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PoM - Principles of Medicine Week 2 > Lymphocytes > Flashcards

Lymphocytes Flashcards

1
Q

What does the immune system do?

A

Recognise self from non-self, then work to only kill the non-self

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2
Q

Where do lymphocytes come from?

A

Starts off in the bone marrow - from a common lymphoid progenitor

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3
Q

What is adaptive immunity?

A

2 broad responses - humoral and cell mediated
Made up of B cells and T cells, a specific response against a foreign body / antigen - takes time to develop
Gives memory and protection against recurring infections
Can help clear the infection due to the specificity (unlike innate which controls it i.e. stops it from spreading etc.)

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4
Q

Why is adaptive immunity important / necessary?

A

To fight off recurring infections - improves efficacy
Primary immune response, requires time and high activation energy e.g. to find the right variable region to initiate complement cascade, and more damage to the host
However, once the memory cells develop, an immune response from memory cells require a lower activation energy to clear the pathogen, therefore is quicker and much larger production of immune cells
Kinetically, useful
And clears pathogen before it can cause serious harm

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5
Q

What is the condition called where children have primary immunodeficiency, where they lack adaptive immunity?

A

SCID - must be very protected

Very susceptible to infections

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6
Q

How is immunological memory used medically?

A

Vaccines - long term immunity against many common / deadly infections

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7
Q

What are the 2 types of adaptive response?

A

Humoral - B cells, make antibodies

Cell mediated - T cells, cytokines, killing

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8
Q

What is an antigen?

A

Unique fingerprint of the pathogen / foreign body that the adaptive immune system sees and recognises
They can be proteins or polysaccharides
So molecules that act to induce an immune response

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9
Q

What is an epitope?

A

The region (small molecular protein) on the antigen to which the T or B cell binds to

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10
Q

What are the 2 types of epitope that the immune system recognises?

A

Structural and Linear

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11
Q

Which epitope does the B cell recognise?

A

3D structures i.e. how the protein folds in space into shape (tertiary structure)
B cells and antibodies recognise structural epitopes

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12
Q

Which epitope does the T cell recognise?

A

Linear

Recognise the primary structure of the protein i.e. the sequence of amino acids

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13
Q

Using the knowledge that antibodies and B cells recognise tertiary structures, explain why vaccines are always stored in cool areas?

A

A B cell or antibody will not recognise an epitope if the protein is linearised
Therefore, is the antigens in a vaccine denature due to high temperatures, a different set of Abs will be made to fit the structure of the denatured antigens rather than the ones present on the actual pathogen
The vaccine then cannot serve its purpose

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14
Q

Normally in a blood sample, how do the B or T cells exist?

A

In a random array - each B or T cell will have a different gene coding for it as there is great diversity of the receptors

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15
Q

Why is there such a great diversity of T and B cell receptors in the blood?

A

The pathogen exists, it is the body’s job to find the right B / T cell receptor combination that is complementary to the pathogen’s antigens

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16
Q

What triggers the activation of a T or B cell?

A

The interaction with its cognate antigen
Causes clonal expansion - the T or B cell that recognises its complementary antigen is activated, so it divides and differentiates to carry out further immune functions

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17
Q

During an infection, in a blood sample, how do the T or B cells exist?

A

Now, mainly that specific one B or T cell that is present as it is dividing and expanding to clear the infection / invading pathogen

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18
Q

What are the downstream effects of the measles infection? (i.e. which type of cells do measles affect and what are the consequences?)

A

Measles virus infects B cells, hence Abs produced kill many B cells, losing many combinations of genes that code for different / specific shapes of antigens (lose diversity)
More likely to die from secondary infection many years later due to loss of recognition

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19
Q

What is an issue with forming many different receptors to recognise many different antigens?

A

May form a receptor site that is complementary to a self-antigen
Causes autoimmune disorders - immune system recognises epitopes on self rather than on pathogens

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20
Q

How is the variable region on the Ab determined?

A

The gene that codes for the specific BCR (B cell receptor) on the surface, is the same to code for the shape of the variable region on the Ab
BCR gives unique mRNA for a unique antibody

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21
Q

How many unique variable sites on antibodies can the body theoretically make?

A

10 ^10

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22
Q

How does the body develop such a huge range / diversity of BCRs?

A

Immunoglobulin gene rearrangement
The separate multigene families on different chromosomes coding for the 3 different chains (kappa, lamda and heavy) on the BCR are can recombine

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23
Q

An antibody has light chains and heavy chains, how is it manufactured genetically?

A

The looping of 2 different genes - one set to make the V (variable) region, one set to make the J (joining) region

24
Q

What on the T cell recognises pathogens?

A

TCR (T cell receptor) - recognises linear epitopes, fragments of the antigen proteins produced by other cells

25
Q

What occurs when the T cell sees it’s specific antigen?

A

Receptor clustering - bring other T cell receptors together

Undergoes intra-cellular signalling (signalling inside the cell)

26
Q

How does the T cell see their antigen?

A

Via the Major Histocompatibility Complex (MHC) which is present on antigen presenting cells / target cells

27
Q

Features of the MHC:

A

Encoded by the HLA genes in humans
Important in surgery and donor matching (close HLA family as possible for bone marrow transplants)
Polygenic - several genes for different classes
Co-dominant - both, maternal and paternal are equally expressed

28
Q

What are the 2 classes of MHC and their features?

A

Class I - all nucleated cells present this

Class II - only antigen presenting cells present this e.g. dendritic cells

29
Q

Why is it important for all nucleated cells to present MHC I and how does it do this?

