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CMB2004 - Cell and Molecular Biology of the Immune System > Lectures 4-7: Cell biology of the specific immune system > Flashcards

Lectures 4-7: Cell biology of the specific immune system Flashcards

1
Q

How do B cells develop?

A

From haematopoietic stem cells in bone marrow that express PAX5 transcription factor
Re-arrangement and expression of Ig genes
Removal of self-reactive cells

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2
Q

How do B cells react to antigens?

A

B-cell precursor rearranges Ig genes
Immature B cells bound to self cell-surface antigen is removed from the repertoire using negative selection
Then bind to foreign antigens activating B cells giving rise to plasma and memory cells

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3
Q

How are pre-B cells produced?

A

H chain genes rearrange then move to cell surface with Ig alpha and beta and express with surrogate light chain
Produces pre-B cell receptor

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4
Q

Which proteins determine good heavy chain binding for the surrogate light chain?

A

V preV and λ5

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5
Q

How are immature B cells produced?

A

Light chains rearrange and displace proteins to produce IgM BCR

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6
Q

What is the function of a pre-BCR?

A

Delivers a signal to pre-B cell that H chain looks functional
No Ag required yet

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7
Q

What signals are emitted from pre-BCR?

A

Turns off RAG-1&2
5-6 rounds of cell division
Surrogate light chain expression stops
RAG-1&2 turned on again
L chain rearrangement starts

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8
Q

What is the gene arrangement on the H-chain in a B-cell?

A

D-J rearrangement on both chromosomes
↓
V-DJ rearrangement on first chromosome
↓ (-)
V-DJ rearrangement on second chromosome
↓ (-)
Cell loss

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9
Q

What is the gene arrangement on the L-chain in a B-cell?

A

Rearrange Kappa gene on first chromosome
↓(-)
Rearrange Kappa gene on second chromosome
↓(-)
Rearrange Lambda gene on first chromosome
↓(-)
Rearrange Lambda gene on second chromosome
↓(-)
Cell loss

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10
Q

Which part of B-cell development has the largest chance of survival?

A

Pre-B cell

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11
Q

What are factors of Ig gene re-arrangement?

A

Error prone
If cell fails to productively re-arrange both H and L genes, it dies

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12
Q

Why does the light Kappa chain have so many chances at rearrangement?

A

Because there are 5 J Kappa genes on each chromosome

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13
Q

What are the 2 different mechanisms immature B cells do to multivalent self-antigens?

A

Clonal deletion - cell dies by apoptosis
Receptor editing - further light chain gene rearrangements of variable regions

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14
Q

When does the immature B cell become anergic?

A

When it binds soluble self antigen
Anergic = becomes unresponsive

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15
Q

What is the process of T cell development?

A

Originate from bone marrow
Re-arrange receptor genes in thymus
Express pre-T receptor
Eliminate self-reactive T cells via negative selection
Undergo development/selection in thymus
T cells expressing αβ TCR must bind with self MHC expressed in thymus

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16
Q

How are T cells made and activated?

A

Precursors use Notch signalling to initiate T cell receptor gene rearrangements
Immature T cells recognising self MHC receive signals for survival ones that interact strongly with self antigen are removed from the repertoire
Mature T cells encounter foreign antigens in the peripheral lymphoid organs and are activated
Activated T cells proliferate and eliminate infection

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17
Q

What is the thymus?

A

Bi-lobed organ in anterior mediastinum
Lobe divided into many lobules
Lobules have outer cortex and inner medulla
Cells - lymphoid cells, epithelial cells, macrophage and dendritic cells

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18
Q

How does the T cell mature in the thymus?

A

Pro-thermocytes enter cortex via blood vessels from bone marrow
Inside, TCR genes re-arranged (TCRβ first, expressed along with pre-T cell receptor, proliferation then re-arrange TCRα genes)
Express TCR together with CD3 and both CD4 and 8

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19
Q

How is the full TCR complex assembled?

A

Requires CD3 complex (δ,ε,γ)
CD3 transmits signal to T cell

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20
Q

What are the differences between γδ TCR in comparison to αβ?

A

Similar structure
γδ do not express CD4 or CD8
γδ have less diversity
γδ expressed on separate T cell population (1-5% in circulation , epithelial cells + mucosal surfaces)
Recognise different antigens
Depends on which genes are rearranged successfully first

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21
Q

What are the disadvantages of cells expressing randomly rearranged αβ?

