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MICRO > Ch7: Hypersensitivity and Autoimmunity > Flashcards

Ch7: Hypersensitivity and Autoimmunity Flashcards

1
Q

What are allergens?

A

Things that the immune system develops an over-active response to

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2
Q

What are 4 common sources of allergens?

A
  1. inhaled materials
  2. injected materials
  3. ingested material
  4. contacted materials
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3
Q

How many types of hypersensitivity are there?

A

4

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4
Q

Name of each hypersensitivity reaction?

A
  1. Type I: Immediate Hypersensitivity
  2. Type II: Antibody-mediated diseases
  3. Type III: Immune complex mediated diseases
  4. Type IV: T cell mediated diseases
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5
Q

What are the steps of Type I Hypersensitivity’s sensitization?

A
  1. Allergens taken up by APC’s
  2. Proteins degraded
  3. Peptides presented as peptide:MHC to specific T cells
  4. Th2 cells then produce cytokines to isotype switch to IgE
  5. IgE binds to Fc-epsilon-RI receptors on Mast cells
  6. Repeat exposure of allergen causes activation of mast cell and release of mediators
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6
Q

Two kinds of mediators that mast cells release?

A
  1. Vasoactive amines and lipid mediators immediately after repeat exposure
  2. Cytokines released hours later
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7
Q

Does IgE need antigen to bind and coat mast cells?

A

No

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8
Q

Basophils and mast cells are very similar but differ in what terms?

A

Mast cells: tissues

Basophils: Blood

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9
Q

5 main classes of products released by mast cells and which are prestored?

A
  1. enzymes (prestored)
  2. toxic mediators (prestored)
  3. cytokines (TNF-alpha only prestored)
  4. chemokines
  5. lipid mediators
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10
Q

Effect of enzymes released by mast cells?

A

Remodeling of CT matrix

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11
Q

Two main toxic mediators released by mast cells?

A

Histamine and heparin

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12
Q

Function of histamine and heparin release?

A
  1. Toxic to parasites
  2. leaky vessels
  3. Smooth muscle contraction
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13
Q

Function of mast cell TNF alpha? 3

A
  1. promotes inflammation
  2. stimulates cytokine production
  3. activates endothelium
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14
Q

Function of IL4 and IL13 release

A

Stimulate and amplify TH2 cell response

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15
Q

Function of IL3, IL5, and GM-CSF release?

A

Promote eosinophil production and activation

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16
Q

Function of CCL-13 release of mast cells?

A

Chemotactic for phagocytes

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17
Q

Function of leukotriene release of mast cells?

A
  1. Smooth muscle contractin
  2. Increase vessel leakiness
  3. Cause mucus secretion
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18
Q

Function of platelet activating factor

A
  1. Chemotactic for leukocytes
  2. Amplifies production of lipid mediators
  3. Activates neutrophils, eosinophils, and platelets
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19
Q

Function of prostaglandins?

A

Vascular dilation

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20
Q

Function of vasoactive amines?

A

Vascular dilation

Smooth muscle contraction

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21
Q

IMmediate Phase Type I hypersensitivity involves what cells?

A

Mast

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22
Q

Late phase Type I hypersensitivity involves what cells?

A

Eosinophils

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23
Q

What causes the wheal and flare of a Type I reaction?

A

Mast cell degranulation

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24
Q

Late-phase reaction occurs 6-8 hours later because of what?

A

Leukotrienes, chemokines, cytokines synthesized by mast cells

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25
Q

Degranulation in GI tract of Type I causes what?2

A

Diarrhea and vomiting

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26
Q

Degranulation in Airways causes what? 2

A

Phlegm and coughing

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27
Q

Degranulation in blood vessels causes what? 3

A

Edema
Inflammation
Increased lymph flow

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28
Q

Treatment for Type I involves what?

A

Block effects of inflammatory mediators (histamine and leukotrienes)
Can’t stop the cause: IgE crosslinking

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29
Q

When allergen is in skin, what results? (2)

A
  1. urticaria

2. angioedema

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30
Q

Where do recruited eosinophils go in Type I?

