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Immunology > Memory & Vaccination > Flashcards

Memory & Vaccination Flashcards

1
Q

Which parts of adaptive immune response will be short-lasting & which will be long-lasting?

A

Effector lymphocytes = short
Plasma cells, memory T & B cells = long (circulate in blood & occupy lymphoid tissue)

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2
Q

What is the primary immune response?

A

-Naive cells activated for first time - as not seen antigen before (lots in children)
-Due to infection OR vaccination (should give safe 1st dose - not infectious)

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3
Q

What is the secondary (or tertiary/quaternary) immune response?

A

-After already been exposed to antigen before (2nd/3rd…)
–> cells = antigen experienced
-Have immunological memory cells
-Imm resp - memory cells = qual & quan improved - make more cytokine & antibodies & qual too (higher affinity)
-Asymptomatic/mild disease (as often imm resp is cause of symptoms not pathogen)

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4
Q

How will T cell, B cells & antibody levels change over time for virus - after vaccination for virus?

A

-Get CD8+ cytotoxic T cell resp
-Get CD4+ helper too (which help inc. no. of CD8+)
–> so peak no of memory CD8+ & CD4+ T cells after vacc
-Peak no. antibodies - plasma cells = long-lived

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5
Q

How are B cells different to other APCs?

A

-B cells only phagocytose specific antigen (via BCR)
-Other APCs phagocytose ANY antigen in env

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6
Q

Which MHC do B cells have?

A

MHC II & I

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7
Q

What do T cells do to B cells when they bind to MHC antigen complex?

A

-Activate B cells - signal to B cell what pathogen is - so tells which antibody to make - makes high affinity antibody - then class switches to antibody which is needed for this infection

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8
Q

Where do memory B cells come from in germinal centre of secondary lymphoid organ?

A

NOT IN GC YET - just primary follicle
-Follicular B cell interacts w/ T cell - after B cell is APC & after T cell has been activated by DC (3 signals)
-T cell activates B cell - 3 signals
-Activated B cell = proliferates
-Some cells in prolif are now plasma cells - so can make IgM (high avidity, but low affinity - as no somatic hypermutation yet) immediately - short-lived plasma cells

INTO/FORMS GC
-Non differentiated B cells enter GC
-B cell undergoes somatic hypermutation - alters BCR
-Follicular DC presents antigen to B cell again - checks BCR
-If B cell uptakes correct antigen from follicular DC = gets survival signals (x3) from T follicular helper cell
(if BCR not bind or binds to self = no surv signal as T cell not see same antigen - so apoptosis)
-More prolif
-Class switching (recombination) of B cell - produce specific antibody type (helpful for this infection) —> due to specific cytokines from TFH
-Differentiation of B cells to become plasma or memory cells

OUT OF GC
OUTCOME = LONG-lived plasma cells & memory B cells
Get affinity maturation - plasma cells produce high affinity antibodies

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9
Q

2 types of B cell in secondary lymphoid tissue?

A

-Mantle zone B cells - don’t recognise that specific antigen - BCR isn’t comp
-Follicular B cells - interacts w/ T cell

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10
Q

What dictates which B cells enter GC or become short-lived plasma cell making IgM?

A

-Location in cell - are they pushed away during prolif - so do they recieve signals to
-No. of mitochondria entering daughter cells

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11
Q

Characteristics of memory B cells?

A

-High affinity antibody (than plasma)
-Make class switched antibody
-Antibody made more quickly
-Can re-enter GC - somatic hypermutation & affinity maturation again
-Have higher MHC & costim molecules - attract Th help

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12
Q

What are the 2 subsets of T memory cells?

A

-Central memory T cells - become memory cells earlier (before has decided which cytokine will make)
-Effector memory T cells (after decided which cytokine will make)
–> found in diff places
–> can have same TCRs (or not)
NOT SAME AS NAIVE & EFFECTOR T CELLS!

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13
Q

Process of T cell effector & memory cell formation?

A

-Naive T cell goes to LN - due to chemokine rec
-DCs activate naive T cell
-T cell differentiates into effector cell (cytotoxic or helper - effector phenotypes) –> some effector cells go on to = memory cells, OR die (apoptosis) OR become ‘useless’ effector cells - quiescent (can’t respond to antigen)
-Memory cells become central OR memory (based on which markers on surface - chemokines)
*central mem = has CCR7 - LN chemokine - stays in LN
*effector mem = has no CCR7 - goes to tissue where infection is

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14
Q

Why do memory T cells survive?

A

Get survival signals from cytokines (IL-7 & IL-15)
-central or memory difference = chemokines recs on surface

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15
Q

Purpose of having 2 types of memory T cells?

