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Fundamentals of P > Generation of Diversity in The T Cell Repertoire > Flashcards

Generation of Diversity in The T Cell Repertoire Flashcards

1
Q

Antigen – define

A

Antigen – A combination of ‘antibody’ and ‘generate’.
Any molecule that can bind specifically to an
antibody

Proteins,
carbohydrates and lipids capable of binding to B-cell receptors, T-cell
receptors and/or innate immune receptors

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2
Q

Explain the immune reactions to epitopes

A

• Adaptive immune reactions occur to specific epitopes (portions of the antigen)
as opposed to the entire antigen itself

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3
Q

Infection and vaccination usually induce what

A

Infection and vaccination usually induce polyclonal T- and B-cell responses

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4
Q

Which immune cells recognise and process antigen? - list

A

MONOCYTES MACROPHAGES
DENDRITIC CELLS
B-CELLS

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5
Q

“Professional” Antigen-Presenting Cells (APCs): - define

A

“Professional” Antigen-Presenting Cells (APCs): Immune cells that express
high levels of surface MHC Class II and can efficiently induce T-cell responses

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6
Q

• Highly phagocytic cells - which ones and their effect

A

Macrophages + DC

Highly phagocytic cells – induce strong T-cell responses and inflammation.
Important for protection against Mycobacterium tuberculosis

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7
Q

Compare specific functions of macrophages vs dendritic cells

A

• Macrophages better-equipped to kill pathogens (higher NO production); DCs
better at migrating to lymph nodes (via CCR7) and presenting antigen to Tcells

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8
Q

B-CELLS - distribution

A

• Highly abundant in blood and mucosal tissues

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9
Q

Macrophages + DC - distribution

A

• Rare in peripheral blood - enriched in mucosal tissues

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10
Q

B-CELLS - functions

A

Receptor-mediated internalisation of antigens, as opposed to phagocytosis
• Primary function to make antibody (plasma cell) – but still very good at antigen
presentation
• Possibly main inducer of T-cell immune response to pathogens such as
Neisseria meningitidis

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11
Q

Endogenous antigen processing - describe

A

UPTAKE
Antigens/pathogens already present in cell

DEGRADATION
Antigens synthesised in the cytoplasm undergo limited
proteolytic degradation in the cytoplasm

ANTIGEN-MHC COMPLEX FORMATION
Loading of peptide antigens onto MHC class I molecules
is different to the loading of MHC class II molecules

PRESENTATION
Transport and expression of antigen-MHC complexes on
the surface of cells for recognition by T cells

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12
Q

Macrophages function

A

Macrophages have welldeveloped lysosomal systems
• Specialised for motility,
phagocytosis and the introduction
of particles to the lysosomal system

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13
Q

Is exogenous antigen processing sufficient?

A

Most cell types do not have lysosomal systems
developed as well as macrophages
BUT
Viruses can infect most cell types
A non-lysosomal mechanism to process antigens for presentation to T cells is required

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14
Q

Non-lysosomal antigen processing - list types

A

ANTIGENS FROM INACTIVE VIRUSES ARE PROCESSED VIA THE EXOGENOUS PATHWAY

ANTIGENS FROM INFECTIOUS VIRUSES ARE PROCESSED VIA THE
ENDOGENOUS PATHWAY

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15
Q

Immune response for inactive virus vs infectious virus

A

Inactive virus raises a weak CTL response

The processing of antigens from inactive viruses is sensitive to
lysosomotrophic drugs

I fectious virus raises a strong CTL response

The processing of antigens from infectious viruses is NOT sensitive to
lysosomotrophic drugs

Most CTL recognise antigens generated via a non-lysosomal pathway

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16
Q

Requirements for non-lysosomal antigen processing

A

Protein synthesis is required for non-lysosomal antigen processing

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17
Q

Exogenous pathogens eliminated by

A

Antibodies and phagocyte activation by T helper cells that use antigens generated by exogenous processing

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18
Q

Endogenous pathogens eliminated by

A

Killing of infected cells by CTL that use antigens generated by endogenous processing

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19
Q

MHC class I - describe:

  • Expressed where
  • Binds what
  • Presents to
  • Antigens from
A

Expressed on
all nucleated
cells

Binds short
peptides (8-10
amino acids)

Presents to
CD8+ T-cells

Antigens from
the cytosol (+
crosspresentation)

20
Q

MHC class II - describe:

  • Expressed where
  • Binds what
  • Presents to
  • Antigens from
A

Expressed on
APCs and
activated T-cells

Long peptides
(typically 15-24
amino acids)

Presents to
CD4+ T-cells

Antigens from
phagosomes
and ensodomes

21
Q

The T-cell receptor - binds what

A

Binds to peptide-MHC
(pMHC) complexes –
cannot recognise peptide
alone

22
Q

The T-cell receptor - diversity and structure

A

Huge diversity – potentially
up to 1 x 1013 different TCRs

Exists in a TCR complex
with accessory molecules
such as CD3

23
Q

T cell receptor and B cell receptor - Similarities to B cell receptor/antibody:

