy? Case study?

A 
MMR vaccine and autism
Samoa measles outbreak
Themes include:
Control (body autonomy)
Parenting style
Past issues
Risk of vaccine vs disease not understood
Fear of chemicals
Distrust of gov/corporations
21
Q

Herd immunity?

A

1 unvaccinated individual in Samoa caused the catastrophic measles outbreak
Threshold depends on pathogen virulence and susceptibility

22
Q

What is central tolerance?

A

Negative selection of self-recognising T and B cells to avoid autoimmunity

23
Q

Why do we need tolerance?

A

Self - avoid attacking own cells
External - avoid attacking harmless non-self cells e.g. fetomaternal antigens, allergic reactions, transplants, commensal gut bacteria

24
Q

Original explanations for self tolerance?

A

Found to be aquired, not inherited, through twin studies which share a blood supply
Thought to be due to clonal deletion - immature cells that encountered antigens would die. However, this would = holes in our repertoire i.e. loss of our broad non-specific range of antigen detection

25
Q

Mechanisms of tolerance?

A

Inactivation of self-reactive clones
Immune regulation
Self-epitopes hidden from recognition factors

26
Q

B cell central regulation?

A

Checkpoint - does receptor bind self antigens in bone marrow?
Those that bind self = clonal deletion or receptor editing

27
Q

Receptor editing in B cells?

A

Way of rescuing self reactive cells
RAG genes stay active to allow recombination at light chain locus
If this creates a non-self binding receptor = rescue
If not = deletion

28
Q

Further interactions in B cell development?

A

A soluble self-antigen may interact leading to inactivation/anergy, as IgM is not expressed (IgD is, though) and the cell cannot signal, so migrates to the periphery and dies

Autoreactivity - cell is ignorant to self-antigens, maybe because they do not bind strongly enough or it is unavailable
This leads to a clonally ignorant B cell separated from dangerous self-reactions

29
Q

Central tolerance in T cells?

A

Interactions in thymus determine fate

Interactions with antigen on MHCI and II, through 3 CDR loops

30
Q

Role of checkpoints of T cell development?

A

T cells dont express TCR on surface, can’t recognise self MHC or recognise self-MHC:self-antigens too strongly - removed

Useful TCR, recognising self-MHC but not binding self-antigens strongly = kept

31
Q

Checkpoint 1 of T cell development?

A

Antigen independent quality check, like B cells, checking beta chain rearrangements will express on the surface using a surrogate alpha chain, down regulating RAG

32
Q

Checkpoint 2 of T cell development?

A

Positive selection
If alpha BTCR recognises self-peptides
Double positive thymocytes (express CD4 and 8 on surface) interact with self-peptide:MHCI/II
Recognition = survival

Non-recognition- recovery via receptor editing or death via apoptosis

33
Q

Checkpoint 3 of T cell development?

A

Is alpha/beta TCR recognition too strong?
Single positive cells (i.e. express either 4 or 8) enter medulla, interacting with antigens presented by TFs AIRE and Fexf2

Exact mechanism unclear:
affinity hypothesis, where those with intermediate self-peptide affinity survive to exit the thymus

34
Q

Need for peripheral tolerance?

A

Central removes most dangerous clones, peripheral picks up on the rest

35
Q

Mechanism of B cell peripheral tolerance?

A

Lack of T cell assistance
If T cells cannot recognise self-antigen, even though they are taken up by B cells, T cells wil ignore these and so no plasma cells that recognise self antigens are made
This is also evident during affinity maturation in germinal centres, where Tfh cells don’t aid

36
Q

DCs in T cell peripheral tolerance?

A

Presenting an antigen in a non-activation context i.e. without co-stimulatory signal is tolerogenic
Only signal 1 (antigen) = anergic T cells
Induces peripheral Tregs

37
Q

Tregs in tolerance?

A

Induced by antigen and signal 3
induced pTreg = Foxp3+, restrain self-responses
thymic derived tTreg = Foxp3+ and - = recognise self and harmless non-self

38
Q

Effector mechanisms of Tregs?

A 
Anti-inflammatory and pro-regulatory cytokines, TGFb, IL10, IL35
Modulate DCs
Outcompete effector T cells for IL2
Directly kill T cells
Affect transcription of T cells
39
Q

Immune privilege sites?

A 
Some regions more exposed e.g. the gut, where pathogen antigens are better tolerated
Brain
Eye
Testes
Uterus

These are enclosed by a physical barrier, blocking lymphatic drainage
Low MHCI
Suppressive cytokines like TGFb
Express FasL for apoptosis of Fas expressing cells

40
Q

Sympathetic opthalmia?

A

TRauma to one eye = release of the sequestered self antigens, carried to lymph nodes for T cell activation
Effector T cells in bloodstream attack both eyes
This breaks immune privilege

41
Q

Tumours?

A

Use immune suppression to gain immune privilege at the tissue
-exploit earlier mechanisms

42
Q

When is T cell regulation favoured?

A

When tTregs and T cells are triggered in presence of suppressive cytokines, skewing their function

43
Q

Examples of self tolerance?

A 
Central tolerance
Antigen segregation
Peripheral anergy
Tregs
Functional deviation
Activation-induced cell death

Immunology (12 decks)

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