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DMD 5244 (Immunity) > Autoimmune Diseases (complete) > Flashcards

Autoimmune Diseases (complete) Flashcards

1
Q

What happens in a normal immune response to a microbe

A

you have proliferation and differentiation of lymphocytes, an immune response

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2
Q

what happens in a normal response to self-antigens

A

you have anergy, deletion, or change in specificity of the lymphocyte

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3
Q

microbes are tolerogenic and self antigens are immunogenic. T or F

A

False, microbes are immunogenic and self antigens are tolerogenic

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4
Q

what are autoimmune diseases

A

diseases caused by failure of self tolerance and the subsequent immune responses against self antigens

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5
Q

what are the three things that combine to lead to the breakdown of self tolerance, and autoimmunity

A

Genetic factors (HLA)
Infections
Environmental factors

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6
Q

What is immune tolerance

A

the lack of a response to an antigen that is induced by a previous exposure to that antigen

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7
Q

how do normal individuals achieve self-tolerance

A

via self/non-self descrimination

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8
Q

When do we induce immune tolerance (when is immune activity too high)

A
  1. organ transplantation
  2. autoimmune diseases
  3. allergic diseases
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9
Q

What is central tolerance

A

immunological tolerance to self antigens induced in immature lymphocytes in the central lymphoid organs

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10
Q

What are the mechanisms of central tolerance

A

Deletion
receptor editing in B-cells (change in BCR)
development of Treg cells

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11
Q

what are the levels of Treg like in many autoimmune diseases

A

low levels of Treg cells are often found in autoimmune responses

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12
Q

What is the positive selection in thymus portion of central tolerance for T-cells

A

T-cells with low-affinity interactions of TCR with self MHC molecule positively selects, and saves thymocytes from apoptosis

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13
Q

What is the negative selection in thymus portion of central tolerance for T-cells

A

thymocytes that bind self MHC too tightly undergo apoptotic death

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14
Q

what is peripheral tolerance

A

immune tolerance to self-antigens encountered in peripheral tissues by mature lymphocytes

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15
Q

What are the mechanisms of peripheral tolerance

A
  1. clonal anergy (lacking second signal)
  2. Deletion (cell death)
  3. supression (via Treg secretions of IL-10 and TGF-beta)
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16
Q

What are the three mechanisms of mucosal intolerance

A
  1. ignorance of the antigen by immune system (anergy)
  2. Deletion of T-cells that respond to inhaled/ingested antigen.
  3. Tregs supress inflammatory response
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17
Q

is self tolerance learned/acquired or innate to lymphocytes

A

learned/acquired

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18
Q

do all lymphocytes have the potential to become autoreactive

A

yes

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19
Q

what usually leads to autoreactive lymphocytes

A

failure in central and peripheral tolerance mechanisms

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20
Q

what leads to autoimmune diseases

A
  1. breakdown of central and or peripheral tolerance
  2. failure of immune system to distinguish between self and non-self
  3. autoreactive T and B cells
  4. auto Abs or autoreactive T-cells attack the body
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21
Q

what do autoimmune diseases all cause

A

inflammation and tissue damage (through hypersensitivities 2,3, and 4 and uncontrolled compliment activation)

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22
Q

what are the three methods by which complement activation clears infection

A
  1. C3b opsonization-phagocytosis and killing of microbes
  2. cytolysis or killing of microbes
  3. activation of inflammation
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23
Q

what does the lack of complement proteins C1q, C2 or C4 lead to

A

defective clearance of immune complexes and apoptotic cells which is often found in autoimmune disease development