A

Recognise self MHC + peptide from foreign antigen (immunity)
Recognise self MHC + peptide from self antigen (autoimmunity)
Not able to recognise self-MHC (useless)

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22
Q

What happens in positive selection of T cells?

A

Recognise self MHC
Double positive T cells recognise MHC on cortical epithelial cells in thymus - apoptosis if not recognised
Rearrangement gives random TCR repertoire

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23
Q

What happens in negative selection of T cells?

A

Recognise self MHC on thymus dendritic cells/macrophages with high affinity
TCR binding to MHC/self-peptide with high affinity causes T cell to die (apoptosis)

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24
Q

When does positive and negative selection of T cells occur?

A

Sequentially, at different regions of the thymus

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25
Q

What is the paradox of positive and negative selection?

A

T cells positively and negatively selected on self MHC + self peptide
T cells positively selected aren’t always subsequently eliminated by negative selection

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26
Q

What is the basis for selection of TCR affinity for p/MHC?

A

All T cells recognising self MHC are positively selected
Highest affinity TCR are negatively selected
GOAL: population of T cells with low affinity for self peptide + self MHC

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27
Q

What percentage of T cells survive thymus selection?

A

<5%
Express TCR capable of binding self MHC
Depleted of self-reactive cells
(CD8+ T cells MHC class I)
(CD4+ T cells MHC class II)

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28
Q

What is T cell mediated immunity?

A

Naive T cells recirculate via blood/lymphatics through secondary lymphoid tissue
Contact with specific Ag and APC -> clonal proliferation and differentiation
Naive -> effector/memory T cells
CD8+ kill infected cells
CD4+ secrete cytokines

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29
Q

What are naive T cells?

A

They haven’t yet recognised foreign antigen

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30
Q

What do the lymphoid tissues contain?

A

T cells that recognise antigen/MHC on antigen presenting cells
Array of APC, some specialised, trap and present antigens
Lymph nodes
Spleen

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31
Q

Where do T cells go one activated?

A

They leave the lymphoid tissues and migrate to the sites of infection

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32
Q

How do T cells get to where they need to be?

A

They enter the lymph node from blood via high endothelial venues (HEV)
Move to T cell area rich in dendritic cells and macrophages
APC presents antigen and delivers other activation signals (cytokines)

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33
Q

What happens to T cells that are not activated?

A

They leave the lymph via cortical sinuses into the lymphatics and re-enter the circulation (re-used)

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34
Q

What are the signals required for T cells to get where they need to be?

A

Molecules are expressed on the surface of T cells (chemokine receptors) bind ligands (chemokine) expressed/released by other cells
Once close to other cells different molecular sets of cell adhesion molecules mediate cell-cell interactions

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35
Q

What are examples of CAMs mediating cell-cell interactions?

A

Naive T cells with high endothelial venules (HEV)
T cell with APC
Effector T cell and target cell

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36
Q

What are CAMs?

A

Cell adhesion molecules

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37
Q

What happens once T cells make contact with the APC?

A

Contact using CAMs
TCR scans APC peptide-MHC complexes
(no recognition -> disengages)
(recognition -> signal from TCR complex)
- Increased affinity of CAM interactions
- T cell divides
- Progeny differentiate to effector cells, exit lymph

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38
Q

What is LFA-1?

A

Leukocyte function associated antigen

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39
Q

What is ICAM-1?

A

Intercellular adhesion molecule

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40
Q

How do T cells initially become activated?

A

They bind to APC through low affinity LFA-1:ICAM-1 interactions then this binding leads to TCR signalling LFA-1
Conformational change in LFA-1 increases affinity and prolongs cell-cell contact

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41
Q

How are T cells signalled?

A

They receive a signal from TCR contacting MHC/peptide on APC
Involving CD3 chain

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42
Q

How many signals are required for T cell activation?

A

3

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43
Q

What is co-stimulation in T cells?

A

APC express co-stimulatory molecules that bind CD28 expressed by naive T cells and deliver signal 2
APC release cytokines which bind cytokine receptors now up-regulated on naive T cells with deliver signal 3

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44
Q

What are the B7.1/2 molecules?

A

They are the co-stimulatory molecules required to release the second signal

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45
Q

What is CD28?

A

It is a molecule required for the release of the second signal to activate T cells

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46
Q

What examples of cytokines are required for the third signal to activate T cells?

A

IL-6, IL-12, TGF-β and IL-4

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47
Q

Why is the co-stimulatory signal and cytokine signal not required when the effector T cell releases the effect?

