MICRO > Ch7: Hypersensitivity and Autoimmunity > Flashcards

Ch7: Hypersensitivity and Autoimmunity Flashcards

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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
Degranulation in GI tract of Type I causes what?2
Diarrhea and vomiting
26
Degranulation in Airways causes what? 2
Phlegm and coughing
27
Degranulation in blood vessels causes what? 3
Edema Inflammation Increased lymph flow
28
Treatment for Type I involves what?
Block effects of inflammatory mediators (histamine and leukotrienes) Can't stop the cause: IgE crosslinking
29
When allergen is in skin, what results? (2)
1. urticaria | 2. angioedema
30
Where do recruited eosinophils go in Type I?
To the lung
31
Why is mast cell degranulation bad in the heart and vascular system?
Leakage of fluids into tissue resulting in drop in cardiac output leading to anaphylactic shock and possibly death
32
Most extreme outcome of hypersensitivity is what?
IgE mediated systemic anaphylaxis
33
What reverses systemic anaphylaxis? | How? (3)
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
34
Activated mast cells release what to stimulate eosinophils?
IL-5
35
What is the most important chemokine for eosinophils?
CCL11 (Eotaxin)
36
Do resting eosinophils express IgE receptors on surface?
No, not first responder
37
Presence of eosinophils is associated with what?
Chronic allergic inflammation
38
What is preformed in eosinophils for release?
Enzymes and toxic proteins
39
Chronic responses involve what?
Th2 cells and eosinophils
40
Allergic asthma is due to what?
Mast and Th2 cells activating eosinophils to cause damage in the lungs
41
Chronic asthma is what type of hypersensitivity?
Type 4
42
Why is chronic asthma different from allergic asthma?
Hyper-responsiveness of airways and exposure to the allergen is no longer needed to initiate attack
43
Chronic asthma involves what cells?
Th2 cells
44
Role of corticosteroids in type I HS?
Reduce inflammation
45
Role of leukotriene antagonists in type I HS?
Relax bronchial smooth muscle and reduce inflammation
46
Desensitization works how in type I?
Giving low doses of allergens may inhibit IgE production and cause production of IgG instead.
47
What is Anti-IgE antibody used for in type I HS?
Just destroy IgE
48
What does cromolyn do?
Stabilizes membranes of mast cells so no degranulation
49
How to induce regulatory T cells for type I?
Give cytokines (IL-10 and IFN-gamma)
50
How does penicillin become an allergen?
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
51
Penicillin allergy is what type of hypersensitivity?
Type 1, 2, and 3
52
Type II hypersensitivities are mediated by what?
IgG directed at cell surface antigens
53
Since penicillin binds to erythrocytes, what could happen?
Ab's attack penicillin epitopes on RBC's leading to lysis of RBC's
54
A person that has A blood is said to have what antibody?
Anti-B antibody
55
A person that has AB blood is said to have what antibody?
No antibody
56
A person that has type O blood is said to have what antibody?
A and B antibody
57
What is the A antigen?
GalNAc
58
What is the B antigen?
Gal
59
What does it mean if someone is Rh-?
They possess an anti-Rh antibody so that their blood has no Rh.
60
What type of hypersensitivity is hemolytic disease of the newborn?
Type II
61
What is a type III hypersensitivity reaction?
When a antigen-antibody-complement complex forms which deposits into mast cell causing degranulation
62
Accumulation of immune complexes results in what?
Complement fixation
63
What are the two molecules that stimulate histamine release?
C3a and C5a (anaphylatoxins)
64
Type III hypersensitivity reactions involve what antibody?
IgG
65
What is the arthus reaction?
IgG reacting with mast cells at injection site of inoculations for desensitization
66
Symptoms of type III HS?
Hemorrhaging in skin and urticarial rashes
67
What type of HS is serum sickness?
HS
68
What happens in serum sickness?
First exposure to antibodies from foreign species takes 7-10 days to develop. Subsequent exposure is far faster and stronger.
69
Apply serum sickness to real life.
Can only use one type of anti-venin in life. Then switch to another animal's.
70
Type IV hypersensitivity involves what cells?
T cells
71
Why is type IV HS so delayed?
Have to develop whole immune response against it and direct T cells
72
How long does it take for Type IV HS to peak?
2-3 days
73
What type of HS is contact dermatitis?
Type IV
74
What causes contact dermatitis?
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
Why is it bad is pentadecacatechol penetrates the skin?
Crosses plasma membrane of cells and modifies proteins inside causing CD8 cytotoxic killing of thsoe cells
76
Key feature of Type IV HS?
Antigens are presented to T cells and effector response is provided by these T cells
77
Celiac disease is what type of HS?
IV
78
What happens in celiac disease?
CD4 T cells tell Galt to respond to gluten which activates tissue macrophages, causing inflammation in SI that destroys tissue.
79
How can celiac disease be controlled?