A 
Similarities to B cell receptor/antibody:
• Belongs to Ig superfamily
• Like Fab fragment of antibody
• Large diversity
• Single specificity
24
Q

T cell receptor and B cell receptor - Differences to B cell receptor/antibody:

A 
• Lower affinity
• Cannot be released
• No Fc fragment, so no cellular
functions
• Single rather than two binding sites
• B cell receptor/Ab: 5 classes
• T cell receptor: 2 classes (ab and gd)
25
Q

Mechanisms which generate B-cell receptor diversity (before/after AT stim)

A

Mechanisms which generate B-cell receptor diversity

Before antigen stimulation: Somatic recombination

After antigen stimulation: Somatic hypermutation

26
Q

Mechanisms which generate T-cell receptor diversity

before/after AT stim

A

Mechanisms which generate T-cell receptor diversity

Before antigen stimulation: Somatic recombination

After antigen stimulation: None

27
Q

T cell receptor diversity - Receptor gene rearrangement takes place during

A

Receptor gene rearrangement takes place during T-cell

development in thymus

28
Q

Three signal model of T-cell activation - list + compare them

A
  1. Peptide-MHC (pMHC) →
  2. Co-stimulation →
  3. Cytokines →

Signals 1 + 2 alone will activate a naïve T-cell, but Signal 3 is also
important for a strong response and also determining T-cell phenotype

29
Q

APC-T-cell interactions - describe signal one

A

The main signal (Signal One) is delivered from the APC by a

peptide-MHC complex to the TCR

30
Q

APC-T-cell interactions - describe signal two

A

The co-stimulatory signal (Signal Two) is delivered from the
APC by germline-encoded accessory receptors such as the ‘B7
family’ (CD80 and CD86) – although many of these receptors
are not fully characterised or understood

31
Q

APC-T-cell interactions - describe signal three

A 
Lastly, Signal Three is formed of cytokines secreted by the
APC to determine the T-cell phenotype.
• IL-12 promotes TH1 cells
• IL-4 promotes TH2 cells
• IL-23 promotes TH17 cells
32
Q

The immunological synapse - define

A

Complex interaction of many molecules – but simplistically Signals 1 and 2
are central, and surrounding integrins and accessory molecules help to
stabilise the interaction

33
Q

Negative regulators of antigen presentation provide

A

Negative regulators of antigen presentation provide an ‘immune
checkpoint’ to limit T-cell activation→HOMEOSTASIS

34
Q

Negative regulators of antigen presentation - important molecules

A

Two important molecules – CTLA4 (Cytotoxic T-Lymphocyte-Associated
Protein 4) and PD-L1 (Programmed Death-Ligand 1) are crucial for
dampening the T-cell response

35
Q

T-cells - explain positive selection

A

• T-cells arise from the thymus, which is a ‘school’ for T-cells.

T-cells are exposed to self-antigens and tested for reactivity

T-cells that can’t bind self antigen-MHC are deleted →
POSITIVE SELECTION

• These T-cells are useless because they won’t protect
against pathogens

36
Q

T-cells - explain negative selection

A

T-cells that bind self antigen-MHC too strongly are also
deleted → NEGATIVE SELECTION

• These T-cells are dangerous because they are too selfreactive

37
Q

the ‘master

controller’ of Regulatory T-cells (TREG) - define

A

In some models (STOCHASTIC MODEL), a proportion of Tcells that are strongly reactive to self-antigen will express
the transcription factor FOXP3, which is the ‘master
controller’ of Regulatory T-cells (TREG)

38
Q

the ‘master

controller’ of Regulatory T-cells (TREG) - function

A

Thymically-derived TREG that are reactive
for self-antigen can compete with any
autoreactive T-cells and secrete antiinflammatory cytokines

39
Q

IMMUNE EVASION - describe

A

Many organisms depend on human host for survival (‘obligate parasites’) –
need to co-exist with the host immune system → IMMUNE EVASION

40
Q

Mycobacterium tuberculosis - effects on immune system

A

• Up-regulates PD-L1 on APCs
to shut down T-cell activation
• Blocks MHC Class II expression via multiple
mechanisms

41
Q

Neisseria meningitidis - effects on immune system

A

• Blocks DC activation –
low CD40, CD86 and MHC Class I & II
expression

• Antigens (capsule) with homology to selfantigen, therefore anergic T-cells

42
Q

Neisseria gonorrhoeae - effects on immune system

A

Expresses Opa protein, which binds to T-cells
and induces tyrosine phosphatases that ‘switch
off’ key molecules involved in TCR signalling

43
Q

HIV - effects on immune system

A

• Up-regulates PD-1 on T-cells,
which antagonises TCR signalling

• Binds to DC-SIGN to suppress DC activation
via Rho-GTPases

44
Q

Herpes Simplex Virus (HSV) - effects on immune system

A

• Herpes Simplex Virus (HSV)
• Produce protein which binds to and
inhibits TAP
• Prevents viral peptide transfer to ER

45
Q

Adenovirus - effects on immune system

A 
Adenovirus
• Produce protein which binds MHC class
I molecule
• Prevents MHC class I molecule from
leaving ER

Fundamentals of P (62 decks)

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