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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
Q

what does the binding of IgG or IgM to an antigen cause

A

a cytotoxic immune response that kills the antigenic target cell

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26
Q

what are the three mechanisms of cytotoxicity

A
  1. complement mediated cell lysis
  2. cell injury by inflammatory cells
  3. phagocytosis of antibody coated cells
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27
Q

what type of hypersensitivity is caused by immune complexes

A

type 3

28
Q

what usually removes immune complexes

A

phagocytes and complement activation

29
Q

what determines whether an immune complex is likely to persist and deposit into the tissues

A

its size, there is an optimum size, medium and small complexes are more likely to deposit than large ones.

30
Q

what diseases are associated with immune complex deposition

A

autoimmune disease
SLE
RA

31
Q

what is it called when immune complexes deposit into vessels

A

vasculitis

32
Q

what are the factors that lead to vasculitis

A

platelet aggregation and complement activation
microthrombi formation
C5a, C3a recruitment of PMN that damage the cell wall

33
Q

which type of hypersensitivity is associated with idopathic thrombocytopenia purpura, and autoimmune hemolytic anemia

A

type 2 Ab-induced

34
Q

which type of hypersensitivity is associated with grave’s disease, myasthenia gravis, and insulin receptorAb syndrome

A

type 2 Ab-induced receptor stimulation or blockade

35
Q

which type of hypersensitivity is associated with SLE and vasculiitis

A

type 3

36
Q

which type of hypersensitivity is associated with Insulin-dependent diabetes mellitus, hasimoto’s thyroiditis, (rheumatoid arthritis?), multiple sclerosis

A

type 4

37
Q

what are the four different types of autoantibodies

A

Anti-DNA antibody
complement fixing autoantibodies
tissue specific autoantibodies
autoantibodies to cell-surface receptors

38
Q

what type of auto antibody is seen in lupus nephritis

A

anti DNA autoantibody

39
Q

what type of auto antibody is seen in autoimmune anemias and thrombocytopenia

A

complement fixing autoantibodies

40
Q

what type of auto-antibody is seen in SLE, RA, and type 1 diabetes mellitus

A

tissue specific autoantibodies

41
Q

what type of auto-antibody is seen in graves disease and myasthenia gravis

A

autoantibodies to cell surface receptors

42
Q

what does the pathogenic role of autoantibodies depend on

A

concentration and charge of the auto-antigen

affinity and charge of the auto-antibody

43
Q

which is more pathogenic auto-antibodies with high or low affinity for auto-antigens

A

high (they form more stable complexes and activate complement more effectively)

44
Q

what kind of charge do anti-dna antibodies have, and what does it cause

A

weak positive charge that causes it to bind to the negatively charged glomerular basement membrane

45
Q

what is glomerulonephritis

A

inflammation of the glomeruli caused by uncleared immune complexes

46
Q

what causes grave’s disease

A

autoantibodies binding to the TSH receptor on thyroid cells. this causes the cell to secrete unregulated amounts of thyroid hormones (hyperthyroidism)

47
Q

what causes myasthenia gravis

A

autoantibodies binding to the ACH receptor, inhibits binding of ACH, causes muscle weakness and paralysis

48
Q

what are cross reactive antigens

A

autoreactive B-cells that recognize both a self-antigen and a forgein antigen

49
Q

what happens when a cross-reactive B-cell binds a self antigen

A

you get no Th cell help via cytokine secretion

50
Q

what happens when a cross reactive B-cell binds a non-self antigen

A

you get Th cell help via cytokine secretion. this leads to B-cell proliferation
secretion of antibodie to control infection

51
Q

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

A

because the remaining/residual auto antibodies that are produced can go on and bind to self antigens

52
Q

what causes rheumatic fever

A

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
Q

what can be a similar cause of insulin dependent diabetes mellitus and guillan-barre syndrome

A

a cross reactive antigen reaction

54
Q

What are the signs of Grave’s disease

A

exophthalmos

enlarged thyroid gland

55
Q

What are the T-cell mediated autoimmune diseases

A

Type 1 diabetes (attacks islet cell Ag)
RA (attacks synovial fluid Ag)
MS (attacks myelin protein)
Hasimoto’s thyroiditis (attacks thyroglobin)

56
Q

what is the link between RA and periodontitis

A

citruillination of proteins.

57
Q

how does periodontitis lead to RA

A

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
Q

what is CCP

A

cyclic citruillinated protein

59
Q

Heat shock protein comes from p. gingivalis and is implicated in

A

periodontitis and autoimmune atherosclerosis

60
Q

what does the link between RA and periodontitis mean clinically

A

it means that treatments for one may benefit the other condition as well

61
Q

how are autoimmune diseases normally diagnosed

A

determining the auto-Antibody participating

62
Q

what are the 4 treatments of autoimmune diseases

A
  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
Q

what is ADCC that occurs in patients treated with mAb drugs

A

antibody dependent cellular cytotoxicity

64
Q

how do mAb drugs work

A

the target cells are coated/marked with the mAb, and the NK cells kill them

65
Q

how is allergen immunotherapy done

A

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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