A

To the lung

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31
Q

Why is mast cell degranulation bad in the heart and vascular system?

A

Leakage of fluids into tissue resulting in drop in cardiac output leading to anaphylactic shock and possibly death

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32
Q

Most extreme outcome of hypersensitivity is what?

A

IgE mediated systemic anaphylaxis

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33
Q

What reverses systemic anaphylaxis?

How? (3)

A

Epinephrine

  1. Reforms tight junctions in between cells
  2. Reduces permeability Preventing fluid loss from blood
  3. Relaxes constricted bronchial smooth muscle and stimulates heart
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34
Q

Activated mast cells release what to stimulate eosinophils?

A

IL-5

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35
Q

What is the most important chemokine for eosinophils?

A

CCL11 (Eotaxin)

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36
Q

Do resting eosinophils express IgE receptors on surface?

A

No, not first responder

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37
Q

Presence of eosinophils is associated with what?

A

Chronic allergic inflammation

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38
Q

What is preformed in eosinophils for release?

A

Enzymes and toxic proteins

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39
Q

Chronic responses involve what?

A

Th2 cells and eosinophils

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40
Q

Allergic asthma is due to what?

A

Mast and Th2 cells activating eosinophils to cause damage in the lungs

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41
Q

Chronic asthma is what type of hypersensitivity?

A

Type 4

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42
Q

Why is chronic asthma different from allergic asthma?

A

Hyper-responsiveness of airways and exposure to the allergen is no longer needed to initiate attack

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43
Q

Chronic asthma involves what cells?

A

Th2 cells

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44
Q

Role of corticosteroids in type I HS?

A

Reduce inflammation

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45
Q

Role of leukotriene antagonists in type I HS?

A

Relax bronchial smooth muscle and reduce inflammation

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46
Q

Desensitization works how in type I?

A

Giving low doses of allergens may inhibit IgE production and cause production of IgG instead.

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47
Q

What is Anti-IgE antibody used for in type I HS?

A

Just destroy IgE

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48
Q

What does cromolyn do?

A

Stabilizes membranes of mast cells so no degranulation

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49
Q

How to induce regulatory T cells for type I?

A

Give cytokines (IL-10 and IFN-gamma)

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50
Q

How does penicillin become an allergen?

A
  1. Binds to bacteria and opens its Beta-lactam ring which forms covalent bond with amino acid residue. B cells recognize this ring or ring with the protein and uptake it. They present the modified peptides to T cells which cause B cells to release IgE and IgG against penicillin
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51
Q

Penicillin allergy is what type of hypersensitivity?

A

Type 1, 2, and 3

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52
Q

Type II hypersensitivities are mediated by what?

A

IgG directed at cell surface antigens

53
Q

Since penicillin binds to erythrocytes, what could happen?

A

Ab’s attack penicillin epitopes on RBC’s leading to lysis of RBC’s

54
Q

A person that has A blood is said to have what antibody?

A

Anti-B antibody

55
Q

A person that has AB blood is said to have what antibody?

A

No antibody

56
Q

A person that has type O blood is said to have what antibody?

A

A and B antibody

57
Q

What is the A antigen?

A

GalNAc

58
Q

What is the B antigen?

A

Gal

59
Q

What does it mean if someone is Rh-?

A

They possess an anti-Rh antibody so that their blood has no Rh.

60
Q

What type of hypersensitivity is hemolytic disease of the newborn?

A

Type II

61
Q

What is a type III hypersensitivity reaction?

A

When a antigen-antibody-complement complex forms which deposits into mast cell causing degranulation

62
Q

Accumulation of immune complexes results in what?

A

Complement fixation

63
Q

What are the two molecules that stimulate histamine release?

A

C3a and C5a (anaphylatoxins)

64
Q

Type III hypersensitivity reactions involve what antibody?

A

IgG

65
Q

What is the arthus reaction?

