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GBA Immunology > Week 10 - Hypersensitivity > Flashcards

Week 10 - Hypersensitivity Flashcards

(56 cards)

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1
Q

When did allergic diseases start to increase drastically in number?
What does it mean?

A

1990~

Hypersensitivity is dependent of Genetic but probably more important environmental reasons.

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2
Q

What is necessary to be uninfluenced by the genetic and environmental stimulus in order to form Hypersensitivity?
(Simplified)

A

DC and T regulatory cells

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3
Q

What is the leading Hypothesis for the reason of allergies cause?

A

High Hygiene level is causing the immune system to be inconsistently stimulated - Biodiversity Hypothesis

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4
Q

Organize the Hypersensitivities reaction time and severity according to types?

A

4 to 1

Increasing in severity and Reaction times

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5
Q

Examples for allergies with the following sites of entry -

Skin, Respiratory, GI

A

Skin - Atopic Dermatitis, Acute urticaria
Respiratory - Asthma, Hay Fever
GI - Food allergy

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6
Q

What is a common epithelial phenomenon occurring with allergy formation (sensitization) ? What is the hypothetical paradox associated with it?

A

Epithelial Injury - Not obvious if it is caused by the sensitization or it is a participating factor in its development?

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7
Q

What is the most critical point of sensitization in Allergy formation? Determined by DCs

A

TH2 development from naive T cells accompanied by IL4 (not known if from TH2) and the Interaction with Antigen bound B cell.

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8
Q

When is the patient called Sensitized?

A

IgEs in blood stream are present

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9
Q

Sensitizing agents in Hypersensitivity come from 3 pathways -

A

Environmental
Tissue
Persistent Microbes

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10
Q

Definition of Hypersensitivity

A

Pathological immune response for harmless or self antigen

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11
Q

First contact with the sensitizing agent are ____________ but the second contact will show uncontrolled attack against on tissue.

A

First contact with the sensitizing agent are asymptomatic but the second contact will show uncontrolled attack against on tissue.

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12
Q

Type 1-3 have something in common in the immune reaction propagation

A

Type 1 - IgE dependent
Type 2 and 3 - IgG dependent
Antibody dependent

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13
Q

What are the effector meachnism of each Hypersensitivity

A

1 - Mast cell Degranulation
2 -Complement or Antibody signaling Phagocytosis
3 - IC accumulation
4 - T mediated (Delayed - 2-3 days)

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14
Q

Why is it important that HSN 1 involves protein antigen?

A

Presentation by DC cells and B cells by MHC2

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15
Q

Why is it possible the antigens presented by B cells and DCs will be the same?

A

Only 6 types of MHC2 types allows the binding

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16
Q

What is the importance of IL4 release by the TH2 for the progression of HSN1?

A

Class switch to IgE

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17
Q

If in “time 0” we are exposed to allergen when will there be a IgE produced for it by TD Follicular B cells?

A

After two weeks

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18
Q

If in “time 0” we are exposed to allergen when will there be a IgM produced for it by Extra-follicular B cells? Why does it lowers afterwards?

A

Few days

These cells are short lived

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19
Q

What will happen if the IgEs for Allergen cover the Mast cells? (without an antigen on them)

A

Nothing

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20
Q

What will happen if the IgEs for Allergen cover the Mast cells? (with an antigen on them)

A

Mast Degranulation and Memory cells will produce more and more IgE for Allergen

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21
Q

How will the immune response change from exposure to exposure?

A

Increases as the Memory cells are more equipped for IgE synthesis.

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22
Q

What is the cause of the signaling effectively of the FC-epsilon-R?

A

ITAM presences

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23
Q

Contents of Mast cells granules - Early mediators

Study These Flashcards
A

Histamine, Tryptase, Chimase, Carboxypeptidase

24
Q

How long does it take for a mast cell to degranulate?