A

-Central (don’t know which cytokine will make) = so can tackle same infection @ diff site in body - as stay in lymphoid tissue - can help B cells make antibody needed
-Effector (know which cytokine will make) = so can tackle same infection @ same site in body

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16
Q

Compare central & effector memory T cells.

A

Central = can make any cytokine - why is more useful if infected @ diff site in body - respond like naive cells but faster (no need for 3 signals to activate)
Effector = already changed its epigenetics to produce certain cytokines

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17
Q

What happens to effector memory T cells?

A

They WILL specialise –> become a specific type of T cell

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18
Q

What is trained immunity?

A

Ability of innate imm resp to show memory –> when activated many times quickly
-Short-lived (not like adaptive immunity)
-But not specific to an antigen
-If in env where exposed to diff antigens for long time?
-Involves epigenetic, metabolic changes & improved effector function (e.g., macrophages - if see INFy)
-Cells will revert back to same start point (NOT IN ADAPT IMM!)

(Strength of imm resp = in terms of TNFa, cytokine, neutrophil no.s into tissues = for innate immunity)

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19
Q

Why is it important innate trained immunity is only short-term?

A

Can be dangerous - constantly ready for inflamm resp - as is not antigen specific
(but adaptive = v. specific so not dangerous)

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20
Q

Graph of primary (vaccination) & secondary infection.

A

-Higher conc of antibodies on reinfection - more T & B cells made - faster & better - antibodies made faster & have higher affinity (class switching)

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21
Q

Role of vaccines & how?

A

-Give long-lasting immunity
–> antibodies to prevent toxin damage from pathogen OR neutralise pathogen - STOP entry of pathogen
–> done by recognition of foreign antigen, B cell activation, antibodies made
–> also activate T cell immunity (best for viruses)

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22
Q

Balance between immunity & safeness of vaccine?

A

-Vaccine MUST activate adaptive imm resp - if killed by innate then = NO = immunity
–> so need dose great enough for adaptive resp - but not too much that = unsafe

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23
Q

Who needs to be most vaccinated, & why is this an issue?

A

-Old, young & immunocompromised = most need to vacc
BUT
-Vacci = least effective in these groups - as their imm systems are weakened

24
Q

What is herd immunity?

A

-Point where a pop is protected from a disease, either by enough people being vacc OR by people having developed antibodies by having the disease

% of pop - need to vaccinate - to achieve herd immunity varies for each infection

25
Q

What does herd immunity achieve?

A

Protection for people in pop that can’t be vaccinated - old, young, immunocompromised

26
Q

Requirements of vaccines?

A

-Safe - no illness/death
-Protect against illness by live pathogen
-Give infection lasting ideally years
-Low cost per dose
-Biological stability - ability to keep stable easily? - does it need to be refrigerated?
-Ease of administration - training?, for when in rural places must be easy to do
-Few side-effects
–> imm resp will = side-effects - need balance

27
Q

Types of vaccine?

A

-mRNA
-Live attenuated pathogen (changed)
-Subunit or toxoid
-Synthetic or conjugated
-Whole inactivated pathogen

NEVER GIVE ‘NORMAL’ PATHOGEN!

28
Q

What are live attenuated pathogen vaccines?

A

-Often = viral vaccines
-Can replicate = strong stimulation to imm system - stimulate Tc, Th resp & antibodies

29
Q

How are live attenuated pathogen vaccines made - old way?

A

-Isolate virus
-Culture on animal (often monkey) cells - adapts to this - changes its genetics - alters tropism of virus (VIA mutations)
-So virus grows well in monkey cells
-Choose virus that will not damage human cells - use as virus

30
Q

How are live attenuated pathogen vaccines made - new way?

A

-Isolate virus
-Identify virulence genes (ones which cause damage to cells) - encoding: rec binding prots, virulence prots, core structural prots
-Mutate OR delete these genes = attenuates virus

31
Q

Examples of live attenuated pathogen vaccines?

A

MMR
Rotavirus

32
Q

+ves & -ves of live attenuated pathogen vaccine?

A

+ves
-Immune recognition at multiple life cycle stages
-Long lasting immunity including T cell mediated effects
-ves
-Theoretically could revert to a pathogenic strain
-May act as virulent opportunistic pathogen in immunocompromised patients.
-Need special storage conditions

33
Q

What are whole inactive pathogen vaccines?

A

Whole pathogens which = inactive OR dead

34
Q

How are whole inactive pathogen vaccines made?

A

-Isolate live pathogen
-Inactivate pathogen - use heat OR formaldehyde
= structurally intact BUT inactive pathogen
-can’t enter cells or replicate - proteins have been denatured in capsid
-prots can’t be seen by B cells = not as good as vacc

35
Q

Examples of whole inactive pathogen vaccines?