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24
Q

what are the mediators of type 2 hypersensitivity

A

IgG and IgM

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25
what does the binding of IgG or IgM to an antigen cause
a cytotoxic immune response that kills the antigenic target cell
26
what are the three mechanisms of cytotoxicity
1. complement mediated cell lysis 2. cell injury by inflammatory cells 3. phagocytosis of antibody coated cells
27
what type of hypersensitivity is caused by immune complexes
type 3
28
what usually removes immune complexes
phagocytes and complement activation
29
what determines whether an immune complex is likely to persist and deposit into the tissues
its size, there is an optimum size, medium and small complexes are more likely to deposit than large ones.
30
what diseases are associated with immune complex deposition
autoimmune disease SLE RA
31
what is it called when immune complexes deposit into vessels
vasculitis
32
what are the factors that lead to vasculitis
platelet aggregation and complement activation microthrombi formation C5a, C3a recruitment of PMN that damage the cell wall
33
which type of hypersensitivity is associated with idopathic thrombocytopenia purpura, and autoimmune hemolytic anemia
type 2 Ab-induced
34
which type of hypersensitivity is associated with grave's disease, myasthenia gravis, and insulin receptorAb syndrome
type 2 Ab-induced receptor stimulation or blockade
35
which type of hypersensitivity is associated with SLE and vasculiitis
type 3
36
which type of hypersensitivity is associated with Insulin-dependent diabetes mellitus, hasimoto's thyroiditis, (rheumatoid arthritis?), multiple sclerosis
type 4
37
what are the four different types of autoantibodies
Anti-DNA antibody complement fixing autoantibodies tissue specific autoantibodies autoantibodies to cell-surface receptors
38
what type of auto antibody is seen in lupus nephritis
anti DNA autoantibody
39
what type of auto antibody is seen in autoimmune anemias and thrombocytopenia
complement fixing autoantibodies
40
what type of auto-antibody is seen in SLE, RA, and type 1 diabetes mellitus
tissue specific autoantibodies
41
what type of auto-antibody is seen in graves disease and myasthenia gravis
autoantibodies to cell surface receptors
42
what does the pathogenic role of autoantibodies depend on
concentration and charge of the auto-antigen | affinity and charge of the auto-antibody
43
which is more pathogenic auto-antibodies with high or low affinity for auto-antigens
high (they form more stable complexes and activate complement more effectively)
44
what kind of charge do anti-dna antibodies have, and what does it cause
weak positive charge that causes it to bind to the negatively charged glomerular basement membrane
45
what is glomerulonephritis
inflammation of the glomeruli caused by uncleared immune complexes
46
what causes grave's disease
autoantibodies binding to the TSH receptor on thyroid cells. this causes the cell to secrete unregulated amounts of thyroid hormones (hyperthyroidism)
47
what causes myasthenia gravis
autoantibodies binding to the ACH receptor, inhibits binding of ACH, causes muscle weakness and paralysis
48
what are cross reactive antigens
autoreactive B-cells that recognize both a self-antigen and a forgein antigen
49
what happens when a cross-reactive B-cell binds a self antigen
you get no Th cell help via cytokine secretion
50
what happens when a cross reactive B-cell binds a non-self antigen
you get Th cell help via cytokine secretion. this leads to B-cell proliferation secretion of antibodie to control infection
51
what is a so bad about cross-reactive antigens if they don't illicit an immune response when the B-cell binds a self antigen, but only when it binds a non-self antigen
because the remaining/residual auto antibodies that are produced can go on and bind to self antigens
52
what causes rheumatic fever
the auto-antibodies that were created in response to an antigen on group A strep infection, that antigen is cross-reactive with the self-antigen on the heart valves. so those auto-antibodies attack the heart valves
53
what can be a similar cause of insulin dependent diabetes mellitus and guillan-barre syndrome
a cross reactive antigen reaction
54
What are the signs of Grave's disease
exophthalmos | enlarged thyroid gland
55
What are the T-cell mediated autoimmune diseases
Type 1 diabetes (attacks islet cell Ag) RA (attacks synovial fluid Ag) MS (attacks myelin protein) Hasimoto's thyroiditis (attacks thyroglobin)
56
what is the link between RA and periodontitis
citruillination of proteins.
57
how does periodontitis lead to RA
p. gingivalis creates CCPs, which are also found in the patients gingiva. so as you create an immune response against the CCPs, you also lose self-tolerance, and those anti-CCP antibodies can get to the synovial fluid and break down the citruillinated proteins there. causing RA
58
what is CCP
cyclic citruillinated protein
59
Heat shock protein comes from p. gingivalis and is implicated in
periodontitis and autoimmune atherosclerosis
60
what does the link between RA and periodontitis mean clinically
it means that treatments for one may benefit the other condition as well
61
how are autoimmune diseases normally diagnosed
determining the auto-Antibody participating
62
what are the 4 treatments of autoimmune diseases
1. NSAIDs/COX inhibitors to reduce inflammation 2. cyclophosphamid prevents B-cell proliferation 3. Anti-TNF-a mAb (infliximab/remicade) controls inflammation 4. anti-CD20 mAb (Rituximab) eliminates B-cells in RA, SLE
63
what is ADCC that occurs in patients treated with mAb drugs
antibody dependent cellular cytotoxicity
64
how do mAb drugs work
the target cells are coated/marked with the mAb, and the NK cells kill them
65
how is allergen immunotherapy done
a series of injections of an allergen with the attempt of densensitizing the patient to the allergen (chaning from IgE to IgG and TH2 to TH1)

DMD 5244 (Immunity) (16 decks)

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