NO GLUTEN DIET
80
Allergic response is defined by what?
Presentation of symptoms
81
What happens in autoimmune hemolytic anemia?
IgM or IgG bind to RBC antigens and cause opsonization which leads to phagocytosis in spleen. However RBC's are functional until destroyed
82
What is autoimmune neutropenia?
IgM or IgG binds to neutrophil antigens and leads to their destruction
83
What is Good pasture's syndrome?
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
Treatment of Goodpastures?
Plasma exchange to remove antibodies and immunosuppressive drugs
85
What is Grave's disease?
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
Short term Grave's disease treatment?
Drugs to inhibit thyroid
87
Long term grave's disease treatment?
remove thryoid
88
Symptoms of Grave's disease?
Heat intolerance, irrtability, weight loss, bulging of eyes and thyroid
89
What is Hashimoto's Thyroiditis?
Th1 response against thyroid antigens causing lymphocytes to destroy thyroid tissue leading to hypothyroidism
90
Treatment for hashimoto's thyroiditis?
Thyroid hormone replacement
91
What is multiple sclerosis?
Th1 cells produce IFN-gamma and activated macrophages release proteases to destroy myelin sheaths in CNS.
92
What can reduce severity of multiple sclerosis?
High doses of immunosuppressives
93
What is myasthenia gravis?
Antibodies against acetylcholine receptors form leading to loss of NMJ function which causes droopy eyelids, weak face muscles, and impaired breathing
94
Treatment of myasthenia gravis is?
Azathioprine which prohibits autoantibody production
95
What is systemic lupus erythematosus?
IgG antibodies against cell surfaces, cytoplasm and nucleus.
96
Lupus autoantibodies cause what?
Inflammation, tissue destruction, release of soluble cellular components and formation of immune complexes.
97
What is rheumatoid arthritis?
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
What is Type I diabetes?
Antibody against Beta cells in pancreas in which CD8 cells eliminate Beta cells.
99
What type of HS is Type I diabetes?
Type IV
100
When using animal insulin to treat type I diabetes what might develop?
Type III HS
101
What does autoimmunity tell you about where the problem started?
Problem with central and peripheral tolerance
102
Autoreactive B cells should undergo peripheral tolerance how?
Stay in lymph node and die.
103
What removes most autoreactive T cells?
Negative selection/Central tolerance
104
Tregs produce what cytokines? | Result of these?
IL-4, IL-10, TGF-Beta Suppress CD4 autoreactive cells
105
What TF do tregs express?
FoxP3
106
A problem with FoxP3 leads to what?
Absence of tregs --> Autoimmunity against a number of tissues
107
What is a dysfunction in FoxP3 called?
IPEX (x linked deficiency of Fox P3)
108
How are anergic T cells dealt with?
No B7 exposed by APC so no secondary activation of T cells
109
How are T cells dealt with in suppression?
Regulatory T cells block activation
110
How are autoreactive T cells dealt with through deletion?
Apoptosis
111
Is there a genetic predisposition to autoimmunity?
Yes, for example ankylosing spondylitis is due to MHC allele HLA-B27
112
What does a problem with the AIRE gene result in?
APS-1 or APECED
113
What is APS-1 or APECED?
No AIRE gene results in no presentation of self antigen to T cells in thymus so autoreactive T cells develop
114
A deficiency in AIRE is breaking which tolerance?
CENTRAL
115
How does a B cell break peripheral tolerance?
B cell binds self antigen and is activated by a T cell causing differentiation of B cell into plasma cells secreting self antibody
116
What is sympathetic opthamalia?
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
How might a mother pass Grave's disease to fetus?
In grave's disease, IgM from mother against TSHR crosses placenta and stimulates babies Thyroid
118
What can remove maternal antibodies?
Plasmapheresis
119
Will Type IV HS cross to the fetus?
No, T cells can't cross barrier
120
Explain acute rheumatic fever?
Antibodies toward bacterial cell wall of strep pyogenes react with epitopes in heart, joints, and kidneys causing widespread inflammation leading to heart failure
121
Why might acute rheumatic fever occur?
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
What cells that don't express MHC-II, will do so after IFN-gamma upregulates it?
Thyroid cells, Pancreatic Beta cells, astrocytes and microglia
123
What is pemphigus vulgaris?
Develop Ab's against desmogleins of keratinocyte cell junctions. First the EC5 which is symptomless and then EC1 and EC2 causing disease.
124
How does the response toward DNA in SLE develop?
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
Treatment for rheumatism is what?
Ab against TNF-alpha called infliximab
126
What does rituximab do?
Initiates ADCC (NK Cells) against CD20 on B cells thus alleviating rheumatoid
127
How does one treat B cells in autoimmunity?
CD20 mAB
128
In MS, how would one attack HMG-CoA reductase?
Statins
129
How would one attack T cells in autoimmunity?
CD3 mAB
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