A

Flu & polio

36
Q

+ves & -ves of whole inactive pathogen vaccines?

A

+ves
-Pathogen can’t replicate in the body (non-pathogenic)
-Safe to use in immunocompromised people
-Vaccines can be easily stored and transported without affecting them
-ves
-Less effective than live vaccines often require booster doses
-Don’t induce a CD8+ T Cell response or effective mucosal immunity
-Failure to adequately inactivated virus might produce a pathogenic strain

37
Q

What are conjugate vaccines, & when are they used?

A

-Combine antigen recognised by B cell (e.g., polysaccharide) & 2nd antigen that will induce T cell help (e.g., protein toxoid)
–> used in young children as some antigens can’t effectively induce a memory response on their own

38
Q

How are conjugate vaccines made?

A

-B cell recognises polysacc - & takes up whole vaccine molecule
-B cell = APC w/ peptides of polysacc & toxoid on MHC II
-T cell recognises toxoid on B cell
-T cell binds to toxoid on B cell
-T cell activates B cell (3 signals) - & causes class switching
-B cell = antibodies to polysacc - imm resp to polysacc caused

39
Q

Example of conjugate vaccine?

A

Meningitis C

40
Q

+ves & -ves of conjugate vaccines?

A

+ves
-Create a complete adaptive immune response involving CD4+ T cells
-Don’t use whole pathogens so can’t cause disease
-Can elicit protection in v. young children
-ves
-Expensive to produce
-Don’t induce a CD8+ T Cell response or effective mucosal immunity
- Need to be engineered to include a whole range of different antigens to be sure of a response to all pathogenic strains

41
Q

What are toxoid vaccines?

A

Pathogen component - combine w/ adjuvant to induce immunity

42
Q

How are toxoid vaccines made?

A

-Toxins of some bact = harm
-Purify toxins from bact & inactivated - now = toxoids
-Antibodies made against toxoid - no disease caused

43
Q

What are subunit vaccines?

A

Pathogen component - combine w/ adjuvant to induce immunity

44
Q

How are subunit vaccines made?

A

-Isolate pathogenic bact
-Isolate prot from bact that induces imm resp
–> put in vaccine = DCs phagocytose = APCs

45
Q

Example of toxoid/subunit - pathogen component vaccine?

A

Toxoid = Tetanus
Subunit = Whooping cough (pertussis)

46
Q

+ves & -ves of pathogen component vaccines?

A

+ves
-Very safe, there is no pathogen being introduced so no chance of infection
-Vaccines can be easily stored and transported without affecting them
-ves
-Less effective at inducing long-lasting immunity
-Don’t induce a CD8+ T Cell response or effective mucosal immunity
-Need to engineer to include a range of different antigens to ensure body responds to pathogen strain

47
Q

How are DNA/RNA vaccines made?

A

-Make DNA/RNA strand - codes for prot
-Inoculate this into body cell (often muscle)
-Cells take up nuc acid & make prot & express on surface/excrete
-Imm syst recognises as foreign = CD8+ & CD4+ resp (often both)

48
Q

+ves & -ves of DNA/RNA vaccines?

A

+ves
-Potentially effective against cancers
-Antigen presentation by MHCI and MHCII
-Long term persistence of the antigen
-ves
-Possibility of inducing tolerance (switching immune responses off!) if insufficient adjuvant is given

49
Q

What are adjuvants?

A

Compound which enhances imm resp - put into pathogen component vaccines

50
Q

Examples of adjuvants?

A

-Alum
-Bact cell wall components
-Mineral salts

51
Q

How are adjuvants used?

A

-Mix w/ antigen/pathogen

52
Q

Role of adjuvants?

A

-Enhance immunogenicity by giving danger signal
-Reduce amount of antigen needed
-Aid delivery at mucosa

53
Q

What 3 types of vaccines are in development?

A

-Reverse vaccinology (for meningitis B)
-CAR T cell (for leukaemias)
-Dendritic cell vaccines (for rheumatoid arthritis & cancer)

54
Q

How does reverse vaccinology work?

A

-Examine genome of pathogen & try identify novel antigens (often surface prots)
-Synthetically make prots
-Test for effective imm resp & antibody production

55
Q

+ves & -ves of reverse vaccinology?

A

+ves
-Find many targets very quickly
-Don’t need to use live organisms
-ves
-Peptide may not be bound by everyone’s MHCII molecules
-Need to pick peptides large enough that DC’s will present them

56
Q

Types of COVID vaccines?

A

Immunology (6 decks)

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