Session 7: Adaptive Immunity 2

Question 1

Where are B and T lymphocytes produced?

+ mature

Answer 1

T = produced in bone marrow and mature in thymus
B = produced in bone marrow and mature in tissues following contact with antigen

Question 2

When does lymphadenopathy occur?

Answer 2

When B and T cells are activated by antigens

Question 3

Where do T and B lymphocytes accumulate?

Answer 3

In key lymphoid tissues:
MALT (mucosa associated lymphoid tissue)
Lymph nodes
Spleen

Question 4

What are the antigen recognition receptors found on T-lymphocytes?

Answer 4

T cell receptors (TCR) with alpha and beta chains

Question 5

What forms of antigens are recognised?

Answer 5

Peptides displayed by MHC molecules

Question 6

There are different subtypes of antigen recognition.
What do helper T cells recognise?
What do Cytotoxic T cells recognise?

Answer 6

Helper T (CD4+) recognise peptide presented by MHC class II molecules
Cytotoxic T cells (CD8+) recognise peptide presented by MHC class I molecules.

Question 7

Binding by antigen to a TCR does not activate the T cell. What else is needed?

Answer 7

CD3 complex

Question 8

Explain the costimulation of T-helper cells.

Answer 8

There are three signals needed to fully activate T cells.
Signal 1 which is the presentation of the peptide by the antigen presenting cells on the MHC class I or class II.
Signal 2 which is the activation of CD28 by B7
Signal 3 which is the activation of T cell by cytokines.

Question 9

What different T helper cells can Th0 differentiate into?

Answer 9

Th1
Th2
Th17
Treg

Question 10

Explain how Th0 (naive CD4+ T cell) turns into Th1.

Explain the role of Th1

Answer 10

This depends on the cytokine environment.
IL-12 (cytokine) will turn Th0 into Th1.

Th1 is a part of the cell mediated immunity response and excels at defence against intracellular and extracellular pathogens like bacteria, viruses and fungi.
Th1 stimulates activation and differentiation of CD8+ T cells, recruits and activates macrophages. Stimulates B cells to produce IgG or IgA.

Question 11

Explain how Th0 turns into Th2.

Explain the role of Th2.

Answer 11

IL-4 will turn Th0 into Th2.
Th2 is a part of the humoral immunity which excels at defence against extracellular pathogens like parasites and worms.
Th2 stimulates B cells to produce IgE.
Stimulates Eosinophils and Mast cells.

Question 12

Explain how Th0 turns into Th17.

Explain the role of Th17.

Answer 12

IL-1 and IL-6 which will recruit and activate Neutrophils.

Question 13

Explain how Th0 turns into Treg.

Explain the role of Treg.

Answer 13

IL-10 and TGFbeta will turn Th0 into Treg.

Treg is important in tolerance and immune suppression.

Question 14

Explain the differentiation of CD8+ T cells.

Answer 14

Naive CD8+ T cells goes to become Memory CD8+ T cells or Effector CD8+ T cells.
Effector CD8+ T cells can then become cytotoxic T cells and kill pathogens.

Question 15

What does effector CD8+ T cells need in order to become cytotoxic T cells?

Answer 15

They need Th1 to stimulate the differentiation.

Question 16

What is the antigen recognition receptor on B cells?

Answer 16

B cell receptor or BCR which are found on the membrane and bound to antibodies.

Question 17

What’s unique for BCRs?

Answer 17

Every B cell has its unique specificity/combination of the antigen binding site.

Question 18

What forms of antigens are recognised by BCR?

Answer 18

Macromolecules like proteins, polysaccharides, lipids and nucleic acids.
Small chemicals.

It’s important to note that BCR and therefore B cells do not need processed antigens presented by MHCs.

Question 19

Explain activation of B lymphocytes.

Answer 19

It requires multiple signals.
Signal 1: An antigen can bind to BCR and cause processing of the antigen. This phagocytose the antigen.
There is also increased B7 costimulator numbers.

Signal 2: An already activated T helper cell (Th1 or Th2 depending on the antibody needed to be produced). This is TCR engagement and CD40L will switch IgM to a different isotype (IgA, IgG or IgE).

Signal 3: Cytokines and CD40 activation.

This causes proliferation of B cells and antibody production.

Question 20

How does production of IgM differ to production of IgG, IgE and IgA?

Answer 20

IgM production is T helper independent.

The rest of the antibodies need T helper cells to isotype switch IgM into them.

Question 21

How does affinity maturation occur?

Answer 21

By prolonged or repeated exposure of an antigen.

Question 22

What are memory B cells?

Answer 22

B cells produced after exposure to an antigen. Upon re-challenger the memory B cells will give a faster, stronger and longer antibody response.

Question 23

Explain how antigen stimulated B cells produce IgM.

Answer 23

They turn into plasma cells and then the plasma cells produce IgM.

Question 24

Explain how antigen stimulated B cells produce IgG.

Answer 24

Needs stimulation by effector T helper cells (Th1) by the presence of IFNgamma.

Question 25

Explain how antigen stimulated B cells produce IgE.

Answer 25

Needs stimulation by effector T helper cells (Th2) by the presence of IL-4.

Question 26

Explain how antigen stimulated B cells produce IgA.

Answer 26

Needs stimulation by effector T helper cells (Th1) by the presence of TGFbeta.

Question 27

What are the fates of B cells?

Answer 27

Plasma cells
IgG, IgE or IgA producing B cells.
Memory B cells

Question 28

Why is the ratio of IgG to IgM important?

Answer 28

Because it will tell us whether an infection is acute or chronic?

Question 29

How can you tell if an infection is chronic vs acute?

Answer 29

In a chronic infection IgG will be high.

In an acute infection IgM will be high.

Question 30

Effector functions of IgG.

Answer 30

Fc-dependent phagocytosis
Complement activation
Neonatal immunity
Toxin/virus neutralisation

Question 31

Effector functions of IgA.

Answer 31

Mucosal immunity

Question 32

Effector functions of IgE.

Answer 32

Immunity against helminths and mast cell degranulation in allergies.

Question 33

Effector functions of IgM.

Answer 33

Complement activation.