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IMM > Tolerance and Autoimmune > Flashcards

Tolerance and Autoimmune Flashcards

1
Q

As B cells and T cells randomly recombine their V,D, J gene segments to create antigen receptors, it is inevitable that some receptors will be——–

A

Specific for self antigens

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2
Q

These self reactive lymphocytes must be deleted or rendered anergic to prevent——

A

autoimmune reactions from occuring

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3
Q

——is induced when self-reactive B cells and T cells are DELETED in the central lymphoid tissues

A

Central Tolerance

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4
Q

——-is induced when the few self-reactive lymphocytes that escape deletion in the central lymphoid organs are rendered ANERGIC in the peripheral lymphoid organs

A

Peripheral tolerance

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5
Q

——result when the occasional anergic lymphocyte becomes re-activated and starts attacking self tissues

A

Autoimmune diseases

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6
Q

——-occurs when thymocytes are rescued from apoptosis by moderate affinity interactions with sefl-MHC molecules

A

Positive selection

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7
Q

Positive selection occurs by epithelial cells where—–

A

in the cortex of the thymus

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8
Q

—–occurs when autoreactive T cells are deleted when the T cells interact with dentritic cells or epithelial cells that display non-MHC self antigens along with self-MHC molecules

A

negative selection

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9
Q

Negative selection occurs where?

A

at the cortico-medullary junction and in the medulla of the thymus

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10
Q

When the T cell progenitors produced in the bone marrow enter the thymic cortex, these pro-T cells express neither—–nor—-(double negative thermocytes)

A

CD4 nor CD8

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11
Q

Pro-T cells develop into pre- T cells, which express the—–chain of the—-

A

beta chain of the TCR

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12
Q

Pre- T cells develop into double positive immature T cells, which express both —-and—–, along with——levels of complete TCR molecules

A

CD4 and CD8/low

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13
Q

The double positive thymocytes interact with thymic—–that express high levels of both—–and——MHC molecules

A

cortical epithelial cells/class I/class II

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14
Q

Thymocytes with——-for these self-MHC molecules are allowed to develop further, while thymocytes with affinities—-or——for self MHC are induced to die by——–

A

moderate affinities/too high/too low/apoptosis

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15
Q

The positively selected thymocytes begin to express—-of TCR molecules, some of which recognize normal body components other than self-MHC

A

high levels of TCR molecules

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16
Q

—– —- —-present self antigens that are always present within the thymus at the————

A

Intergigitating dendritic cells (IDCs)/at the cortico-medullary junction

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17
Q

in the—–the thymocytes interact with “non-thymic” self antigens processed and presented by—- —— ——

A

in the medulla/medullary epithelial cells

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18
Q

—– —- —–produce a transcription factor regulator called——- that allows these cells to synthesize non-thymic antigens typically found in the peripheral tissues

A

medullary epithelial cells/AIRE

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19
Q

People with an AIRE gene defect suffer from—– —– —-due to autoreactive T cells that are not deleted (pt present with hypothyroidism/adrenal insufficiency/thyroiditis/type 1 diabeties/ovarian failure

A

autoimmune polyendocrine syndrome

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20
Q

Only thymocytes that—-to recognize self antigens are allowed to survive and proceed along the maturation process, with the remainder undergoing apoptosis

A

fail

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21
Q

T cells that survive the negative selection process lose either CD4 or CD8, becoming —- —-T cells

A

single positive

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22
Q

Some immature CD4+ T cells that recognize self antigens in the thymus do not die by instead develop into—–regulatory T (Treg) that enter the peripheral tissures

A

CD25+

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23
Q

Development of Treg cells is controlled by the transcription factor —-under the influence of —–

A

Foxp3/TGFbeta

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24
Q

T reg cells protect the host from the harmful effects of other self-reactive lymphocytes, namely— —- —- by secreting —- and —–

A

TH1, TH2, TH17 by secreting TGFbeta and IL10

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25
Q

Tregs also cause down regulation of the —–co-stimulatory molecule on dendritic cells, resulting in poor antigen presentation to T cells

A

B7

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26
Q

The anergic T lymphocyte remains alive but is inactivated by interaction with antigen presented by an APC lacking the —–co-stimulator