A

Because the signals have already changed the naive T cell to the effector T cells which allows it to have an effect in the secondary lymph tissue

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48
Q

What are the ICOS and CTLA-4 molecules?

A

ICOS is related to CD28 binding ICOSL (ligand) on the APC to induce cytokine secretion by T cells
CTLA-4 is highly related to CD28, shows stronger binding to B7.1/2 than CD28 (competition)

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49
Q

What happens once CTLA-4 has bound to B7.1/2 on APC?

A

A negative signal is delivered which deactivates the T cell

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50
Q

Why does the T cell express the ICOS and CTLA-4 molecules?

A

After 3 signals released and T cells are activated they proliferate and express these molecules

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51
Q

What is the importance of CTLA-4?

A

Mutations within the molecule are associated with several autoimmune diseases as the T cell cannot become inactivated
Cancer patients are often treated with anti-CTLA-4 which can enhance the immune response to the tumour (melanoma and renal carcinoma)

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52
Q

What is the significance of the co-stimulatory molecules?

A

B7.1/2 are the most important and contain functional differences
The expression varies - constitutive on mature dendritic cells, inducible on macrophages and B cells

53
Q

How are APCs activated?

A

They express receptors for microbial molecules (PRR)
Binding of pathogen-associated molecules activates the APC (danger signal)
Leads to up regulation of MHC and co-stimulatory molecules
Ensuring signal 2 released to activate T-cell mediated response only occurs during infection

54
Q

What is signal 3?

A

It is the release of cytokines to dictate the differentiation of activated CD4 cells into different sub-sets of effector cells

55
Q

What are the different types of cytokines that can be signalled?

A

TGF-β, IL-6, TGF-β&IL-6, IL-12&IFN-γ, IL-4

56
Q

What does TGF-β cytokine lead to?

A

A transcription factor FoxP3 produces TGF-β and IL-10 which leads to Treg cells (regulation)

57
Q

What does IL-6 cytokine lead to?

A

A transcription factor Bcl6 expressing IL-21 and ICOS which leads to Tfh cells

58
Q

What does TGF-β and IL-6 lead to?

A

A transcription factor RORγT expressing IL-6 and IL-17 which leads to Th17 cells

59
Q

What does IL-12 and IFN-γ lead to?

A

A transcription factor T-bet expressing IL-2 and IFN-γ leading to Th1 cells

60
Q

What does IL-4 lead to?

A

A transcription factor GATA3 expressing IL-4 and IL-5 leading to Th2 cells

61
Q

What are the different types of T cells?

A

Treg cells, Tfh cells, Th17 cells, Th1 cells, Th2 cells

62
Q

What are the different types of APCs?

A

Dendritic cells (only present Ags) crucial for activation of naive T cells
Macrophages and B cells that present antigen to receive help from effector cells

63
Q

What are the different types of DC?

A

Myeloid conventional DC (DC2,3)
Plasmacytoid DC (pDC, DC6)

64
Q

What is myeloid DC?

A

DC2,3 which have potent APC and are involved in activation of naive T cells

65
Q

What is plasmacytoid DC?

A

pDC, DC6 have important viral infection and secrete several type 1 α and β interferons and also express TLR 7 and 9

66
Q

Why are myeloid DCs significant?

A

It is a key APC that initiates T cell responses
Bone-marrow derived
Immature form found in epithelia
Macropinocytic and phagocytic
Do not express co-stimulatory molecules till activated
Induced to mature and migrate to lymph node following danger signal activation

67
Q

How do dendritic cells act as efficient activators of naive T cells?

A

They are found in T cell areas of lymphoid tissue
DC MHC I and II loaded with peptides from pathogens from peripheral tissues
Levels of co-stimulatory molecules will be very high
Express high levels of adhesion molecules

68
Q

How do immature dendritic cells go to mature dendritic cells?

A

In peripheral tissues encounter pathogens and are activated by PAMPs (Pathogen-associated molecular patterns)
TLR signalling induces CCR7 and enhances processing of pathogen-derived antigens
CCR7 directs migration into lymphoid tides and augments expression of co-stimulatory molecules and MHC
Mature dendritic cell in T-cell zone primes naive T cells

69
Q

What is cross presentation?

A

Specialised DC (DC1) take up and process exogenous Ag and present it via MHC I
Allows these DC to activate CD8+ T cells, CD8 effector cells can kill infected cells that are not APCs so they aren’t expressing co-stim

70
Q

What is the significance of macrophages?

