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Y2 MECHANISMS OF DISEASE > Autoimmunity & Immunodeficiency > Flashcards

Autoimmunity & Immunodeficiency Flashcards

1
Q

Why does the immune system need to be tightly regulated?

A

It has to deal with threats from outside the body as well as internal threats

e.g. cancer cell surveillance

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2
Q

Why can severe burns make someone more susceptible to infection?

A

The skin provides a barrier to prevent pathogen entry

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3
Q

What are the main cellular components of the innate immune system?

A
  1. neutrophils
  2. complement & PRRs
  3. dendritic cells
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4
Q

What are the 3 main characteristics of the innate immune system?

A
  1. it is pre-programmed
  2. it has no memory
  3. it is triggered within seconds
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5
Q

What is the role of pattern recognition receptors (PRRs)?

A

They inform the immune system about the type of threat

e.g. bacterial, viral, etc.

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6
Q

What is the role of the dendritic cells and macrophages in the innate immune response?

A

They inform the adaptive immune system about they type of threat that is present

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7
Q

What is the role of the antigen presenting cells in the innate immune system?

Which cells are these?

A

Dendritic cells & macrophages/monocytes

They engulf debris and microorganisms, digest them and present the antigen on their cell surface

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8
Q

What are the types of phagocytes in the innate immune response?

What is their role?

A

They engulf and destroy pathogens

Macrophages and neutrophils

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9
Q

What are the granulocytes that are part of the innate immune response?

A
  1. neutrophils
  2. eosinophils
  3. mast cells
  4. basophils
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10
Q

What are the 3 types of proteins that are part of the innate immune system?

A
  1. cytokines
  2. complement
  3. acute phase proteins
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11
Q

What is the role of cytokines in the innate immune system?

A

they are chemical signals that modulate cell activity or attract cells (chemokines)

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12
Q

What is the role of acute phase proteins in the innate immune system?

A

They opsonise or present pathogens to the immune system

They coat the pathogen to make it more visible to the immune system

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13
Q

What is the most commonly measured acute phase protein?

A

CRP

It is measured as a marker of inflammation

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14
Q

What is the role of complement proteins in the innate immune system?

A

It is a cascade of proteins with multiple functions

e.g. opsonisation, killing, activation, chemoattraction

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15
Q

What are the cells of the adaptive immune system?

A

B cells, T cells and high affinity antibodies

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16
Q

What are the 3 characteristics of the adaptive immune response?

A
  1. highly tailored to infction
  2. it has memory
  3. it takes 4-6 weeks
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17
Q

What is meant by the Th1 response?

A

cytotoxic T cells directly destroy infected cells

there is less need for antibodies

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18
Q

What is meant by the Th2 response?

A

Many antibodies are produced for opsonisation of extracellular pathogens

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19
Q

What is the main difference between the Th1 and Th2 responses?

A

Th1 response targets intracellular pathogens

Th2 response targets extracellular pathogens

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20
Q

What is produced if there is no dangerous signal associated with tissue damage when the naive T cell comes into contact with an APC?

A

Regulatory T cells

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21
Q

What are the 3 categories that can influence autoimmune diseases?

A
  1. genetic background
  2. environment
  3. immune regulation
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22
Q

Why do autoimmune diseases tend to be more common in women?

A

There are a number of immune chains on the X chromosome

2 copies in a woman can lead to a higher degree of autoreactivity

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23
Q

In which locations are B and T cells generated?

A

B cells - bone marrow

T cells - thymus gland

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24
Q

How does the molecular structure of pathogens compare to that of our body?

A

Many pathogens have molecular structures that are similar to structures found in the body

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25
Q

What is meant by negative selection of T cells?

A

If the MHC molecules of T cells show a high degree of engagement with self-proteins, they are destroyed

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26
Q

What is a crucial factor in deciding whether a T cell can survive or not?

A

The T cells must be able to engage their T cell receptors (they must be working)

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27
Q

Why do all T cells released from the thymus have some degree of autoreactivity?

A

The only way to check that the T cell receptor is working is to check it against self proteins

All T cells may recognise some native proteins

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28
Q

How may a B or T cell develop a higher degree of autoreactivity?

A

Through somatic hypermutation

This can lead to development of a clone with a high degree of autoreactivity

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29
Q

What happens in the periphery to ensure there are no autoreactive cells present?

A

If there is engagement between an APC that is NOT carrying a harmful antigen and a T cell, T cell anergy occurs

The T cell becomes a peripheral regulatory T cell

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30
Q

What are the 3 categories of factors that have a causative association with autoimmunity?

A
  1. sex hormones
  2. age
  3. environmental triggers
31
Q

How does age affect development of autoimmune conditions?

A

autoimmunity is more common in the elderly

the immune system becomes less effective with age as B and T cells shrink

32
Q

What are the 3 main environmental triggers for autoimmune diseases?

A
  1. infection
  2. trauma tissue damage
  3. smoking
33
Q

How can infection trigger an autoimmune response?

A

Infection may cause a clone of a T cell to proliferate

The T cell has the ability to recognise both self proteins and pathogen proteins

Some pathogen proteins are very similar to self proteins and can trigger an autoimmune response

34
Q

What is meant by the shared epitope of rheumatoid arthritis patients?

A

Most rheumatoid arthritis patients have a certain type of HLA molecules - HLADRB51

35
Q

How do HLA molecules vary between individuals?

A

Everyone has a different HLA makeup, allowing them to respond to a variety of pathogens

36
Q

What is the role of a HLA molecule?

What does it stand for?

A

human leukocyte antigen

it encodes cell surface molecules that present antigenic molecules to the T cell receptor

37
Q

How can HLA molecules make someone more prone to rheumatoid arthritis?

