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BM 212: Introduction to Immunology > Block C Lecture 4: Tolerance > Flashcards

Block C Lecture 4: Tolerance Flashcards

1
Q

What can the adaptive immune system generating a diverse range of antigen-specific cells potentially result in?

A

These cells recognising self-antigens
(Lecture 4, Slide 6 )

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2
Q

How does the immune system prevent antigen-specific cells by recognising self-antigens?

A

Selection in the thymus
(Lecture 4, Slide 6)

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3
Q

What is central tolerance?

A

Deletion of inappropriate T cells through positive and negative selection in the thymus
(Lecture 4, Slides 6 and 7)

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4
Q

What is thymic selection dependant on?

A

The affinity of the TCR for MHC receptors
(Lecture 4, Slide 7)

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5
Q

What occurs in positive selection in the thymus?

A

T cells which don’t have enough affinity for MHC receptors don’t receive a “survive signal” and undergo “death by neglect”
(Lecture 4, Slide 7)

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6
Q

What does positive selection in the thymus select for and what does this ensure?

A

T cells with a TCR of moderate / high affinity for MHC, ensuring T cells can recognise MHC and antigens in the periphery
(Lecture 4, Slide 7)

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7
Q

What does negative selection in the thymus removes and what does it ensure?

A

It removes T cells which bind too strongly, ensuring self-reactive T cells are clonally deleted
(Lecture 4, Slide 7)

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8
Q

What happens to T cells that fail negative selection?

A

They undergo apoptosis
(Lecture 4, Slide 8)

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9
Q

What is the problem with negative selection?

A

It ensures T cells do not have high affinity for self-antigens presented by MHC, but not all antigens are presented in the thymus, meaning some T cells which are self-reactive to antigens in other parts of the body could slip through
(Lecture 4, Slide 9)

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10
Q

What is required on top of negative selection to ensure T cells are not self-reactive to any antigen in the body?

A

Peripheral tolerance mechanisms
(Lecture 4, Slide 9)

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11
Q

What do peripheral tolerance mechanisms ensure?

A

That mature T cells don’t activate inappropriately (such as to self-antigens)
(Lecture 4, Slide 10)

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12
Q

How do peripheral tolerance mechanisms ensure mature T cells don’t activate inappropiately?

A

T - cells need multiple signals to activate (recognition of antigen via TCR-MHC complex, presence of CD4, co-stimulatory molecules and eventually cytokines) and won’t activate without one of these signals being present
(Lecture 4, Slide 10)

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13
Q

What can co-stimulatory molecules (such as B7.1) interact with, instead of interacting with CD28?

A

CTLA-4
(Lecture 4, Slide 11)

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14
Q

What is CTLA-4?

A

An immune checkpoint
(Lecture 4, Slide 11)

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15
Q

Why is the fact that CTLA-4 can bind more strongly with B7 than CD28 important?

A

As binding to CTLA-4 can turn off an activated T cell, whereas CD28 activates a T cell, so the turn off mechanism needs to be stronger than the turn on mechanism to prevent inappropriate immune responses
(Lecture 4, Slide 11)

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16
Q

Other than T Cells needing multiple signals to become active, what is another peripheral tolerance mechanism?

A

Induction of Treg cells
(Lecture 4, Slide 12)

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17
Q

How do regulatory T cells (Tregs) work?

A

By secreting Interleukin 10 (IL-10) and transforming growth factor beta (TGF-ß)
(Lecture 4, Slide 12)

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18
Q

What do regulatory T (Treg) cells do to self-reactive T cells?

A

They inhibit them to prevent them from continuing to respond inappropriately
(Lecture 4, Slide 12)

19
Q

What do regulatory T (Treg) cells often play an important role in?

A

Regulating immune response after an infection has been cleared
(Lecture 4, Slide 12)

20
Q

What do central and peripheral tolerance do?

A

Central tolerance removes self-reactive T cells in the thymus
Peripheral tolerance mechanisms counteract cells which are responding inappropriately by turning these cells off - but not deleting them
(Lecture 4, Slide 13)

21
Q

What is antigen segregation?

A

Antigens being separated or distributed within different cellular or tissue compartments
(Lecture 4, Slide 15)

22
Q

What is an example of antigen segregation?