A

Function as scavengers of pathogens also important APC for extracellular pathogens
Highly phagocytic
Express MHC II and B7 increasing following T cell help
Resident in many tissues at peripheral sites as well as in lymphoid tissue and other tissues around the body
One activated by T cells secrete many inflammatory cytokines

71
Q

What is the significance of using B cells as APCs?

A

Vary poor at phagocytosis (don’t engulf MOs)
Internalise soluble antigens for processing and presentation by BCR
Antigen binding to BCR up-regulates B7 (provide signal 2 to T cell)
Similar to DC, found in lymph nodes presenting to T cells
Role as APC may be more important after initiation of immune response by APC
Use BCR to physically extract antigen from other cells

72
Q

How is IL-2 important for T cell survival?

A

It is an important autocrine T cell growth factor (naive T cells have low affinity)
Activated T cells (after signal 1+2+3) have high affinity IL-2R and secrete IL-2
IL-2 binding to IL-2R on activated T cells leads to lots of T cell proliferation

73
Q

What is the significance of IL-2 in drug development?

A

Target of immunosuppressive drugs (stopping T cell proliferation)

74
Q

What are the different T cells once activated?

A

Effector T cells
CD8+ cytotoxic (kill MHC I/peptide complexes)
CD4+ by secreting cytokines (effects on other T cells)

75
Q

What is the significance of effector T cells?

A

Display effector function when TCR engaged
Dont require co-stimulation
Change expression of adhesion molecules
No longer enter lymph nodes
Enter tissues activated by endothelia (sites of infection and inflammation)

76
Q

Where do B cells move once they have survived in the bone marrow?

A

Into the blood and lymphatics

77
Q

What are the different functions B cells can differentiate into?

A

Neutralisation
Opsonisation
Complement activation

78
Q

How are B cells activated?

A

Using several signals
Naive B cells express membrane Ig/BCR
Encounter non-self antigen in secondary lymphoid tissue
Binding of antigen to BCR provides signal 1 to B cell

79
Q

What is the molecular basis of BCR signal 1?

A

BCR-associated polypeptides involved (Igα and Igβ)
Cross-linking BCR activates intracellular kinases

80
Q

What are ITAMs?

A

Immunoreceptor tyrosine-based activation motif which are involved in signalling (Igα and Igβ)

81
Q

How is signal 1 increased/enhanced?

A

When antigen activates complement cascade
Lots of C3b
complement receptor 2 (CR2) on B cell surface (CD21)
CR2/CD19/CD81 form BCR co-receptor complex
Augments the signal

82
Q

What are the 2 different ways B cells receive signal 2?

A

Thymus-independent antigen (TI)
Provided by:
antigen itself
extensive cross linking of BCR
Thymus -dependent antigen (TD)
Provided by CD4+ T cells

83
Q

How does TI-1 antigen signalling work?

A

IgM production with no T cell involvement
TI-1 antigen: binds BCR and other receptors on all B cells providing signal 2, high concentrations these antigens act as polyclonal activators for B cells
The 2 signals lead to B cell activation proliferation and antibody secretion

84
Q

How does TI-2 antigen signalling work?

A

Contain repeated epitopes
- often polysaccharides
- important in some bacterial infections
Cross-link many BCR molecules on the same B cell surface
Take longer to induce B cell activation (more Ag required)
Antibody responses don’t develop until >5 years old in humans

85
Q

How does TD antigen signalling work?

A

Antibodies require the presence of CD4+ T cells
Responses are much better compared to TI antigen response
T cells activated by peptide-MHC on APC
BCR binds antigen - signal 1
B cell internalises antigen, processes and presents antigen to CD4+ cells - signal 2 (via CD40/CD40 ligand interaction)
Cytokines are then secreted by T cell

86
Q

Which classes of antibody can be produced by TD antigen?

A

ALL!

87
Q

What is the process of TD antigens recognising a virus?

A

B cell binds virus through viral protein coat
Virus particle is internalised and degraded (using lower pH)
Peptides from internal proteins of the virus are presented to the T cell (CD154(CD40L)-CD40) which activates the B cell by producing signal 2
Activated B cell produces antibody against viral coat protein

88
Q

How are epitopes recognised by antibody and T cell physically linked?

A

From different parts of the same molecule
OR
Different molecules of the complex

89
Q

How can a vaccine against pathogens be made more efficient?

