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Infection and Immunity > 28 Autoimmunity > Flashcards

28 Autoimmunity Flashcards

1
Q

what is the immunological responses

A

regulated response

exaggerated response

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2
Q

what does the regulated response lead to

A

protection

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3
Q

what does the exaggerated response lead to

A

tissue protection

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4
Q

what leads to autoimmune response

A

If self-responding to and self being damaged

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5
Q

examples of organ-specific autoimmune diseases

A

type 1 diabetes mellitus
Crohn’s syndrome
grave’s disease

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6
Q

examples of systemic autoimmune diseases

A

rheumatoid arthritis
Scleroderma
polymyositis

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7
Q

examples of organ specific diseases

A

multiple sclerosis -myelin sheath of nerve fibres

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8
Q

what are organ specific diseases

A

antigens (self-proteins/components) recognised – immune responses are organ specific, only in a particular area

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9
Q

examples of systemic diseases

A

systemic lupus erythematosus – ds (native) DNA, histones, ribonucleoprotein

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10
Q

what are systemic diseases

A

not one area, affects different

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11
Q

how many types of hypersensitivity are there

A

4

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12
Q

what is type 1 hypersensitivity

A

allergy

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13
Q

what is type 2 hypersensitivity

A

hypersensitivity reaction / autoimmunity – binding of auto antibody to self can trigger immune response = destruction

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14
Q

what is the type 3 hypersensitivity

A

immune complex disease

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15
Q

what is the type 4 hypersensitivity

A

delayed hypersensitivity – takes time to develop, cell-mediated response, cell has to have T cell on by APC, can trigger macrophages – macrophages damage as well as T cell related damage

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16
Q

what are autoimmune diseases

A

complex/multifactorial diseases

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17
Q

what effects the autoimmune diseases

A

Genetics effects how likely to get autoimmune disease, particular variants in genes, can give decrease or increased risk in developing an autoimmune disease
Infections and environmental factors effect too
Smoking is a risk factor for increasing risk
Lead to immune dysregulation and can lead to triggering of immune response

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18
Q

what mechanism is controlled for central tolerance

A

deletion

editing

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19
Q

where is the site of action of central tolerance

A 
thymus (T cells)
bone marrow (B cells)
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20
Q

what mechanism is controlled for antigen segregation

A

physical barrier to self-antigen access to lymphoid system

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21
Q

where is the site of action of antigen segregation

A

peripheral organs

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22
Q

what mechanism is controlled for peripheral anergy

A

cellular inactivation by weak signalling without co-stimulus

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23
Q

where is the site of action for periphery anergy

A

secondary lymphoid tissue

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24
Q

what mechanism is controlled for regulatory T cells

A

suppression by cytokines, intracellular signals

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25
Q

where is the site of action for regulatory T cells

A

secondary lymphoid tissue and sites of inflammation, multiple tissues in steady state

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26
Q

what mechanism is controlled for functional deviation

A

differentiation of regulatory T cells that limit inflammatory cytokine secretion

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27
Q

where is the site of action for functional deviation

A

secondary lymphoid tissue and sites of inflammation

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28
Q

what is mechanism of activation induced cell death

A

apoptosis

29
Q

where is the site of action for activation induced cell death

A

secondary lymphoid tissue and sites of inflammation

30
Q

examples of Graves disease causes - Hyperthyroidism

A 
Weight loss
Twitching
Palpitations
Restlessness
Heat sensitive
31
Q

what do autoantibodies do in grave’s disease

A

Autoantibodies that stimulate TSH receptors

  • Hyperthyroidism
  • Type II HS
32
Q

what does the pituitary gland secrete

A

thyroid-stimulating hormone which acts on thyroid to induce release of thyroid hormones

33
Q

what do thyroid hormones do following pituitary gland secretion

A

act on pituitary to shut down production of TSH, suppressing further thyroid hormone synthesis

