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Bio 432 > Endocrine Autoimmunity - Final Exam > Flashcards

Endocrine Autoimmunity - Final Exam Flashcards

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Biology 101 flashcards
1
Q

What does autoimmune disease involve? (2)

A
  1. Immune response

2. Attack against a host organ

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2
Q

What is the statistic/percentage that epidemiologists suggest suffer from some type of autoimmune disease in the world?

A
  • 2.5 in 30 people

~ 7-9%

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3
Q

What are 4 examples of autoimmune diseases?

A
  1. Addisons disease
  2. Graves disease
  3. Type 1 diabetes
  4. Hashiomto thyroiditis
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4
Q

What is an autoimmune disease?

A

A disease in which the body produces antibodies that attack its own tissues, leading to the deterioration and in some cases to the destruction of such tissue.

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5
Q

What are 5 endocrine organs that are sensitive to autoimmune disease?

A
  1. Adrenals
  2. Gonads
  3. Pancreas
  4. Pituitary
  5. Thyroid
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6
Q

What is a key feature to a healthy immune system?

A

Establishment and maintenance of immunologic tolerance to “self”

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7
Q

What does the cellular immune system contain? (2)

A
  1. Ag presenting cells (innate immune)

2. Adaptive T-cells that present T cell receptors

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8
Q

What is the humoral immune system?

A

Is the aspect of immunity that is mediated by macromolecules found in extracellular fluids such as secreted antibodies, complement proteins, and certain antimicrobial peptides

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9
Q

What is the cellular immune system?

A

Is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.

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10
Q

What does Treg do?

A

Inhibits Th and Tc

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11
Q

What is a macrophage?

A

A large phagocytic cell found in stationary form in the tissues or as a mobile white blood cell, especially at sites of infection

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12
Q

What are the humoral immune system made up of?

A

B cells

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13
Q

What does adaptive T-cells do?

A

Suppress the immune system

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14
Q

What are the T-cell receptors?

A

first line of defences against diseases

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15
Q

What are the recognition possibilities for TCR? (2)

A
  1. Linear genome

2. Rearrange their DNA during development for a wide range of recognition

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16
Q

TCR

A

T-cell receptors

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17
Q

What is the estimated recognition diversity?

A

10^15

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18
Q

What else does the diverse mechanism of rearrangement apply to?

A

B cells of Ab synthesis

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19
Q

What kind of receptors do T and B cells have?

A

Self reactive receptors

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20
Q

How are T and B receptors eliminated?

A

By negative selection in the thymus and bone marrow

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21
Q

CTLs

A

Cytotoxic T cells

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22
Q

What do CTLs develop?

A

TCRs that have antibody like molecules on the surface

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23
Q

What do the TCR antibody like molecules have on their surface display?

A

Ab like recognition for a specific pathogen

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24
Q

APCs

A

Antigen presenting cells

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25
Q

What happens after phagocytosis of foreign bodies?

A

Antigen presenting cells process the foreign proteins

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26
Q

What are 2 examples of foreign proteins that APCs process?

A
  1. Proteaosome

2. Lysosome

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27
Q

Where do the foreign proteins move after processing?

A

To the surface with major histocompatibility

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28
Q

MHC

A

Major histocompatibility

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29
Q

What class of receptors are MHC?

A

Class II receptors

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30
Q

Where do major histocompatibility receptors display their info and what is that info?

A
  • Displays info on the plasma membrane

- Info is about what the macrophage had found

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31
Q

How does MHC break down proteins?

A

Through phagocytosis

32
Q

What 3 ways are antigens taken up by?

A
  1. Phagocytosis
  2. Pinocytosis
  3. Endocytosis
33
Q

What do antigen presenting cells deliver and through where?

A

An antigen-specific signal through the major histocompatibility complex

34
Q

What is the required second signal for antigen recognition presentation complex? And where does it come through?

A

T cell activation via CD80/86

35
Q

What does CD28 do?

A

Induces the expression of CD 154 first and CD152 later on

36
Q

What does T cell CD154 bind to on APCs?

A

CD40

37
Q

What does the interaction between CD154 and CD40 induce?

A

The activation and proliferation of downstream effector cells

38
Q

How long after T cell activation is CD152 expressed?

A

48-72 hours

39
Q

Why does CD152 preferentially bind to CD80-86 on APCs? What does it do?

A

Because of its higher affinity

- It displaces CD28 and as a result suppresses T cell activity

40
Q

What do productive immune cells synthesize?