A

By converting a TI antigen signalling to TD antigen signalling

90
Q

What types of vaccines are made when the TI is switched to TD antigen signalling?

A

Conjugate vaccines

91
Q

What is an example of a conjugate vaccine?

A

Haemophilus influenza type B
Protective response requires antibodies to capsular polysaccharide
Coupling this to a protein such as tents toxoid converts it to a TD antigen
So young children can be immunised and protected
(other e.g. MenC(meningitis) and pneumococcal conjugate vaccine)

92
Q

Which responses are important for good antibody responses?

A

B-CD4+ T cell interactions

93
Q

Why are B-CD4+ T cell interactions important for good antibody response?

A

B cells enter lymph from blood
B cell comes into contact with its specific antigen which becomes activated
If antigen is TD then B cell presents peptide from antigen to CD4+ Th cells at the boundary of T/B areas within the lymph forming B/T cell conjugates

94
Q

What happens once the T cell expresses CD40 ligand and secretes cytokines?

A

B cell receives signal 2 from T cell via CD40/CD40L binding and via cytokine from T cells binding receptors -> B cell proliferation
CD40 signal also induces activation induced deaminase (AID) which is required for class-switching and somatic hypermutation (SHM)

95
Q

How are B cells activated using a TD antigen?

A

Conjugates of B lymphoblasts and T cells move to primary follicles
Germinal centres (GC) are formed within a B cell follicle in secondary lymphoid tissues
B cells divide rapidly becoming centroblasts and undergo:
- SMH of Ig genes
- isotope switching
Differentiate into non-dividing centrocytes (smaller)

96
Q

What happens to B cells once they are in the Germinal Centres(GC)?

A

Either differentiate into plasma cells
- secrete various isotypes
- high affinity antibody, somatically mutated
Or form long-lived memory cells
- recirculate
Or die within lymphoid tissue
- if BCR no longer binds to antigen

97
Q

What is somatic hypermutation?

A

It introduces point mutations into V regions of the Ig
Approx one mutation/V region/cell division (10^6 x normal DNA mutation rate)
Enzymes primarily involved includes activation induced deaminase (AID) and DNA repair genes

98
Q

What other cells are located within GCs?

A

Follicular dendritic cells (FDCs)

99
Q

What are follicular dendritic cells(FDCs)?

A

Not bone-marrow derived dendritic APCs
Cells in primary follicle that capture intact antigen for centrocytes brindles via BCR

100
Q

Why are follicular dendritic cells important in B cell maturation?

A

Centrocytes that have undergone SMH express mutated BCR on surface
- centrocytes compete with each other for antigen on FDC and signals from Tfh cell
- if mutated BCR binds antigen on FDC better than the un-mutated, presents more efficiently and receive CD40 signal from Tfh cell (failure = apoptosis/re-cycle to dark zone)
- centrocytes with higher affinity for BCR survive and differentiate into plasma cells

101
Q

Which B cell interactions are good for antibody responses?

A

Follicular T helper cells (Tfh)

102
Q

What is the basis for affinity maturation?

A

Mutated BCR with low affinity for antigen:
Germinal centre B cell with mutated low-affinity surface Ig
BCR not cross-linked and B cell cannot present antigen to T cell -> apoptosis
Mutated BCR with high affinity for antigen:
Germinal centre B cell with mutated high affinity surface Ig
T-cell help and BCR cross-linking sustain B cell proliferation and maturation -> memory B cell/ plasma cell

103
Q

What is the role of CD40?

A

CD40 single using CD40L expressed on Tfh
- protects centrocytes from apoptosis
Induced isotope switching
- different cytokines induce different isotopes to be produced

104
Q

How is isotope switching controlled?

A

By different antigens
- polysaccharides: IgM (TI)
- proteins: IgG1 & IgG3 or IgG4 (TD)
Antigen at mucosal surfaces induce IgA
Some antigens elicit IgE
Role of cytokines(Tfh cell):
- e.g. IL-4 important for IgE switch

105
Q

Why is immunological tolerance needed?

A

To allow random generation of repertoire of BCR and TCR
Many self-reactive specificities will be produced
No tolerance means auto reactivity would lead to serious pathology

106
Q

What is T cell tolerance?

