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YR2: Immunology > Tolerance and Autoimmunity > Flashcards

Tolerance and Autoimmunity Flashcards

1
Q

What type of immune response is involved in autoimmunity?

A

Adaptive immune response with specificity for self antigens

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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 have 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 6 main factors that contribute to autoimmune disease?

A 
Genetic susceptibility  
Sex
Infections  
Diet
Stress
Microbiome
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5
Q

Why are autoimmune conditions chronic?

A

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 + 4)

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7
Q

What % of people affected by autoimmune disease are female?

A

~ 80% overall

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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

Autoantibodies against RBCs, which bind to RBCs + activate complement
Results in clearance + complement-mediated lysis of autologous RBCs

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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 BM in the glomerulus
Results in deposition of autoantibodies in the renal corpuscle + activation of complement leading to infiltration of inflammatory cells + kidney damage

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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 (damage more systemic)

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16
Q

What is the autoantigen in multiple sclerosis? What pathology results?

A

Myelin basic protein
Brain degeneration (demyelination)
Paralysis

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17
Q

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

A

Co-stimulation

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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

Early exposure to foreign antigens allows development of tolerance to those antigens

20
Q

Define immunological tolerance.

A

The acquired inability to respond to an antigenic stimulus

21
Q

3 A’s of immunological tolerance

A

Acquired : involves cells of acquired immune system + is “learned”
Antigen specific
Active process in neonates

22
Q

What are the 2 types of immunological tolerance?

A

Central Tolerance: occurs during lymphocyte development

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

23
Q

What are the 3 main mechanisms of peripheral tolerance?

A

Anergy
Active suppression (T regs)
Ignorance / immune privilege

24
Q

What are the 3 outcomes for T cells based on how strongly they bind to MHC in the thymus?

A

Useless: don’t recognise self MHC: die by apoptosis
Useful: associate weakly with self MHC
Dangerous: associate too strongly with self MHC: die by apoptosis

25
Q

What % of thymocytes survives selection?

A

5%

26
Q

What class of immunoglobulin are the B cell surface receptors?

A

IgD + IgM

27
Q

What happens to B cells that recognise soluble autoantigens?

A

They migrate to the periphery but don’t express normal levels of IgM + they are anergic (Not very responsive)
Eliminated with time

28
Q

What is the role of the AIRE transcription factor?

A

Important for low-level expression of a large variety of tissue specific self-peptides e.g. insulin in the thymus, against which T cells are selected

29
Q

What is APECED caused by?

A

Mutation in the AIRE transcription factor means T cells can’t be selected against for a wide range of self-peptides
Lots of self-reactive T cells get released into the circulation + can cause AI disease

30
Q

What is anergy caused by?

A

Presentation of an antigen in the absence of co-stimulation: this makes the lymphocytes enter a refractory state

31
Q

What is immunological ignorance caused by?

A

Occurs when antigen concentration is too low in periphery
Can be due to the absence of APCs- most cells in periphery are MHC class II negative
Occurs at immunologically privileged sites where the immune cells don’t normally penetrate e.g. eye, CNS
Ignorance: 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 + lymph nodes
Antigens are recognised by T cells, which become activated against the eye antigens
The T cells return to both eyes + cause damage

33
Q

What are the 4 main receptors expressed by Tregs?

A

CD4
CD25: IL-2 receptor, an important growth factor for T cells
CTLA-4: binds to B7 + sends a negative signal
FOXP3: essential transcription factor for T reg development

34
Q

What is IPEX caused by? List 3 symptoms

A 
Mutation in FOXP3 
Mutation in FOXP3 leads to accumulation of autoreactive T cells 
Early onset insulin dependent DM
Severe infections
Eczema
35
Q

What are the 2 types of Treg?

A 
Natural Tregs (nTregs): generated in thymus  
Inducible Tregs (iTregs): 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? (6 ways)

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 e.g. Th1 to Th2
Activation of APCs by pathogens leads to upregulation of costimulatory molecules
Tissue damage at immunologically privileged sites

37
Q

What mechanisms does the adaptive immune system use in autoimmune disease?

A

Same mechanisms as immune reactions against pathogens

38
Q

What does autoimmune disease involve breaking?

A

T-cell tolerance

39
Q

How does pregnancy influence inflammatory responses in autoimmunity?

A

There are more Th2 responses (rather than cell mediated)
Antibody mediated AI condition symptoms worsen
Cell mediated AI condition symptoms improve

40
Q

List 5 common autoimmune diseases

A 
Rheumatoid Arthritis
Type 1 Diabetes 
Multiple Sclerosis
SLE
Autoimmune thyroid disease
41
Q

Give 3 examples of Type 2 autoimmune disease

A

Pemphigus vulgaris
Graves disease
Goodpastures syndrome

42
Q

Give an examples of Type 3 autoimmune disease

A

SLE

43
Q

Where do B and T cells mature?

A

T cells: Thymus

B cells: Bone marrow

44
Q

Defects in which processes are associated with autoimmune disease?

A

Induction of tolerance: autoantibody production
Apoptosis: failure in cell death
Clearance of antigen: persistence of autoantigen

YR2: Immunology (5 decks)

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