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SEM 4: Immunology > Development of Lymphocytes > Flashcards

Development of Lymphocytes Flashcards

1
Q

What are the cells in the innate immune system?

A
  • Neutrophils
  • Monocytes
  • NK cells
  • Basophils
  • Eosinophils
  • Macrophages
  • Tissue cells and endothelial cells (not immune cells necessarily)
  • Platelets (not immune cells necessarily)
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2
Q

What are the cells in the adaptive immune system?

A
  • B cells
  • T cells
  • Plasma cells
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3
Q

What may happen when a person doesn’t have lymphocytes?

A
  • Paraesthesia in the head and arm (numbness and tingling/0
  • MRI shows area of oedema caused inflammation
  • Ring enhancing vascular permeability
  • Ring of inflammation, with ring of swelling
  • Infection of the brain
  • Likely have a toxoplasma infection
  • Low CD4 count has allowed an opportunistic infection to get through the immune defences
  • Patient is given anti-viral treatment for toxoplasmosis and is doing well
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4
Q

Which cells do primary/secondary lymphocyte deficiency affect?

A

B cells or T cells

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5
Q

What are the lymphocyte deficiencies that can occur in B cells?

A
  • Congenital agammaglobulinemia: lose the Ig
  • Common variable immunodeficiency
  • May be due to side effects of certain drugs such as Rituximab
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6
Q

What are the lymphocyte deficiencies that can occur in T cells?

A
  • Severe combined immunodeficiency (SCID)
  • DiGeorge syndrome
  • Acquired HIV, chemotherapy/novel biologics
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7
Q

Define a lymphocyte

A

A white blood cell part of the adaptive immune response either a T cell or B cell.

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8
Q

What is the morphology of a lymphocyte?

A

Small cell with a large nucleus

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9
Q

What is the functions of lymphocytes?

A
  • A helper cell
  • A cytotoxic cell
  • A regulatory cell
  • Etc
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10
Q

What are the specifities of a lymphocyte?

A

It has specificity which can be which type of antibody it produces or, what epitope it recognises via the TCR which can be different. It can produce different cytokines

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11
Q

What are the two key features of adaptive immunity?

A

Specificity and memory

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12
Q

What is the specificity of B cells?

A
  • One cell will produce one Ig.
  • The Ig may have class switch (go from IgM to IgG), but it will always be the same basic Ig.
  • It may undergo affinity maturation.
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13
Q

What is the specificity of T cells?

A
  • One cell will have one TCR receptor and recognise one antigen.
  • There will selection and expansion of that clone
  • This will lead to retention in memory of the clonal progeny
  • Leads to continued production of antibodies and a more rapid specific response.
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14
Q

How is specificity of the adaptive lymphocyte achieved?

A

This is done due to the hypervariable region on the TCR, meaning there is diversity between the binding region of each T cell and therefore more specific to the antigen.

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15
Q

How does the immune system predict the infection?

A
  1. Whether it looks like a foreign body: pathogens display generic recognisable features (PAMPs and TLRs) which allow the immune system to recognise them as foreign etc
  2. If the presence is associated with damage: the danger hypothesis meaning whether the pathogen will lead to tissue damage producing DAMPs which the immune system will be able to recognise.
  3. Previous exposure to pathogen: memory cells against previous infection.
  4. Recognising non-self: attacking accordingly based on what is self and non-self. If this goes wrong, it leads to autoimmune diseases.
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16
Q

How does the immune system predict pathogens that are unknown?

A

Through the huge diversity between TCRs and BCRs; this means that by chance one of them should be complementary to the antigen. However, this might have some issues.

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17
Q

What are the issues with the immune system trying to predict unknown pathogens?

A
  • The response will be delayed, this is why the primary response is slow.
  • Might miss some pathogens if the TCR/BCR is not complementary
  • May lead to self-recognition as enemy
18
Q

How does the immune system recognise cancer cells?

A

It is harder for the immune system to detect because cancer cells are still self-cells.

  1. Cancer cells express cell signals such as MHC.
  2. The immune system is able to recognise these signals and express signals but only specific to cancer cells.
19
Q

Describe the binding of TCR-MHC peptide binding

A
  1. MHC I molecule binds to the antigen peptide via its groove.
  2. It expresses it on the surface for CD8 T cells. Every cell will express MHC I.
  3. MHC II molecule binds to the antigen peptide via it’s groove and expresses it on the surface for CD4 T cell.s
20
Q

How is thymic selection carried out?

A

This is done via positive selection and negative selection in the thymus. T-cells are trained to recognise antigens and not self-cells, they need to be active but not overreactive or underactive.

21
Q

What is positive selection of B cells?