A

Random TCR rearrangements
Leads to T cells expressing TCR that:
-fails to recognise self-MHC (dies by neglect
- recognises self-MHC + peptide generated from antigen present in thymus (potential dangerous)
- recognise self-MHC + any other peptide not present in thymus (potentially useful)
2&3 expanded by positive selection
2 eliminated by negative selection

107
Q

What is AIRE?

A

An autoimmune regulator protein

108
Q

What is the use of AIRE?

A

Transcription factor
Role in tolerance induction
Allows expression of many tissue-specific antigens(TSA)
Negative selection/deletion of T cells that recognise these antigens

109
Q

What happens to patients with AIRE deficiency?

A

They have a major autoimmune syndrome

110
Q

What is B cell tolerance?

A

Random Ig gene rearrangement many B cells could express self-reactive BCR
Auto-reactive B cells are negatively selected/deleted
B cells get second chance to re-arrange self-reactive BCR

111
Q

What is anergy in B cells?

A

When immature B cells bind to self antigen

112
Q

What is tolerance via anergy?

A

Lymphocytes recognise self antigen can become unresponsive
Immature B cells: BCR encounters antigen in bone marrow that is not multivalent, down regulate BCR and leave bone marrow as unresponsive
Many potentially self-reactive B cells but anergia B cells leave bone marrow

113
Q

How do T cells become anergic?

A

When T cell only receives signal 1 so no co-stimulatory signal is delivered so T cells have not recognised a nonbacterial antigen

114
Q

What are other mechanisms of tolerance?

A

Immunological ignorance: antigens not presented at sufficient levels to activate T cells
Privileged sites: antigens sequestered from immune system
B cell responses that are T cells dependent: if antigen-specific T cells are absent/tolerant no help fro B cell is available = no antibody response

115
Q

What are regulatory T cells?

A

They are another CD4+ T cell subset surpassing immune responses
Crucial for autoimmune responses
Arise in thymus from T cells with high affinity TCR for self antigens
Express Fox P3 transcription factor
Natural and induced regulatory T cells

116
Q

What happens during regulatory T cell deficiency?

A

Leads to severe autoimmune syndrome IPEX (immune dsyregulation, polyendocrinopathy, enteropathy, X-linked syndrome) very serious autoimmune condition

117
Q

What are regulatory B cells?

A

Secrete IL-10 crucial in preventing autoimmunity

118
Q

Why is regulation of the immune response required?

A

To ensure responses only continue for as long as they are needed
Minimise collateral damage
Ensure responses are qualitatively appropriate

119
Q

What are CD4+ Th1 cells required for?

A

Activation of macrophages, NK cells, cytotoxic T cells

120
Q

What are CD4+ Th2 cells required for?

A

Promoting responses mediated by eosinophils and mast cells; role in antibody responses especially IgE

121
Q

What are CD4+ Th17 cells required for?

A

Promote responses against fungi
Secrete IL-17
Recruit neutrophils early
Implicated in autoimmune disease
Evolutionary oldest form of acquired immunity

122
Q

What are CD4+ Treg/Breg cells required for?

A

Suppress unwanted responses
Mix of CD4+CD25+
CD8+ T cells can have Treg activity
Arise in thymus or circulating T cells in peripheral tissues

123
Q

What are CD4+ Tfh cells required for?

A

Specialised Th found in germinal centres to help B cells (produce other T cell subsets)

124
Q

How do Th1 cells help macrophage function?

A

They activate macrophages via secretion of cytokines
Express CD40L which binds to CD40 on macrophage
Can kill chronically-infected macrophages
Fas ligand-Fas induce apoptosis
released bacteria destroyed by healthy macrophages
->other cells can then kill the pathogens

125
Q

What are Treg cells mode of action?

A

Secretion of suppressive cytokines
TGF-β and IL-10
Can also involve cell-cell contact
IL-10 inhibits APC function

126
Q

What are the key cytokines involved in naive T cell activation by APC?

A

IL-12 and IFN-γ play a key role in induction of Th1 responses
IL-4 important for induction of Th2 responses

127
Q

What is the importance of polarised responses?

A

Ensures correct responses for different types of pathogens
Can go wrong may lead to allergy
Control of auto-reactivity/pregnancy

128
Q

What are follicular T helper cells?

A

Defined as CD4+ Th subset predominantly in B cell follicles of the lymph node
Specialised to provide help to B cell
Secrete either Th1 or Th2 type cytokines
Identified with specific markers that differ from other subsets of CD4 Th cells

CMB2004 - Cell and Molecular Biology of the Immune System (4 decks)

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