A

IgG reacting with mast cells at injection site of inoculations for desensitization

66
Q

Symptoms of type III HS?

A

Hemorrhaging in skin and urticarial rashes

67
Q

What type of HS is serum sickness?

A

HS

68
Q

What happens in serum sickness?

A

First exposure to antibodies from foreign species takes 7-10 days to develop. Subsequent exposure is far faster and stronger.

69
Q

Apply serum sickness to real life.

A

Can only use one type of anti-venin in life. Then switch to another animal’s.

70
Q

Type IV hypersensitivity involves what cells?

A

T cells

71
Q

Why is type IV HS so delayed?

A

Have to develop whole immune response against it and direct T cells

72
Q

How long does it take for Type IV HS to peak?

A

2-3 days

73
Q

What type of HS is contact dermatitis?

A

Type IV

74
Q

What causes contact dermatitis?

A

When hapten pentadecacatechol binds to ECM proteins on skin which are degraded by skin phagocytes which present proteins to Th1 which produce cytokines activating macrophages

75
Q

Why is it bad is pentadecacatechol penetrates the skin?

A

Crosses plasma membrane of cells and modifies proteins inside causing CD8 cytotoxic killing of thsoe cells

76
Q

Key feature of Type IV HS?

A

Antigens are presented to T cells and effector response is provided by these T cells

77
Q

Celiac disease is what type of HS?

A

IV

78
Q

What happens in celiac disease?

A

CD4 T cells tell Galt to respond to gluten which activates tissue macrophages, causing inflammation in SI that destroys tissue.

79
Q

How can celiac disease be controlled?

A

NO GLUTEN DIET

80
Q

Allergic response is defined by what?

A

Presentation of symptoms

81
Q

What happens in autoimmune hemolytic anemia?

A

IgM or IgG bind to RBC antigens and cause opsonization which leads to phagocytosis in spleen.
However RBC’s are functional until destroyed

82
Q

What is autoimmune neutropenia?

A

IgM or IgG binds to neutrophil antigens and leads to their destruction

83
Q

What is Good pasture’s syndrome?

A

IgG forms against alpha3 chain of type IV collagen in BM’s. Is really bad in renal glomeruli leading to loss of kidney function and death

84
Q

Treatment of Goodpastures?

A

Plasma exchange to remove antibodies and immunosuppressive drugs

85
Q

What is Grave’s disease?

A

Anti-TSH receptor antibody (IgG2) binds to TSH receptors but do not fix complement or bind Fc receptors causing over stimulation of thryoid through Th2 response)

86
Q

Short term Grave’s disease treatment?

A

Drugs to inhibit thyroid

87
Q

Long term grave’s disease treatment?

A

remove thryoid

88
Q

Symptoms of Grave’s disease?

A

Heat intolerance, irrtability, weight loss, bulging of eyes and thyroid

89
Q

What is Hashimoto’s Thyroiditis?

A

Th1 response against thyroid antigens causing lymphocytes to destroy thyroid tissue leading to hypothyroidism

90
Q

Treatment for hashimoto’s thyroiditis?

A

Thyroid hormone replacement

91
Q

What is multiple sclerosis?

A

Th1 cells produce IFN-gamma and activated macrophages release proteases to destroy myelin sheaths in CNS.

92
Q

What can reduce severity of multiple sclerosis?

A

High doses of immunosuppressives

93
Q

What is myasthenia gravis?

A

Antibodies against acetylcholine receptors form leading to loss of NMJ function which causes droopy eyelids, weak face muscles, and impaired breathing

94
Q

Treatment of myasthenia gravis is?

A

Azathioprine which prohibits autoantibody production

95
Q

What is systemic lupus erythematosus?

A

IgG antibodies against cell surfaces, cytoplasm and nucleus.

96
Q

Lupus autoantibodies cause what?

A

Inflammation, tissue destruction, release of soluble cellular components and formation of immune complexes.

97
Q

What is rheumatoid arthritis?

