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Infection and Immunity > 28 Autoimmunity > Flashcards

28 Autoimmunity Flashcards

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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
where is the site of action for regulatory T cells
secondary lymphoid tissue and sites of inflammation, multiple tissues in steady state
26
what mechanism is controlled for functional deviation
differentiation of regulatory T cells that limit inflammatory cytokine secretion
27
where is the site of action for functional deviation
secondary lymphoid tissue and sites of inflammation
28
what is mechanism of activation induced cell death
apoptosis
29
where is the site of action for activation induced cell death
secondary lymphoid tissue and sites of inflammation
30
examples of Graves disease causes - Hyperthyroidism
``` Weight loss Twitching Palpitations Restlessness Heat sensitive ```
31
what do autoantibodies do in grave's disease
Autoantibodies that stimulate TSH receptors - Hyperthyroidism - Type II HS
32
what does the pituitary gland secrete
thyroid-stimulating hormone which acts on thyroid to induce release of thyroid hormones
33
what do thyroid hormones do following pituitary gland secretion
act on pituitary to shut down production of TSH, suppressing further thyroid hormone synthesis
34
what does autoimmune B cell make
antibodies toTSH receptor that also stimulate thyroid hormone production
35
what does the thyroid hormone shut down
TSH production
36
what AB do grave's diseases patients make
anti-TSHR
37
can newborns get grave's disease
transfer anti-TSHR AB across placenta to fetus | newborn suffers disease
38
what removes anti-TSHR AB
plasmapheresis
39
what is Graves’ opthalmopathy
eyeballs protrude slightly – increased deposition of fat, pushes eyes out
40
what is Hashimoto’s thyroiditis
Almost exact opposite to graves’
41
examples of Hashimoto’s thyroiditis | causes - Hypothyroidism
``` Low BMR Weight gain Pain, numbness Slow responses Goitre Cold sensitive ```
42
what are grave's disease autoantibodies like
not thought to be part of the pathology of Graves disease, but are pathological in HT
43
what do the autoantibodies do in myasthenia gravis
inhibit acetylcholine receptors Progressive loss of motor function Block or cause degradation of the receptor
44
what does Goodpasture’s disease cause
Kidney damage due to antibody stimulated immune cell activation and complement fixation
45
what do autoantibodies do in goodpastures disease
bind directly to glomerular basement membranes giving a ‘smooth’ staining pattern
46
what happens due to Autoimmune haemolytic anaemia
Autoantibodies to RBC Activation of phagocytosis Activation of complement
47
what HS type is Autoimmune haemolytic anaemia
III
48
what HS type is Goodpasture’s disease
II
49
what HS type is Myasthenia gravis
II
50
what HS type is Systemic lupus erythematosus
III
51
what causes an irregular staining pattern in Systemic lupus erythematosus (SLE or ‘lupus’)
Immune complexes of DNA/anti-DNA in the blood are deposited in the glomeruli
52
what does SLE cause
'butterfly' rash
53
what happens in the failure of clearance of immune complexes
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
what leads to tissue damage in SLE
T cells support the generation of autoantibodies, may contribute directly to tissue damage
55
what do the Islets of Langerhan cells express
different tissue-specific proteins
56
what does the effectorT cell recognise in insulin-dependent diabetes
recognises peptides from a beta cell-specific protein and kills beta cell
57
what do alpha and sigma cells make
Glucagon and somatostatin
58
what cant alpha and sigma cells make
insulin
59
what do B cell specific T cells recognise
peptides from insulin or glutamic acid decarboxylase
60
what increases the risk of Rheumatoid arthritis
Obesity, smoking increase risk
61
what is the first stage that causes Rheumatoid arthritis
1. Unknown trigger sets up initial focus of inflammation in synovial membrane, attracting leukocytes into tissue
62
what is the second stage that causes Rheumatoid arthritis
2. Autoreactive CD4 T cells activate macrophages = pro -inflammatory cytokines made and sustained inflammation
63
what is the third stage that causes Rheumatoid arthritis
3. Cytokines induce production of MMP and RANK ligands by fibroblasts
64
what is the last stage that causes Rheumatoid arthritis
4. MMPs attack tissues. Activation of bone-destroying osteoclasts by RANK ligand results in joint destruction
65
what is needed for the Rheumatoid arthritis disease pathology
both B and T cells are required for disease pathology
66
what are the proposed antigens for Rheumatoid arthritis
collagens, heat-shock proteins, citrullinated derivatives of proteins
67
what contributes to tissue and bone destruction in Rheumatoid arthritis
MMPs and RANKL
68
what causes Synovitis in rheumatoid arthritis
accumulation of cells includes CD4+ T cells, B cells and macrophages

Infection and Immunity (29 decks)

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