A
  1. This is the ability of the T cell to bind to MHC molecules.
  2. Therefore, during positive selection, the T cells are checked for their ability to bind to MHC molecules.
  3. If they can’t they are neglected and killed.
22
Q

What is negative selection of T cells?

A
  1. Once the cells pass positive selection, they undergo negative selection.
  2. This is the ability of the T cell not to bind to self-peptides.
  3. Cells in the thymic medulla express specific tissue antigen such as oesophageal.
  4. For the T cells to pass negative selection, they need to NOT bind to those antigens.
  5. If they bind, they are neglected and killed.
  6. Once all this process is passed an array of naive T cells is set up because they haven’t met antigens yet.
23
Q

What happens in the B cell repertoire selection process?

A

Positive selection, receptor editing and negative selection

24
Q

What is the positive selection of B-cells?

A

B cells don’t recognise MHC because it is not their job.

  1. Positive selection is used to identify the B cells which have completed their antigen receptor gene rearrangment successfully.
  2. This means that only B cells which express functional membrane Ig molecule (BCR) receive constitutive BCR derived signals.
  3. These signals are required to keep the immature B cells alive.
25
Q

What is the selection process of receptor editing in B cells?

A
  1. Some of these immature B cells will be able to bind to self-peptides, and so they will undergo recepto editing.
  2. This is when they change the BCR specificity so that the receptor can no longer bind to self-peptides
  3. This is done via reactivation of the gene RAG and the rearrangement and production of new Ig light chain, so the receptor is different/edited.
  4. If this process fails to stop the B cell from binding to self-peptide, then rearrangement in the lambda chains will occur.
26
Q

What is the negative selection of the B-cells?

A
  1. If receptor editing fails and the B cell still binds to self-peptides , it will die by apoptosis in the bone marrow or spleen.
  2. Once all this process is passed and the transition is made to the IgM and IgD mature cell stage, antigen recognition leads to proliferation and differentiation of B cells.
27
Q

What happens to the T cells after they leave the thymus?

A
  1. Once the naive cells have been made, they recirculate from the blood to the lymphn nodes.
  2. There is an array as it is not known yet which one is needed.
  3. Therefore, it’s important to know how long they survive.
28
Q

How are lymphocytes labelled in vivo with deuterium-labelled glucose?

A
  1. Give a patient glucose or heavy water labelled with deuterium. This allows it to be picked up on the mass spectrometer.
  2. Then, take the T cells out and if they have been dividing during the period, the label should be picked up in the T cells.
29
Q

Why are lymphocytes labelled?

A

To fine out information on naive cells

30
Q

What does lymphocyte labelling show? Why are naive cells called ‘sleeping beauties’?

A
  • If there is little labelling of naive cells:
    • > Indicates a very slow turnover in peripheral blood. This is because naive cells do not divide until they are exposed to antigen.
    • > This is why naive cells are known as ‘sleeping beauties’ of the peripheral blood.
31
Q

Describe the T cell differentiation steps

A
  1. Once the naive cells encounter the antigen, a number of steps occur which involve switching on genes that proliferate the cell, activate it and trigger the amplification cascade.
  2. The amplification process only requires small amounts of the precursor cells are needed to make a lot of effector cells.
32
Q

What are T effector memory cells (TEM)?

A
  • Short lived
  • Continually replenished
  • Doubling time is 15 days
33
Q

What are T central memory cells (TCM)?

A
  • Turnover at a significant rate

- Doubling time in 48 days

34
Q

What are T regulatory cells (Treg)?

A
  • Short lived population
  • Need continual replenishment
  • They prevent overactivation of the immune response
35
Q

What is immunological memory?

A
  • The proliferation to disappearance rate
  • Immunological memory is flexible and changing all the time because we are exposed to different pathogens all the time
  • Long term memory is able to reside in short lived cells due to the formation of clones of that cell
36
Q

What are the concepts of immunological memory?

A
  • Acquired cumulatively over time
  • Stored for future use
  • Readily available when required
  • Dynamic process
37
Q

What happens when B cells develop?

A

Activated B cells transform into plasma cells

They are antibody factories and also produce CD27+ memory B cells

38
Q

What is the anatomy of lymph and lymphocytes?

A

Organised mainly into lymph nodes to optimise the facility for cellular interaction

39
Q

What is the role of the spleen in antibody generation?

A

Splenectomy increases the risk of infection

Especially in pneumococcal infection

40
Q

What is the importance of tissue resident T cells?

A

Important in patrolling and acute responses

41
Q

What is immune senescence?

A

The lymphocyte function deteriorates with age:

  • this is the age of the cell and age of the individual
  • telomers shorten
  • change in functional attributes
  • accumulation of CD57+ cells
42
Q

Which infection is the key driver for immune senescence?

A

CMV

SEM 4: Immunology (15 decks)

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