34
Q

what does autoimmune B cell make

A

antibodies toTSH receptor that also stimulate thyroid hormone production

35
Q

what does the thyroid hormone shut down

A

TSH production

36
Q

what AB do grave’s diseases patients make

A

anti-TSHR

37
Q

can newborns get grave’s disease

A

transfer anti-TSHR AB across placenta to fetus

newborn suffers disease

38
Q

what removes anti-TSHR AB

A

plasmapheresis

39
Q

what is Graves’ opthalmopathy

A

eyeballs protrude slightly – increased deposition of fat, pushes eyes out

40
Q

what is Hashimoto’s thyroiditis

A

Almost exact opposite to graves’

41
Q

examples of Hashimoto’s thyroiditis

causes - Hypothyroidism

A 
Low BMR
Weight gain
Pain, numbness
Slow responses
Goitre
Cold sensitive
42
Q

what are grave’s disease autoantibodies like

A

not thought to be part of the pathology of Graves disease, but are pathological in HT

43
Q

what do the autoantibodies do in myasthenia gravis

A

inhibit acetylcholine receptors
Progressive loss of motor function
Block or cause degradation of the receptor

44
Q

what does Goodpasture’s disease cause

A

Kidney damage due to antibody stimulated immune cell activation and complement fixation

45
Q

what do autoantibodies do in goodpastures disease

A

bind directly to glomerular basement membranes giving a ‘smooth’ staining pattern

46
Q

what happens due to Autoimmune haemolytic anaemia

A

Autoantibodies to RBC
Activation of phagocytosis
Activation of complement

47
Q

what HS type is Autoimmune haemolytic anaemia

A

III

48
Q

what HS type is Goodpasture’s disease

A

II

49
Q

what HS type is Myasthenia gravis

A

II

50
Q

what HS type is Systemic lupus erythematosus

A

III

51
Q

what causes an irregular staining pattern in Systemic lupus erythematosus (SLE or ‘lupus’)

A

Immune complexes of DNA/anti-DNA in the blood are deposited in the glomeruli

52
Q

what does SLE cause

A

‘butterfly’ rash

53
Q

what happens in the failure of clearance of immune complexes

A
  1. Components released by dead and dying cells
  2. Continuous generation of small immune complexes
  3. Deposition on vessel walls, glomeruli, skin, organs
  4. Trigger activation of phagocytosis via Fc receptors
  5. Destruction of cells leads to more immune complexes
    5 –> 1
54
Q

what leads to tissue damage in SLE

A

T cells support the generation of autoantibodies, may contribute directly to tissue damage

55
Q

what do the Islets of Langerhan cells express

A

different tissue-specific proteins

56
Q

what does the effectorT cell recognise in insulin-dependent diabetes

A

recognises peptides from a beta cell-specific protein and kills beta cell

57
Q

what do alpha and sigma cells make

A

Glucagon and somatostatin

58
Q

what cant alpha and sigma cells make

A

insulin

59
Q

what do B cell specific T cells recognise

A

peptides from insulin or glutamic acid decarboxylase

60
Q

what increases the risk of Rheumatoid arthritis

A

Obesity, smoking increase risk

61
Q

what is the first stage that causes Rheumatoid arthritis

A
  1. Unknown trigger sets up initial focus of inflammation in synovial membrane, attracting leukocytes into tissue
62
Q

what is the second stage that causes Rheumatoid arthritis

A
  1. Autoreactive CD4 T cells activate macrophages = pro -inflammatory cytokines made and sustained inflammation
63
Q

what is the third stage that causes Rheumatoid arthritis

A
  1. Cytokines induce production of MMP and RANK ligands by fibroblasts
64
Q

what is the last stage that causes Rheumatoid arthritis

A
  1. MMPs attack tissues. Activation of bone-destroying osteoclasts by RANK ligand results in joint destruction
65
Q

what is needed for the Rheumatoid arthritis disease pathology

A

both B and T cells are required for disease pathology

66
Q

what are the proposed antigens for Rheumatoid arthritis

A

collagens, heat-shock proteins, citrullinated derivatives of proteins

67
Q

what contributes to tissue and bone destruction in Rheumatoid arthritis

A

MMPs and RANKL

68
Q

what causes Synovitis in rheumatoid arthritis

A

accumulation of cells includes CD4+ T cells, B cells and macrophages

Infection and Immunity (29 decks)

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