A

They help the immune system distinguish between self and non-self cells
It constantly produces and presents antigens on its cell surface of the proteins it is currently manufacturing
i.e. constantly flagging up what it is making

30
Q

How does this help distinguish between self and non-self cells?

A

E.g. if a virus infects a cell, they make viral proteins, which are expressed / presented on MHC I and recognised as foreign by T cells
Initiates immune response

31
Q

What do MHC II molecules do?

A

They present linear epitopes i.e. dendritic cells engulf foreign material, digest, and present a fragment (e.g. 10 amino acids) on its surface on the MHC II receptor site

32
Q

What are the 2 types / families of T cells?

A

CD4 - helper cells i.e. depending on what type of infection, signals the next steps of the immune response
CD8 - killer cells

33
Q

Which type of T cell does the MHC I complex communicate with?

A

CD8 cells - when a cell is not presenting self proteins on the MHC I receptor site, they are killed

34
Q

Which type of T cell does the MHC II complex communicate with?

A

CD4 cells

35
Q

Key differences between MHC I and MHC II

A

MHC I - takes up intra-cellular material, processed in cytosol, and presents it to CD4
MHC II - takes up extra-cellular material, processed in endosomes, and presents in to CD8

36
Q

What are the CD8 cells and what do they do?

A

Cytotoxic T cells - killer cells
Important in controlling viral infections and cancers
Recognise non-self / pathogenic cell, and kill it

37
Q

What are the mechanisms of cytotoxic killer cells to kill a cell?

A
  1. Perforin - punctures holes in the cell membrane, affecting cell membrane integrity and so, osmosis
  2. Granzymes - inject this to induce apoptosis (as the cell will collapse in on itself, unlike necrosis, which may cause the cell to burst and so release viral proteins into the blood etc.)
38
Q

Why is CD8 important in cancer therapy?

A

It aims to re-activate the CD8 cells - so they are able to recognise the ‘bad’ cells i.e. cancer cells, and kill them

39
Q

What do CD4 cells do?

A

Produces cytokines
Depending on the infection e.g. bacterial, parasitic, viral etc. shape the immune response by releasing specific cytokines to activate different parts of the immune response

40
Q

What do cytokines do?

A

Signalling molecules for cells to talk to each other that help determine the way T cells activate and differentiate

41
Q

What type of cell produced Abs?

A

B cells, that divide into plasma cells

42
Q

What are antibodies?

A

Highly specific - recognise a very specific antigen structure
Made of a light chain (With a variable region) and a heavy chain (that determines the functionality)

43
Q

Where do the classes of Abs arise from?

A

The change in the heavy chain, class is dependent on the heavy chain of the Ab

44
Q

What are the 5 classes of Abs?

A

IgG - most common (standard)
IgA - mucosal Ab, anti-inflammatory by stopping gut bacteria getting too close to the body and inducing an immune response
IgE - helps prevent parasitic infections (and also role in allergies)
IgM - initial antibody cells first make (less specific in funcitonality)
IgD

45
Q

What are the 3 core protective functions of Abs?

A
  1. Neutralisation - stop pathogens from entering cells e.g. Ab binding and covering the receptors on viruses that are complementary to the host cell receptor so they can no longer bind and enter the host cell
  2. Opsonisation - Signalling to phagocytes to take up the pathogen and digest it
  3. Complement cascade - can lead to bacterial cell death
46
Q

What are the 2 roles of the effector B cells in humoral immunity?

A
  1. Secrete Abs

2. Generate memory cells for long term immunity

47
Q

Where do B cells come from? (Process)

A

Stem cells in bone marrow
Derived from progenitor B cell - contains proto-BCRs (i.e. all the different genes available)
Genes are shuffled around and matures into a mature B cell which has a single BCR
Can only make one specific Ab

48
Q

What is the BCR?

A

Surface bound antibody - the gene that encodes for the BCR also encodes for the Ab (so the have the same shaped binding region)

49
Q

What does the binding of the BCR to its complementary antigen do?

A

Activates mass generation of Abs

50
Q

How is the BCR activated?

A

Complementary antigen

An accessory signal - either directly on the microbial constituents or on the T helper cell

51
Q

What is it called when the BCR is activated by the microbial constituents?

A

Thymus independent (B cells)

52
Q

What are the features of thymus independent B cells?

A

Only make IgM
No class switch
No memory

53
Q

How do the thymus independent B cells work?

A

Directly activated without the help of T cells
Second signal - often via e.g. long (repetitive), bacterial polysaccharide molecule - bind to the BCR, crosslinks hence activates the cell
Signalling cascade activated

54
Q

How strong is this thymus independent activation?

A

Weak, fairly ineffective

55
Q

What is the more common B cell pathway / activation called?

A

Thymus dependent

56
Q

What are the features of thymus dependent B cells?

A 
Leads to immune memory
Form all Ig class types
57
Q

How does the thymus dependent pathway work?

A

Pathogen inside host
Pathogen taken up by antigen presenting cell e.g. dendritic cell and B cell
Dendritic cell takes up any (non-specific) extra-cellular material, B cell only takes up the complementary material to their BCR
Both present the antigen fragments on the MHC II receptor on their surface
Dendritic cell activates CD4 T helper cell (as it recognises molecule in the context of the MHC II molecule)
Activated CD4 communicates with B cell, leading to Ab production, class switch etc.

PoM - Principles of Medicine Week 2 (12 decks)

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