A

Depending on HLA make-up, someone may be more likely to present self antigens to the immune system and initiate an autoimmune response

38
Q

What is significant about the HLADRB51 phenotype in rheumatoid arthritis?

A

Having this phenotype allows you to present citrullinated peptides

The body is more likely to see citrullinated peptides as foreign and start an autoimmune response against them

39
Q

How can smoking and obesity influence rheumatoid arthritis?

A

You are more likely to produce citrullinated peptides

40
Q

What is the role of the CTLA4 protein?

A

It moderates the amount of T cell activation through a negative feedback mechanism

41
Q

What can go wrong with the CTLA4 protein that can lead to rheumatoid arthritis?

A

A variant of the molecule does not work as well

The immune system cannot be suppressed and is more active

Leads to autoimmune conditions

42
Q

What is the aim of treatment to try and prevent development of rheumatoid arthritis?

A

Blocking certain cytokines involved in the development pathway

43
Q

What are the 3 main things involved in the pathophysiology of autoimmune conditions?

A
  1. autoreactive B cells and autoantibodies
  2. autoreactive T cells
  3. general inflammation and end organ damage
44
Q

How can autoreactive B cells and autoantibodies affect the body?

A

Autoantibodies can be directly cytotoxic to cells

They can interfere with normal physiological function of cells

They can activate the complement system, leading to inflammation

45
Q

How can autoreactive T cells affect the body?

A

They can be directly cytotoxic to cells

They can produce inflammatory cytokines

46
Q

What is the end result of having an autoimmune disease?

A

End organ damage

This is the loss of organ function

47
Q

What organs can be affected by autoimmune diseases?

How long do they last for?

A

any organ can be affected

it is a lifelong-chronic condition

48
Q

What types of people are most commonly affected by autoimmune conditions?

A

Women and the elderly

49
Q

What are the 2 different types of autoimmune condition?

A
  1. organ specific

2. systemic

50
Q

What are the characteristics of organ specific autoimmune diseases?

A

They affect a single organ only

Autoimmunity is restricted to autoantigens of that organ only

51
Q

What are the characteristics of systemic autoimmune diseases?

A

They affect several organs simultaneously

Autoimmunity is associated with autoantigens found in most cells in the body

52
Q

What is the most common category of organ-specific autoimmune disease?

A

autoimmune thyroid disease

53
Q

What is the most common category of systemic autoimmune disease?

A

connective tissue diseases

54
Q

What is the process of Hashimotos thyroiditis?

A

Destruction of thyroid follicles by an autoimmune process

This means there is no production of thyroid hormone

This leads to hypothyroidism

55
Q

What type of autoantibodies is Hashimotos thyroiditis associated with?

A

It is associated with autoantibodies to thyroglobulin and thyroid peroxidase

56
Q

What is the outcome of Hashimotos thyroiditis?

A

Hypothyroidism

57
Q

What is the process behind Grave’s disease?

A

Anti-TSH autoantibodies cause inappropriate stimulation of the thyroid gland

This leads to excessive thyroid hormone production

58
Q

What is the outcome of Grave’s disease?

A

hyperthyroidism initially

eventually there is thyroid gland destruction and the patient develops secondary hypothyroidism

59
Q

What are the typical symptoms of systemic lupus erythematosus?

A
  1. fever
  2. general tiredness
  3. joint and muscle aches
  4. headaches
  5. butterfly rash on the face
60
Q

How does small vessel vasculitis come about in SLE?

A
  1. autoantibodies in the circulation recognise fragments of damaged cells
  2. cell fragments and autoantibodies form complexes
  3. complexes activate the complement system
  4. this leads to small vessel vasculitis
61
Q

Which organs are more likely to be affected in SLE and why?

A

Organs with rich capillary networks

e.g. kidney, heart

The blood flow is slower giving more time for the complexes to form

62
Q

What are the 4 main connective tissue diseases?

A
  1. systemic lupus erythematosus
  2. scleroderma
  3. polymyositis
  4. sjogrens syndrome
63
Q

What are the 2 different types of diagnostic tests?

A
  1. non-specific e.g. inflammatory markers
  2. disease specific
    e. g. autoantibody testing, HLA typing
64
Q

When is HLA typing used?

A

to understand the risk factors for someone developing an autoimmune disease

65
Q

What is meant by immunosuppression?

A

a natural or artificial process which turns off the immune response, partially or fully, accidentally or on purpose

66
Q

What is meant by immunodeficiency?

A

the lack of an efficient immune system

this makes someone susceptible to infection

67
Q

When is immunosuppression used in treatment?

A
  1. transplant rejection
  2. autoimmune diseases
  3. lymphoproliferative diseases
68
Q

How are immunosuppression and immunodeficiency related?

A

Immunosuppression can induce immunodeficiency

69
Q

What are the 2 different types of immunodeficiency?

A
  1. Primary - caused by genetic defects in individual components of the immune system
  2. Secondary - caused by the effects of external factors
70
Q

What is the most common cause of secondary immunodeficiency?

A

malnutrition

71
Q

What are other causes of secondary immunodeficiency?

A
  1. stress
  2. surgery/burns
  3. cancer (especially lymphoproliferative diseases)
  4. immunosuppressive drugs
  5. irradiation
  6. AIDS
  7. other infections e.g. measles, TB
72
Q

What does SCID stand for?

A

severe combined immunodeficiency syndrome

73
Q

What causes SCID?

A

It is a primary immunodeficiency disease caused by defects in both B and T cells

74
Q

What are the characteristics of SCID?

A
  1. recurrent infection with opportunistic infections (things that do not usually cause serious symptoms)
  2. presents in childhood
  3. consanguinity can be related

Y2 MECHANISMS OF DISEASE (36 decks)

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