A

B7

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27
Q

Name 5 immunologically privileged tissues

A

brain, anterior chamber of the eye, placenta, pregnant uterus, testis

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28
Q

Interactions between the previleged tissues and T cells are inhibited by——

A

blood-tissue barriers

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29
Q

Privileged tissues contain—–of complement and—–levels of immunosuppressive—– and—–

A

low/high/TGFbeta and IL-10

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30
Q

Many privileged tissues display—-which kills T cells that display—–

A

FasL/Fas

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31
Q

Immature B cells (IgM+IgD-) are easily made tolerant to slef antigens by—-

A

negative selection

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32
Q

When a self reactive, immature B cell encounters a soluble sefl antigen, the B cell becomes—–

A

Anergized

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33
Q

Both cell-bound and soluble self antigens can induce—– ——-, so that the specificity of the immature B cell changes to fereign antigen

A

receptor editing

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34
Q

— —- —-is often induced by a lack of T cell help, if a T cell clone becomes anergic or is deleted, any B cell that depends upon that T cell clone for help in antibody production also becomes—-

A

B cell anergy/anergic

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35
Q

The advent of autoimmune desease is influenced by —-name the 3 things

A
  1. the inheritance of susceptibility genes, including certain HLA molecues, 2) environmental factors, 3) physical trauma
36
Q

The most profound association between autoimmune disease and HLA expression is found between—— —- and the—– —-allele

A

ankylosing spondylitis and the HLA-B27 allele which carries a relative risk of 90.

37
Q

HLA-B27 allele: name the associated diseases: 4

A

Psoriasis, ankylosing spondylitis, inflammatory bowel disease, Reiter’s syndrome (PAIR)

38
Q

HLA-DR2 allele: name associated diseases: 4

A

MS, SLE, Goodpasture syndrome, hayfever

39
Q

HLA-DR3/DR4

A

Type 1 diabetes

40
Q

HLA-DR4

A

Rheumatoid arthritis

41
Q

—-is an important environmental trigger for autoimmune disease

A

infection

42
Q

Some microbes possess antigenic determinants that resemble self molecules

A

molecular mimicry

43
Q

State an example of when trauma may introduce immunologically privileged tissue to the immune system, when then sees the tissue as foreign and mounts a vigorous response to it

A

sympathetic opthalmia

44
Q

Megaloblastic anemia caused by cobalamin (vit B12) malabsorption

A

pernicious anemia

45
Q

Co-factor required for B12 absorption

A

intrinsic factor

46
Q

This disease may be associated with chronic H-Pylori infection

A

pernicious anemia

47
Q

sore tongue/ beefy red smooth tongue, paresthesias

A

pernicious anemia

48
Q

pernicious anemia molecular target is—-

A

intrinsic factor

49
Q

Name the disease with organ target as the the stomach

A

pernicious anemia

50
Q

Megaloblastic madness: —– — — —-

A

delusions, hallucinations, outbursts, paranoia

51
Q

Diagnosis of Pernicious anemia

A

circulation antibodies to intrinsic factor and other parietal cell components, macrocytic erythrocytes in circulation

52
Q

Tx for pernicious anemia

A

clinical trial fo vit B12 IM/SC/oral/nasal spray

53
Q

Target organs for good pasture syndrome

A

Lungs and kidneys

54
Q

In GPS complement fixing autoantibodies is directed toward —– — —- bind to the basement membranes of the glomerular capillaries and pulmonary alveoli

A

Type IV collagen

55
Q

Good pasture syndrome is also called

A

anti-glemerular basement membrane (anti-GBM) disease

56
Q

25 y/o pt present with hemoptysis/dyspnea/cp/arthralgias/cyanosis; what will be in your defferential dx

A

Good pasture syndrome

57
Q

60 y/o pt present to the ED due to SOB; your work-up reveals: hematuria/proteinuria/crackles/patchy consolidations on x-ray; anemia. What’s ur dx?

A

Good pasture syndrome

58
Q

What antibodies will you dectect

A

circulating anti-glomerular basement membrane antibodies

59
Q

In GPS a kidney biopsy will show

A

linear deposition of antibody and complement

60
Q

What are some treatments for GPS?