25
By activation of PLA in the Mast cell we get specific mediators release how and which are they?
Arachidonic acid is produced and allows for PGs and LTs
26
What are the late transcribed mediators that are released from Mast cells? (More than 30 minutes)
IL3–6 and TNFalpha
27
Common Effects of Mast cells Histamine and Lipid mediators
Vascular leak Bronco constriction Intestinal Hyper-motility (Patient should be treated within 30 minutes)
28
IL5 importance in HSN1
Released by TH2 cells - Activation of Eosinophils, LT released (Less massive response since they are less presented than Mast cells)
29
What is the importance of Crocothyrotomy in HSN1?
Supply of air in a severe anaphylaxis causing bronhoconstriction.
30
Atopy definition
Genetic predisposition to exaggerated IgE production. | Eczema, Asthama and Hay fever can occur in increased risk.
31
How is the balance of TH1 and TH2 cytokines determines the diseases one could acquire? (Hypothesis)
TH1 - Protective Immunity for Infections | TH2 - Allergic Diseases like asthma
32
Where can find the FCgR ? How does it relate to HSN2 and 3?
Macrophages and Neutrophills | Both cause Phagocytosis in HSN2 and HSN3
33
Rh incompatibility is an example of - | How?
HSN2 | After first birth Rh-IgG produced and may attack the RBCs in the second pregnancy with a Rh+
34
Myasthenia Gravis and Graves (Basedow) disease are examples of ? In which way each of them interfere normal function - Agonistic/Antagonistic
HSN2 M. Gravis - Antagonistic by binding of ACh receptors on Muscles Graves - Agonistic by overexpression of T3
35
What is the problem with development of large amounts of IC like in HSN3?
Blockage of small vessels - Capillaries, Glomeruli, Joint vessels
36
What is the further IC function after blockage of small vessels?
Activation of C3a and C5a causing Neutrophills chemotaxis and Frustrated Phagocytosis (Degranulation) that leads to endothelial damage and Vascular permeability
37
SLE is an example of ?
HSN3
38
HSN4 is also called Delayed type (2-3 days) because -
Antigen Presentation by APCs take time in order for T cells to be activated.
39
What kind of molecule is needed to form usually a primary sensitization in HSN4?
Hapten from Environment to combine with skin proteins in order to form an active antigen
40
TH1 releases IFN gamma in HSN4 what is the effect of it?
MHC 2 expression in Epithelial, Mesenchymal cells and Macrophages (More)
41
Gluten sensitivity (Coeliac disease) are examples for
HSN4
42
Which type of HSN can Penicillin form?
All the 4 HSNs
43
Examples for Non Immunological Food Intolerance
Lactose Intolerance | Histamine Rich Intolerance
44
Examples for Immunological Food Hypersensitivity
IgE - Milk, Egg, Peanut, Pollen, Latex | Non-IgE - Celiac (Gluten), Systemic Allergic contact Dermatitis
45
Examples for cross reactivity allergy?
Latex allergy with Fruits | Mellon Allergy with other fruits
46
Drug Therapy for Allergy (5) | Polysensitized
``` Adrenaline Glucocorticoids LT receptor antagonists H1 Histamine receptor Antagonists Mast cell stabilazers ```
47
Therapy for Oligosentisized Pateints
Allergen Avoidance | Immunotherapy
48
Immunotherapy
Desensitization in repeated injection small amount leading to IgG4 instead of IgE development, T reg activation.
49
Allergy Prevention - General Practice
Exposure in small increasing doses (e.g. milk) from early years Teaching the immature immune system for tolerance - Treg/Th3 stimulation by TGFbeta, IL10
50
Asthma Alternative Treatments
Anti-IgE | Anti-IL5
51
Common symptoms of Allergy
Urticaria, Pruritus, Hypotension, Erythema, Responsive to Antihistamines, Increased Tryptase in serum
52
Symptoms of HAE
Possible Hypotension, Possible Erythema, No response for Antihistmines, C4 level in blood decreased
53
Hepten that feats to all types of HSN
Penicillin
54
What is the main cell responsible for the amplification over time of the reaction of DTHSN (HSN4)? What is the Loop is this reaction?
TH1 - Setting a loop of activation of macrophages followed by IFNγ release and MHC-II over expression that activates more TH1 cells!
55
Antibodies formed in Coeliac Disease
Anti-Gliadin, Anti-Transglutaminase and Anti-Endomysial
56
How is Coeliac Disease recognized in biopsy? Morphology? Endoscopy?
Villi Atrophy | "Cracked-mud" appearance to mucosa

GBA Immunology (15 decks)

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