A

Ab

41
Q

How do you get a productive interaction? (2)

A
  1. If the molecular architecture is a fit

2. TH cell activates to display more of this TCR

42
Q

What do TH cells activate in a productive interaction and what does it do?

A
  • Activates B-cells

- It differentiates into plasma cells and makes Ab

43
Q

What info does MHC class I molecule display?

A

Info of the host cells

44
Q

What do all cell types display?

A

Ag on their surface with MHC class I molecules

45
Q

What is Ag formed from?

A

From the proteolytic degradation of endogenous proteins

46
Q

What 2 things can help T cells do?

A
  1. Inducing B cells to make Ab

2. Activate CTLs that can use their TCRs to recognize and bind Ag resented on the cell surface of many cell types

47
Q

What does the activation of CTL result in?

A

In the attack of the Ag displaying cells

48
Q

What do helper T cells often use? (3)

A
  1. Perfornin
  2. Granzyme
  3. FasL
49
Q

What 2 signals T cells require to activate?

A
  1. TCR expressed antigen specific receptor binds to antigenic peptide held by the MHC complex
  2. APC CD80/86 binds to T cell CD28
50
Q

What do pre-T cells first do?

A

Rearrange their T cell receptors

51
Q

What leads to apoptosis?

A

unproductive (nonfunctional) rearrangements

52
Q

What are pre-T cells tested for?

A

Self antigen recognition

53
Q

What does clonal deletion indicate?

A

Elimination of cells based on their high or no avidity for self antigen

54
Q

What happens to T cells when they survive low-avidity?

A

They reach the periphery as mature CD4 and CD8 cells

55
Q

What is a central pathogenic step in the development of autoimmune disease?

A

The breakdown of self-tolerance

56
Q

What kind of mechanism is autoimmunity?

A

Multifactorial

57
Q

What are 5 disruptors of self tolerance?

A
  1. Defects in apoptosis-related molecules (Fas-FasL) of both central and peripheral T-cells
  2. Defects of CD152
  3. Defects of active suppression
    - T reg dysfunction
  4. Defects in B cell tolerance
  5. Hypocortisolism
58
Q

What may prevent apoptosis?

A

Defects of CD152 on T cells may prevent apoptosis of auto-reactive T cells

59
Q

Defects in what may lead to autoimmunity?

A

In active suppression

60
Q

When is active suppression thought to occur?

A

When using T-reg cells

61
Q

What do T reg cells normally suppress?

A

T cell action against those MHC expressing cells

62
Q

What is hypocortisolism?

A

Low cortisol production

63
Q

What are 6 disease characteristics hypocortisolism?

A
  1. Increased autoimmunity
  2. Inflammation
  3. Pain
  4. Fatigue
  5. Asthma
  6. Allergies
64
Q

What are increased autoimmunity, inflammation, pain, fatigue, asthma, allergies involved in?

A

Pathogenesis of autoimmune diseases that attack the endocrine system

65
Q

What 2 factors are necessary for immune self tolerance?

A
  1. Genetic factors

2. Environmental factors

66
Q

What are the 3 environmental factors that are thought to have the greatest influence on disease development?

A
  1. Infectious agents
  2. Diet
  3. Toxins
67
Q

What do 20% of children who are prenatally infected with rubella develop?

A

Type 1 diabetes

68
Q

What is rubella?

A

Is a contagious viral disease, with symptoms like mild measles. It can cause fetal malformation if contracted in early pregnancy

69
Q

Why do children who are prenatally infected with rubella develop type 1 diabetes?

A

Due to development of antibodies against proteins in the beta cells that share a similar molecular architecture to rubella viral proteins and thus autoimmune type 1 diabetes

70
Q

What are children with rubella have an increased incidence of?

A

Other autoimmune disorders

71
Q

What autoimmune disease develops as an attack on the adrenal cortex?

A

Addison’s disease

72
Q

What enzyme antibodies appear to be predictive in children and adults?

A

21-alpha-hydroxylase

73
Q

What controls the level of lymphocytes?

A

Cortisol

74
Q

How does cortisol control the levels of lymphocytes?

A

By inducing apoptosis

75
Q

What is the benefit of having increased glucose levels in the morning?

A

To help you get up and get out of bed

76
Q

Th

A

T helper cells

77
Q

Tc

A

T-cytotoxic

Bio 432 (19 decks)

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