A

IgM, IgG, and IgA’s against Fc region of human IgG (called rheumatoid factor) causes leukocyte infiltration into joints resulting in prostaglandin, leukotriene, and enzyme release.

98
Q

What is Type I diabetes?

A

Antibody against Beta cells in pancreas in which CD8 cells eliminate Beta cells.

99
Q

What type of HS is Type I diabetes?

A

Type IV

100
Q

When using animal insulin to treat type I diabetes what might develop?

A

Type III HS

101
Q

What does autoimmunity tell you about where the problem started?

A

Problem with central and peripheral tolerance

102
Q

Autoreactive B cells should undergo peripheral tolerance how?

A

Stay in lymph node and die.

103
Q

What removes most autoreactive T cells?

A

Negative selection/Central tolerance

104
Q

Tregs produce what cytokines?

Result of these?

A

IL-4, IL-10, TGF-Beta

Suppress CD4 autoreactive cells

105
Q

What TF do tregs express?

A

FoxP3

106
Q

A problem with FoxP3 leads to what?

A

Absence of tregs –> Autoimmunity against a number of tissues

107
Q

What is a dysfunction in FoxP3 called?

A

IPEX (x linked deficiency of Fox P3)

108
Q

How are anergic T cells dealt with?

A

No B7 exposed by APC so no secondary activation of T cells

109
Q

How are T cells dealt with in suppression?

A

Regulatory T cells block activation

110
Q

How are autoreactive T cells dealt with through deletion?

A

Apoptosis

111
Q

Is there a genetic predisposition to autoimmunity?

A

Yes, for example ankylosing spondylitis is due to MHC allele HLA-B27

112
Q

What does a problem with the AIRE gene result in?

A

APS-1 or APECED

113
Q

What is APS-1 or APECED?

A

No AIRE gene results in no presentation of self antigen to T cells in thymus so autoreactive T cells develop

114
Q

A deficiency in AIRE is breaking which tolerance?

A

CENTRAL

115
Q

How does a B cell break peripheral tolerance?

A

B cell binds self antigen and is activated by a T cell causing differentiation of B cell into plasma cells secreting self antibody

116
Q

What is sympathetic opthamalia?

A

When trauma to eye causes self peptide to get in blood stream where it activates T cells in lymph nodes that return to both eyes and cause tissue damage

117
Q

How might a mother pass Grave’s disease to fetus?

A

In grave’s disease, IgM from mother against TSHR crosses placenta and stimulates babies Thyroid

118
Q

What can remove maternal antibodies?

A

Plasmapheresis

119
Q

Will Type IV HS cross to the fetus?

A

No, T cells can’t cross barrier

120
Q

Explain acute rheumatic fever?

A

Antibodies toward bacterial cell wall of strep pyogenes react with epitopes in heart, joints, and kidneys causing widespread inflammation leading to heart failure

121
Q

Why might acute rheumatic fever occur?

A

A pathogenic antigen might very very similar to a self peptide so when an immune response occurs against bacteria, it also occurs against self.

122
Q

What cells that don’t express MHC-II, will do so after IFN-gamma upregulates it?

A

Thyroid cells, Pancreatic Beta cells, astrocytes and microglia

123
Q

What is pemphigus vulgaris?

A

Develop Ab’s against desmogleins of keratinocyte cell junctions. First the EC5 which is symptomless and then EC1 and EC2 causing disease.

124
Q

How does the response toward DNA in SLE develop?

A

CD4 cells recognize specific pieces of self DNA and will all stimulate the same B cells so that the B cell initiates attacks against all different antigens of DNA.

125
Q

Treatment for rheumatism is what?

A

Ab against TNF-alpha called infliximab

126
Q

What does rituximab do?

A

Initiates ADCC (NK Cells) against CD20 on B cells thus alleviating rheumatoid

127
Q

How does one treat B cells in autoimmunity?

A

CD20 mAB

128
Q

In MS, how would one attack HMG-CoA reductase?

A

Statins

129
Q

How would one attack T cells in autoimmunity?

A

CD3 mAB

MICRO (22 decks)

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