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Y2 Immuno (MCD) > Tolerance and Autoimmunity > Flashcards

Tolerance and Autoimmunity Flashcards

1
Q

What type of immune response is involved in autoimmunity?

A

Adaptive immune response

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2
Q

Which cell type is always involved in autoimmunity?

A

Lymphocytes

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3
Q

What proportion of people has lymphocytes with the capability of recognising self-antigens?

A

ALL of us – this is normal autoimmunity

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4
Q

What are the three main factors that affect the transition from normal autoimmunity to autoimmune disease?

A

Genetic susceptibility
Infections
Environmental factors

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5
Q

Why are autoimmune conditions chronic?

A

Because self-tissue is always present

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6
Q

The effector mechanisms in autoimmunity resemble those of which type of immune reaction?

A

Hypersensitivity reactions (types 2, 3 and 4)

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7
Q

What proportion of people affected by autoimmune disease is female?

A

80% overall (this changes between diseases)

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8
Q

What is a possible reason for the increase in incidence of autoimmune disease?

A

Hygiene hypothesis

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9
Q

Describe the pathophysiology of autoimmune haemolytic anaemia.

A

There are autoantibodies against red blood cells, which bind to red blood cells and activate complement
This results in clearance and complement-mediated lysis of the autologous erythrocytes

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10
Q

What is a type II hypersensitivity reaction?

A

Antibody response against cellular or ECM antigens (insoluble antigens)

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11
Q

What is a type III hypersensitivity reaction?

A

Immune complex formation by antibody against soluble antigen

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12
Q

What is a type IV hypersensitivity reaction?

A

T cell mediated disease – delayed type hypersensitivity

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13
Q

What is Goodpasture’s syndrome?

A

Type 2 hypersensitivity reaction in which there are IgG antibodies against a type IV collagen found on the basement membrane in the glomerulus

This results in deposition of autoantibodies in the renal corpuscle and activation of complement leading to infiltration of inflammatory cells and kidney damage

NOTE: the inflammatory cells (e.g. neutrophils) bind to the Fc portion of antibodies via their own Fc receptors

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14
Q

How do type II and type III immune reactions recruit inflammatory cells?

A

Inflammatory cells are recruited via the binding of inflammatory cells to the Fc portion of antibodies via their Fc receptors

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15
Q

What is the main difference between type II and type III hypersensitivity reactions?

A

Type II – insoluble antigens

Type III – soluble antigens

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16
Q

What is the autoantigen in multiple sclerosis?

A

Myelin basic protein

17
Q

Other than antigen-TCR binding, what else is required for the activation of naïve T cells?

A

Costimulation

18
Q

What is the dominant genetic factor affecting susceptibility to autoimmune disease?

A

HLA (class II in particular)

19
Q

What did the freemartin cattle experiment show about tolerance?

A

It showed that early exposure to foreign antigens allows the development of tolerance to those antigens

20
Q

Define immunological tolerance.

A

The acquired inability to respond to an antigenic stimulus

21
Q

What are the main features of immunological tolerance?

A

‘The 3 As’
It is acquired
It is antigen specific
It is an active process in neonates

22
Q

What are the two types of immunological tolerance?

A

Central Tolerance = happens during lymphocyte development

Peripheral Tolerance = once we’ve developed mature lymphocytes, there are mechanisms to develop tolerance

23
Q

What are the three main mechanisms of peripheral tolerance?

A

Anergy
Ignorance
Regulation

24
Q

What are the three outcomes for T cells based on how strongly they bind to MHC in the thymus?

A

Useless = don’t recognise MHC at all – die by apoptosis

Useful = associate weakly with MHC - receive signal to survive

Dangerous – associate too strongly with MHC – die by apoptosis

25
Q

What percentage of thymocytes survives selection?

A

5%

26
Q

What class of immunoglobulin are the B cell surface receptors?

A

IgD and IgM

27
Q

What happens to B cells that recognise soluble autoantigens?

A

They will migrate to the periphery but they do not express normal levels of IgM and they are anergic (they are not very responsive)

28
Q

What is the role of the AIRE transcription factor?

A

It is important for the low-level expression of a large variety of self-peptides in the thymus, against which the T cells are selected

29
Q

What is APECED caused by?

A

Autoimmune polyendocrinolpathy candidiasis ectodermal dystrophy

Mutation in the AIRE transcription factor

This mutation means that the T cells can’t be selected against a wide range of self-peptides so lots of self-reactive T cells get released into the circulation and can cause autoimmune disease

30
Q

What is anergy caused by?

A

The presentation of an antigen in the absence of costimulation – this makes the lymphocytes enter a refractory state

31
Q

What is immunological ignorance caused by?

A

Occurs when the antigen concentration is too low

It can be due to the absence of antigen presenting molecules e.g. most cells in the periphery are MCHII negative so can’t present to CD4+ T-cells

It occurs at immunologically privileged sites where the immune cells don’t normally penetrate

This is ignorance – the T cells never see their antigen

32
Q

Give an example of a failure of ignorance.

A

Sympathetic ophthalmia

Damage to the eye can release eye antigens into the lymphatics and lymph nodes

These antigens are recognised by T cells, which become activated against the eye antigens

The T cells then go back to both eyes and cause damage

33
Q

What are the main receptors expressed by Tregs?

A

CD4
CD25 –IL-2 receptor, which is an important growth factor for T cells
CTLA-4 – binds to B7 and sends a negative signal
FOXP3 – essential transcription factor for Treg development

34
Q

What is IPEX caused by?

A

Mutation in FOXP3
FOXP3 encodes a transcription factor that is critical for the development of T regs
A mutation in FOXP3 leads to the accumulation of autoreactive T cells

35
Q

What are the two types of Treg?

A 
Natural Tregs (nTregs) – these are generated in the thymus  
Inducible Tregs (iTregs) – these are produced as part of the normal T cell response as a mechanism of dampening down an immune response after it has happened
36
Q

How can infections affect tolerant states?

A

Molecular mimicry of self-molecules
Induction of costimulatory molecules or inappropriate MHC class II expression: pro-inflammatory environment
Failure of regulation: effects on Tregs
Immune deviation: shift in type of immune response
Activation of APCs by pathogens leads to upregulation of costimulatory molecules

37
Q

What is a key feature in all autoimmune diseases?

A

Breaking T-cell tolerance

Y2 Immuno (MCD) (5 decks)

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