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MPharm 2 - PH2113 > Unit 3 - Autoimmunity > Flashcards

Unit 3 - Autoimmunity Flashcards

1
Q

What is autoimmunity?

A

Immune response against self (auto-) antigen

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2
Q

How does autoimmunity progress?

A

Development of autoimmunity reflects a combination of susceptibility genes and environmental triggers

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3
Q

What causes autoimmune diseases?

A

Different autoimmune diseases may be systemic or organ specific

  • may be caused by different types of immune reactions
  • antibody
  • T-cell-mediated
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4
Q

What are the two mechanisms to induction of self tolerance?

A
  • central mechanisms

- peripheral mechanisms

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5
Q

What are the central mechanisms which induce self-tolerance?

A

Deletion of lymphocytes reacting to self

- clonal deletion in thymus or bone marrow of lymphocytes reacting to self-antigen

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6
Q

What are the peripheral mechanisms which induce self-tolerance?

A

Direct induction of peripheral lymphocyte tolerance

  • endothelial barrier segregates T cells from self-antigens
  • low levels of antigen will render B cells unresponsive by down regulation of surface IgM expression these B cells are short-lived - clonal anergy
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7
Q

Which is the first organ to be populated with lymphocytes in the unborn child?

A

Thymus

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8
Q

Which type of cells are in the thymic epithelium?

A

Reticular cells

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9
Q

What is the cortex of the thymus comprised of?

A

Almost all lymphocytes - mostly small resting types, packed tight
New arrivals from the marrow are larger and appear mostly under the capsule

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10
Q

What is the medulla of the thymus comprised of?

A

Forms a continuous unit
In addition to epithelium and small lymphocytes as in the cortex - there’s more of a mix of cell with some fibrous tissue extending from the vessels and a variable number of macrophages (both major types), eosinophils, plasma cells

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11
Q

What type of selection processes happen in the thymus?

A

Positive selection

Negative selection

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12
Q

How does positive selection take place in the thymus gland?

A 
Selects T cells that are able to interact with MHC class I and II molecules
- selecting those lymphocytes that are able to interact with self MHC
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13
Q

How does negative selection take place in the thymus gland?

A

Deletes cells that recognise self antigens expressed in conjunction with MHC class I or II molecules on thymic dendritic cells or macrophages

  • if the interaction is of high affinity - T cells will be deleted
  • if the interaction is of low affinity - T cells may escape negative selection

Deleting those lymphocytes that are able to interact with self MHC and respond to self antigen

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14
Q

What is clonal deletion?

A

The process of destroying B and T cells that react to self antigens

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15
Q

What causes alterations in the state of ‘immunological silence’?

A
  • injury causes access to normally sequestered autoantigen
  • induction of MHCII on cells not normally expressing these molecules could lead to presentation of ‘self-antigens’. Coupled with the production by these cells of necessary ‘co-stimulatory’ signals for activation of lymphocytes
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16
Q

What causes cross-reactivity - mimicry of microbial antigens?

A
  • T-cell stimulation by microbial antigen mimicking self-antigen. Once primed by microbial antigen then high avidity primed T-cell could be chronically stimulated by autoantigen e.g. Streptococcal infection of throat leading to auto-antibodies against heart valves (Rheumatic fever)
  • another possibility is that anergic T-cells may be converted to a responsive state by local high concentrations of cytokines released during infectious/inflammatory response
17
Q

Give two examples of genetic factors that cause autoreactivity

A
  • familial incidence

- HLA linkage

18
Q

Give two examples of familial incidence of autoreactivity

A
  • insulin-dependent diabetes

- association of thyroid antibodies with X chromosome

19
Q

Which HLA specificities are common in organ-specific autoimmune disease?

A

HLA-B8

HLA-DR3

20
Q

Which HLA specificities are common in rheumatic heart disease?

A

HLA-DR7

21
Q

Which HLA specificities are common in rheumatoid arthritis?

A

HLA-DR4

22
Q

Which HLA specificities are common in insulin-dependent diabetes?

A

HLA-DR3

HLA-DR4

23
Q

What is Myasthenia gravis?

A

Progressive muscle weakness caused by auto-antibodies against acetylcholine receptors in motor end plates of neuromuscular junctions
Interferes with ACh neuromuscular transmission
- may lead to reduction in number of receptor as a result of increased endocytosis
Results
- failure of muscle to respond to normal neural impulses
- progressive muscle weakness
Treatment
- anticholinesterases which prolong the action of ACh by inhibiting acetylcholinesterases
- corticosteroids
- azathioprine

24
Q

What is Hashimoto’s disease?

A

Autoimmune hypothyroidism

25
Q

What causes Hashimoto’s disease?

A

Thyroid gland bearing receptors for TSH
Interior surface filled with thyroid colloid
- mainly thyroglobulin and membrane bound enzyme thyroid peroxidase (TPO)
TSH interacts with its receptor to
- upregulate of TPO
- increase synthesis of thyroxine (T4)
- triiodothyronine (T3) which are then released into circulation

In Hashimoto’s thyroiditis - thyroglobulin and TPO are the two major antigens. Anti-thyroglobulin antibodies found in 95% of patients with Hashimoto’s disease

26
Q

What are the symptoms of Graves’ disease?

A
  • rapid pulse
  • fatigue
  • muscle weakness and tremors
  • heat intolerance
  • goitre
  • myxedema (swollen legs)
27
Q

What is Graves’ disease?

A

Autoimmune hyperthyroidism

28
Q

How is Graves’ disease diagnosed?

A
  • suppressed TSH
  • raised T4 / T3
  • antibodies against the TSH receptor
29
Q

Why doe 50% of Graves’ disease patients also have exopthalmia?

A

An interaction between the receptor antibodies and epitopes on the orbital fat tissue

30
Q

What is the incidence of Graves’ disease?

A

Increases with age and is 5 x higher in females

31
Q

What is the treatment of Graves’ disease?

A

Aim to lower thyroid hormone production

  • carbimazole (inhibits thyroid peroxide enzyme)
  • radioiodine
  • subtotal thryoidectomy
32
Q

What is SLE?

A

Systemic Lupus Erythematosus

- chronic remitting relapsing multisystem autoimmune disease

33
Q

What is the incidence of SLE?

A

Common between 20 - 60 years, 10 x higher in females

34
Q

What are the symptoms of SLE?

A
  • skin rashes (vasculitis)
  • arthritis
  • glomerulnephritis
  • haemolytic anaemia
  • thrombocytopenia (maybe CNS involvement)
35
Q

What is the treatment of SLE?

A 
Severe = systemic corticosteroids
Mild = non-steroidal
36
Q

What is DILE?

A

Drug-induced Lupus Erythematosus

37
Q

How long does DILE take to develop?

A

DILE can arise months to years after exposure to drugs prescribed to treat various medical conditions

  • antihypertensions
  • antibiotics
  • anticonvulsants

Flares of SLE due to drugs may occur within hours to days

MPharm 2 - PH2113 (50 decks)

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