A

plasmaphoresis/immunosuppressive therapy/hemodialysis/kidney transplant

61
Q

This disease results from cell-mediated immune destruction of beta cells in the pancreas

A

Type 1 diabeties

62
Q

What will happen if insulin is withdrawn in a type 1 diabetic?

A

ketosis and eventually ketoacidosis will develop, therefore these patients are dependent on exogenous insulin

63
Q

20 y/o male present to the ED with fruity breath, thin c/o polyuria/polydipsia/nocturia/blurried vision, weight loss, finger stick reveals elevated glucose level

A

Type 1 diabetes c possible ketoacidosis

64
Q

True of false Type I diabetes pts are prone to develop pancreatitis

A

True

65
Q

Type 1 diabetes will develop peripheral neuropathy in what kind of pattern

A

glove and stocking patter

66
Q

Suppression vs acceleration of type 1 DM is determined by the balance between—-and —-cells specific for —- — —- and enzyme produced by islet beta cells

A

Treg and TH1/glutamic acid decarboxylase

67
Q

When…cells predominate, the IL-10 they produce suppresses——

A

Treg/type 1DM

68
Q

When—- cells predominate, the IFNgamma they produce activates both macrophages and Tc cells to kill the —-cells

A

TH1/beta cells

69
Q

95% of type 1 DM patients are either——or—–

50% of type 1 DM patients are heterozygotes

A

HLA-DR3 or HLA-DR4

70
Q

Name a few ways type 1 DM can be diagnosed

A

asymptomatic: 2 dif fasting glucose >125mg/dL; symptomatic a random glucose of 200 mg/dL, circulating autoantibodies to insulin and beta cell components

71
Q

What’s the treatment for type 1 DM

A

Diet, exercise, insulin

72
Q

Myasthenia Gravis is an autoimmine disorder of peripheral nerves in which IgG autoantibodies form against—– —— ——- at eh neuromuscular junction

A

acetylcholine nicotinic postsynaptic receptors

73
Q

Patients become symptomatic once the number of AChRs is reduced to——of normal

A

30%

74
Q

28 y/o F present c/o specific muscle weakness, sts weakness is more severe later during the day, improves with rest, +ptosis, diplopia, strabismus, nasal twang voice

A

MG

75
Q

—–is a syndrome of generalized muscle weakness, affecting 12% of infants born to women with myasthenia gravis, due to—–antibodies passively crossing the placenta

A

neonatal myasthenia/IgG

76
Q

A thymoma will most likely be present for which autoimmune disease

A

MG

77
Q

Name the disease: +circulating anti-AChR antibodies, +thymoma on CT, anticholinesterase test is positive, muscle biopsies show dec neuromuscular junction (1/3 as many as normal)

A

MG

78
Q

What’s the treatment for MG

A

cholenesterase inhibitors, corticosteroids, immunosuppressive drugs, IVIG, plasmapheresis

79
Q

This disease cause adrenocortical insufficiency due to the destruction or dysfunction of the entire adrenal cortex

A

Addison Disease

80
Q

This disease affects both glucocorticoid and mineralocorticoid function

A

addison disease

81
Q

Destruction of the—- —– leads to overproduction of corticotropin and melanocyte stimulating hormone

A

adrenal cortex

82
Q

Due to autoimmune destruction of melanocytes

A

vitiligo

83
Q

40 y/o F present c/o dizziness, weight loss, nausea/vomiting, amenorrhea, absence of pubic and axillary hair, progressive weakness. Most likely diagnosis is—–

A

addison disease

84
Q

32 y/o female c/o n/v, flank pain, confused, cyanotic, hyperpyrexia >105, later become comatose. What’s the state pt is in—–

A

acute adrenal crisis

85
Q

Name several ways a dx of addison disease can be made

A

Rapid ACTH stimulation test, then plasma levels of cortisol and aldosterone are measured 30 min after, levels will remain near baseline in addison disease, atrophy of adrenal glands on CT, histo: lymphocytic infiltration

86
Q

How to treat Addison Disease

A

Hormone replacement, ex: prednisone or fludrocortisone

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