A

T cells and dendritic cells not be able to cross the blood brain barrier (BBB) and therefore being unable to come into contact with antigens in the central nervous system (CNS)
(Lecture 4, Slide 15)

23
Q

Under what conditions can T cells and dendritic cells gain access through the blood brain barrier (BBB)?

A

Due to infection or injury in the brain
(Lecture 4, Slide 15)

24
Q

How can T cells and dendritic cells entering the blood brain barrier (BBB) end up being harmful?

A

By granting them access to self-antigens they could potentially react with
(Lecture 4, Slide 15)

25
Q

When can activation induced cell death via apoptosis occur?

A

When a large number of cells are activated simultaneously
(Lecture 4, Slide 16)

26
Q

What protein may T cells increase the expression of following activation?

A

Fas proteins
(Lecture 4, Slide 16)

27
Q

What are Fas proteins?

A

The target of a Fas ligand, an apoptotic mediator
(Lecture 4, Slide 16)

28
Q

How can T cells cause allergy?

A

If a T cell escapes clonal deletion in the thymus and isn’t tolerised in the periphery, it can become active to non-harmful antigens, causing allergy
(Lecture 4, Slide 18)

29
Q

What is celiac disease?

A

When antibodies are produced against harmless gluten in wheat, with the resultant inflammatory response in the gut causing gut damage - known as “enteropathy”
(Lecture 4, Slide 18)

30
Q

What 3 ways is the gut damaged in celiac disease?

A

Villi responsible for nutrient absorption are lost, the epithelium becomes leaky and there is an increased number of goblet cells which produce mucus
(Lecture 4, Slide 18)

31
Q

What is asthma?

A

A decrease in the diameter of the airway caused by a build-up of immune cells and the increased muscle concentration that pinches the airway and restricts air flow
(Lecture 4, Slide 19)

32
Q

What occurs when the body responds to self-antigens?

A

Autoimmunity
(Lecture 4, Slide 20)

33
Q

How is autoimmunity usually categorised?

A

Into organ-specific or systematic categories
(Lecture 4, Slide 20)

34
Q

What 3 things determines whether you generate an autoimmune or allergic response?

A

The right genes and environmental exposure and infection
(Lecture 4, Slide 22)

35
Q

What percent of humans carry the gene that predisposes (makes us liable) to allergy and how many people develop these?

A

Around 40% of us carry this gene with few people developing it
(Lecture 4, Slide 22)

36
Q

What is ankylosing spondylitis?

A

An autoimmune condition against MHC receptors
(Lecture 4, Slide 22)

37
Q

Under what conditions is a person likely to develop ankylosing spondylitis?

A

A person harbouring the gene that makes a person liable to ankylosing spondylitis and them being infected with the bacterium shigella
(Lecture 4, Slide 22)

38
Q

Why does a person harbouring the gene making them liable to ankylosing spondylitis and being infected with the shigella bacterium make them likely to develop ankylosing spondylitis?

A

It is likely due to the degree of cross-relativity by also because of innate activation triggers danger signals which triggers increased co-stim expression which can lead to more T-cell activation
(Lecture 4, Slide 22)

39
Q

What percentage of T-cells are deleted in central tolerance as a result of failing either positive or negative selection?

A

95%
(Lecture 4, Slide 23)

40
Q

Why does peripheral tolerance usually work?

A

As danger signals are lacking - no PAMPs or DAMPS resulting in no upregulation of costimulatory molecules - resulting in T cells being anergic - not reacting to antigens (their default state)
(Lecture 4, Slide 23)

41
Q

What is a primary immunodeficiency?

A

A genetically acquired immunodeficiency
(Lecture 4, Slide 24)

42
Q

What are 3 things that can result in secondary (non-genetically acquired) immunodeficiencies?

A

Infections (like HIV)
Metabolic dysregulation
Therapy (such as chemotherapy)
(Lecture 4, Slide 24)

43
Q

How does the trypanosome parasite evade the immune system?

A

They have an antigen coat of them called the variant surface glycoprotein (VSG) and they have the ability to recombine these to produce many different forms of VSG, much like our immune system, and once our immune system recognises its VSG, they start to recombine them to make a new VSG, allowing the parasite to stay one step ahead of our immune system
(Lecture 4, Slide 25)

44
Q

What 3 things are needed to achieve immunological homeostais?

A

The right response, at the right time, in the right place
(Lecture 4, Slide 26)

BM 212: Introduction to Immunology (13 decks)

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