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6 - autoimmunity Flashcards

1
Q

define immunological tolerance?

A

unresponsiveness to an antigen that is induced by previous exposure to that antigen

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2
Q

define tolerogens?

A

antigens which induce tolerance

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3
Q

what is self-tolerance?

A

tolerance to self antigens

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4
Q

what is the result of failure of self tolerance?

A

immune reactions against autologous (self) antigens

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5
Q

what is autoimmunity?

A

immune reactions against autologous (self) antigens

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6
Q

what does autoimmunity cause?

A

autoimmune diseases

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7
Q

what do T and B cells do to avoid autoimmune disease?

A

they must eliminate/ downregulate their self-reactive molecules

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8
Q

2 types of tolerance involved in immunological tolerance?

A

central, peripheral

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9
Q

describe tole of thymus in central tolerance?

A

thymus plays important role in eliminating T cells with high affinity to self-antigens

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10
Q

what is important in B cell tolerance?

A

bone marrow

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11
Q

describe peripheral tolerance?

A

Mature lymphocytes that recognise self antigens in peripheral tissues become incapable of activation or die by apoptosis

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12
Q

what happens to T cells that bind to antigens with high affinity in the thymus?

A

deleted through -ve selection

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13
Q

how are autoreactive T cells managed in peripheral tolerance?

A

they are inhibited by regulatory T cells

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14
Q

what leads to activation-induced death of T cells in peripheral tolerance?

A

repeated antigenic stimulation

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15
Q

5 mechanisms of peripheral tolerance?

A

anergy,
Deletion (cell death), Antigen recognition without co-stimulation,
Treg suppression,
anatomical barriers

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16
Q

define anergy?

A

functional unresponsievness

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17
Q

describe mechanism of anatomical barriers for peripheral tolerance?

A

Some self antigens are sequestered from the immune system by anatomic
barriers

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18
Q

name 3 scenarios where peripheral tolerance can be overcome?

A

Inappropriate access of self-antigens,
Inappropriate or increased local expression of co-stimulatory molecules,
Alterations in self-molecules presentation to immune system

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19
Q

when is peripheral tolerance more likely to happen and what is the reason for this?

A

when inflammation/ tissue damage is present - due to the increased activity of proteolytic enzymes

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20
Q

activity of proteolytic enzymes?

A

cause intra/extra-cellular protein breakdown, therefore increasing concentration of peptides presented to responsive T cells

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21
Q

name 3 factors which may alter the structure of self-peptides?

A

viruses, free radicals, ionising radiation

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22
Q

name 3 factors which aid normal autoimmunity in becoming an autoimmune disease?

A

environmental factors, genetics, infections

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23
Q

define autoimmunity?

A

Adaptive immune responses to self antigens

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24
Q

define autoantibodies?

A

antibodies directed at normal cellular components, referred to as autoantigens

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25
when do autoimmune diseases occur and what are they mediated by?
occurs when autoreactive T cells or autoantibodies | cause tissue damage through hypersensitivity reaction types II, III and IV
26
do healthy individuals produce autoantibodies?
yes but at very low level and low affinity
27
what do B1 cells secrete?
natural antibodies, which are a major source of autoantibodies
28
what activates complement to help clear invading bacteria?
natural antibodies binding to antigens with low affinity on bacteria
29
what does an individual with no inherited A or B antigens produce?
IgM anti-A and anti-B antibodies, even if they have never been exposed to red cells from another person
30
what can natural antibodies bind to?
normal cellular constituents - e.g. DNA
31
name 2 types of factors which lead to the breakdown of T cell tolerance?
genetic predisposition, environmental factors
32
name 3 possible points in the pathway of tolerance which can break down, leading to autoimmune disease?
complement is defective, no regulatory T cells to inhibit T cells, self antigen is missing from thymus
33
which gene mutation leads to central tolerance not taking place?
AIRE
34
what can B27 HLA association lead to?
ankylosing spondylitis, reiter disease
35
what can DR2 HLA association lead to?
goodpasture syndrome
36
what can DR3 HLA association lead to?
addison disease, Sicca syndrome, Hashimoto thyroiditis, Myasthenia gravis
37
what can DR4 HLA association lead to?
insulin-dependent DM
38
what type of mutations are implicated in the breakdown of immune tolerance?
common polymorphisms, rather than rare mutations
39
name 3 environmental factors which can breakdown tolerance?
infection, drugs, UV radiation
40
3 ways in which infection can breakdown tolerance?
Molecular mimicry, Upregulation of co-stimulation, Antigen breakdown and presentation changes
41
2 ways in which drugs can breakdown tolerance?
molecular mimicry, genetic variation in drug metabolism
42
2 ways in which UV radiation can breakdown tolerance?
Trigger for skin inflammation, Modification of self-antigen
43
describe molecular mimicry?
Structural similarity between self-proteins and microbial antigens may trigger an autoimmune response
44
name 3 diseases which are a consequence of molecular mimicry?
rheumatic fever, insulin-dependent DM, guillain-Barre syndrome
45
associated disease - AIRE mutations?
multiple autoimmune diseases
46
associated disease - polymorphisms in insulin gene?
T1 DM
47
associated disease - MHC polymorphisms?
T1 DM, coeliac disease, SLE, etc.
48
associated disease - MBL, complement C1 polymorphisms?
SLE
49
associated disease - infections?
T1 DM, MS,
50
associated disease - medications?
SLE
51
associated disease - UV light?
SLE
52
associated disease - gluten?
coeliac disease
53
how do autoimmune diseases present in families?
show clustering within families
54
M:F - autoimmune diseases?
almost all are more common in women - exception = ankylosing spondylitis
55
what are non-organ specific autoimmune diseases associated with?
autoimmune responses against self-molecules which are widely distributed throughout the body
56
what determines where the autoimmune disease lies in the spectrum?
the location of the antigen
57
how is autoimmunity triggered in SLE?
fragments of DNA persist (not removed by innate immune system) - IgG and DNA form immune complex
58
4 mechanisms for treating the self-reactive lymphocyte in autoimmune diseases?
inhibition of lymphocyte function, re-induction of anergy, removal of co-stimulation, induction of inhibitory T cells
59
how to treat tissue damage caused by autoimmune diseases?
anti-inflammatory drugs
60
how to treat organ dysfunction caused by autoimmune diseases?
replacement therapy
61
disease related to TSH receptor?
hyper/hypo- thyroidism
62
disease related to insulin receptor?
hyper/hypo- glycaemia
63
disease related to acetylcholine receptor?
myasthenia gravis
64
disease related to epidermal cell adhesion molecules?
blistering skin diseases
65
disease related to factor VIII (plasma protein)?
acquired haemophilia
66
disease related to beta-2 glycoprotein I (plasma protein)?
antiphospholipid syndrome
67
disease related to RBCs?
haemolytic anaemia
68
disease related to platelets?
thrombocytopenic purpura
69
name 6 diseases associated with intracellular enzyme self-antigens?
thyroiditis, hypothyroidism, addison disease, autoimmune diabetes, systemic vasculitis, 1y biliary cirrhosis
70
name 4 diseases associated with intracellular molecules involved in transcription and translation as self-antigens?
SLE, diffuse scleroderma, polymyositis, limited scleroderma

Immunology (9 decks)

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