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Immunology > Memory and vaccination > Flashcards

Memory and vaccination Flashcards

1
Q

What is the primary immune response?

A

First time an individual’s immune system comes across a pathogen involving an immune response to an infection/vaccination
Before T/B cells have met their antigen= NAIVE

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2
Q

What’s a secondary (tertiary, quaternary) immune response?

A

the 2nd/3rd/4th time individual comes across same pathogen
Cells are antigen experienced and have immunological memory
Qualitatively and quantitatively improved
asymptomatic/very mid

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3
Q

Levels of antibodies over the years

A

Over the years after a vaccination antibody (Ab) levels rarely decline= long term immunological memory (but T cells - CD4+ and CD8+ do decline)

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4
Q

What makes memory B cells so good in a secondary immune response?

A

Produce higher affinity antibodies than plasma cells
Produce class switched antibody
Produce antibody quickly
Can re enter germinal centre an undergo somatic hypermutation and affinity maturation for a 2nd time
Have higher levels of MHC and costimulatory molecules to attract T helper cell

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5
Q

Characteristics of a primary immune response

A

Ratio of antigen specific B cell= low
IgM produced first in response (IgM>IgG)
Low affinity for antibody
Low somatic hypermutation

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6
Q

Characteristics of a secondary immune response

A

Ratio of antigen specific b cells is higher
More isotypes made (IgG, IgA)
Affinity of antibody= high
Somatic hypermutation= high

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7
Q

2 types of memory T cells

A

Central memory T cell

Effector memory T cell

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8
Q

How do T memory cells differ?

A

Occur in different locations
Traffic differently to naive T effector cells
each= have different effector functions

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9
Q

How do naive/effector/memory T cells

A

They each produce different molecules

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10
Q

How can naive T cell go to lymph node?

A

Have CCR7 chemokine receptor
lymph node has chemokine CCL21
CCR7 and CCL21 are attracted
Takes it to lymph node

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11
Q

Molecules that memory T cells can make

A

CD44- Cell adhesion molecule
CD45R0- modulate TCR signalling
CD45RA- modulate TCR signalling

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12
Q

What do naive T cells have on their surface?

A

CCR7 receptor

CD45RA

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13
Q

How are T memory cells produced?

A

Naïve T cells are activated by dendritic APC in lymph nodes (costimulation, cytokines)
Naive cells differentiate to adopt different effector phenotypes (T helper, cytotoxic cells-perforin and FAS L-made when APC makes IL-2)
Some effector cells become memory cells
Most effector cells die by mitosis after a few days

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14
Q

Difference between central memory t cell and effector memory T cell?

A

Central memory cells= express CCR7 receptor (chemokine receptor) and stay in lymphoid tissue
Effector memory T cell= lack CCR7 and migrate to tissue

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15
Q

How do memory T cells survive?

A

Cytokines IL7 and IL-15 give memory T cells survival signals

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16
Q

What do effector memory T cells have on their surface?

A

CCR3- chemokine
CCR5- receptor for chemokine CCR3
CD45R0- modulates TCR signalling

17
Q

Characteristics of effector memory T cells

A
  1. Stay in tissue (not lymph nodes)
  2. Immediate expansion in reinfection
  3. express receptors for inflammatory cytokines so can be recruited to site of inflammation
  4. Quickly produce IL-4, IL-5, IFN-gamma
  5. Committed to a lineage similar to Th1 and Th2
18
Q

Characteristics of central memory T cells

A
  1. Stay in lymph node (like naive cells)
  2. need antigen presented to them again
  3. Long lived precursors- take longer to respond
  4. Not committed to Th1/Th2 type
19
Q

Why is innate immunity referred to as ‘trained immunity’?

A

Trained immunity- involves epigenetic changes, metabolic changes improved effector functions
These support functions of innate immunity

20
Q

Aim of vaccines?

A

Generate long lasting and protective immunity

Seek to generate antibodies to prevent damage by pathogen toxins or neutralise pathogen to stop infection

21
Q

What must a vaccine do to work?

A 
Incorporate an antigen into the body that the body will recognize as foreign 
B cell must be activated by
Antigen from vaccine binding to BCR= APC (MHC II)
T helper cell binds to B cell APC= Costimulation and cytokine production
Triggers class switching and B cell to differentiate into plasma cells and memory cells
22
Q

What do the best vaccines do?

A

Trigger T cell immunity

23
Q

When will a vaccine not work?

A

If antigen is cleared by innate immunity

24
Q

Which people are vaccines least effective in and why?

A

Young, old, immunocompromised

Weakened immune systems

25
Q

What is herd immunity?

A

Also known as ‘population immunity’
A concept used for vaccination, in which a population can be protected from a certain virus if a threshold of vaccination is reached
% of population that needs to be vaccinated varies for each infection e.g for measales it is 93-95%

26
Q

What are the requirements for a vaccine?

A
  1. Safe- must not cause illness/death
  2. Protective- must protect against illness caused by pathogen
  3. Give sustained protection- last several years
27
Q

Practical considerations for a vaccine

A

Low cost per dose
Biological stability
Ease of administration
Low side effects (side effects from a vaccine means immune response is activated= effective)

28
Q

What are adjuvants?

A

Compounds used to enhance immune response

Mixed with antigen/pathogen (used in subunit/toxoid vaccines)

29
Q

Examples of adjuvants

A

Alum, mineral salts, bacterial cell wall components

30
Q

Purpose of adjuvants

A

Enhance immunogenicity by giving danger signal (PAMPs)
Reduce amount of antigen needed
Aid delivery at mucosa

31
Q

Why can organisms be ‘difficult’?

A
  1. Pathogen is hidden (malaria)
  2. Pathogen changes its surface proteins (trypanosomes- have lots of genes for surface antigens that they can change)
  3. Conserved (Mutated) antigens are hidden (HIV- can mutate and change- hide conserved proteins so antibodies cant target them and neutralise them)
  4. Antibodies aren’t effective (TB)- antibodies aren’t enough to remove pathogen
32
Q

Future of vaccinations

A
  1. Reverse Vaccinology (Meningitis B vaccine)
  2. DNA vaccines (prostate cancer trials)
  3. CAR T cells (in leukaemia)
33
Q

Reverse Vaccinology

A
  1. Examine genome of pathogen- identify best, novel antigens (usually surface proteins)
  2. Synthetically produce the protein
  3. Test for an effective immune response and antibody production
34
Q

Advantages of reverse vaccinology

A
  1. Find many targets v quickly

2. Don’t need live organism

35
Q

Disadvantages of reverse vaccinology

A

Need to chose antigen (peptides) large enough that dendritic cells can process
Antigen (peptide) may not be bound by everyone’s MHC II molecules

36
Q

DNA Vaccines (prostate cancer trials)

A
  1. Produce DNA strand that codes for pathogenic protein
  2. Inoculate into body cells (normally muscle)
  3. Cells take up DNA and produce protein on their surface/secret it
  4. Immune system recognises this as a foreign= immune response- can get CD4+ and CD8+ response
37
Q

Advantages of DNA vaccines

A
  1. Potentially effective against cancers
  2. Antigen presentation by MHC I and MHC II
  3. Long term persistence of antigen
38
Q

Disadvantages of DNA vaccines

A
  1. Limited to protein antigens
  2. Risk of affecting genes involved in cell’s growth
  3. Possibility of inducing tolerance (attack body’s own antigens)

Immunology (7 decks)

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