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GBA Immunology > Week 10 - Hypersensitivity > Flashcards

Week 10 - Hypersensitivity Flashcards

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

A

Histamine, Tryptase, Chimase, Carboxypeptidase

24
Q

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

A

Minutes

25
Q

By activation of PLA in the Mast cell we get specific mediators release how and which are they?

A

Arachidonic acid is produced and allows for PGs and LTs

26
Q

What are the late transcribed mediators that are released from Mast cells? (More than 30 minutes)

A

IL3–6 and TNFalpha

27
Q

Common Effects of Mast cells Histamine and Lipid mediators

A

Vascular leak
Bronco constriction
Intestinal Hyper-motility
(Patient should be treated within 30 minutes)

28
Q

IL5 importance in HSN1

A

Released by TH2 cells - Activation of Eosinophils, LT released
(Less massive response since they are less presented than Mast cells)

29
Q

What is the importance of Crocothyrotomy in HSN1?

A

Supply of air in a severe anaphylaxis causing bronhoconstriction.

30
Q

Atopy definition

A

Genetic predisposition to exaggerated IgE production.

Eczema, Asthama and Hay fever can occur in increased risk.

31
Q

How is the balance of TH1 and TH2 cytokines determines the diseases one could acquire? (Hypothesis)

A

TH1 - Protective Immunity for Infections

TH2 - Allergic Diseases like asthma

32
Q

Where can find the FCgR ? How does it relate to HSN2 and 3?

A

Macrophages and Neutrophills

Both cause Phagocytosis in HSN2 and HSN3

33
Q

Rh incompatibility is an example of -

How?

A

HSN2

After first birth Rh-IgG produced and may attack the RBCs in the second pregnancy with a Rh+

34
Q

Myasthenia Gravis and Graves (Basedow) disease are examples of ?
In which way each of them interfere normal function - Agonistic/Antagonistic

A

HSN2
M. Gravis - Antagonistic by binding of ACh receptors on Muscles
Graves - Agonistic by overexpression of T3

35
Q

What is the problem with development of large amounts of IC like in HSN3?

A

Blockage of small vessels - Capillaries, Glomeruli, Joint vessels

36
Q

What is the further IC function after blockage of small vessels?

A

Activation of C3a and C5a causing Neutrophills chemotaxis and Frustrated Phagocytosis (Degranulation) that leads to endothelial damage and Vascular permeability

37
Q

SLE is an example of ?

A

HSN3

38
Q

HSN4 is also called Delayed type (2-3 days) because -

A

Antigen Presentation by APCs take time in order for T cells to be activated.

39
Q

What kind of molecule is needed to form usually a primary sensitization in HSN4?

A

Hapten from Environment to combine with skin proteins in order to form an active antigen

40
Q

TH1 releases IFN gamma in HSN4 what is the effect of it?

A

MHC 2 expression in Epithelial, Mesenchymal cells and Macrophages (More)

41
Q

Gluten sensitivity (Coeliac disease) are examples for

A

HSN4

42
Q

Which type of HSN can Penicillin form?

A

All the 4 HSNs

43
Q

Examples for Non Immunological Food Intolerance

A

Lactose Intolerance

Histamine Rich Intolerance

44
Q

Examples for Immunological Food Hypersensitivity

A

IgE - Milk, Egg, Peanut, Pollen, Latex

Non-IgE - Celiac (Gluten), Systemic Allergic contact Dermatitis

45
Q

Examples for cross reactivity allergy?

A

Latex allergy with Fruits

Mellon Allergy with other fruits

46
Q

Drug Therapy for Allergy (5)

Polysensitized

A 
Adrenaline
Glucocorticoids
LT receptor antagonists
H1 Histamine receptor Antagonists
Mast cell stabilazers
47
Q

Therapy for Oligosentisized Pateints

A

Allergen Avoidance

Immunotherapy

48
Q

Immunotherapy

A

Desensitization in repeated injection small amount leading to IgG4 instead of IgE development, T reg activation.

49
Q

Allergy Prevention - General Practice

A

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
Q

Asthma Alternative Treatments

A

Anti-IgE

Anti-IL5

51
Q

Common symptoms of Allergy

A

Urticaria, Pruritus, Hypotension, Erythema, Responsive to Antihistamines, Increased Tryptase in serum

52
Q

Symptoms of HAE

A

Possible Hypotension, Possible Erythema, No response for Antihistmines, C4 level in blood decreased

53
Q

Hepten that feats to all types of HSN

A

Penicillin

54
Q

What is the main cell responsible for the amplification over time of the reaction of DTHSN (HSN4)? What is the Loop is this reaction?

A

TH1 - Setting a loop of activation of macrophages followed by IFNγ release and MHC-II over expression that activates more TH1 cells!

55
Q

Antibodies formed in Coeliac Disease

A

Anti-Gliadin, Anti-Transglutaminase and Anti-Endomysial

56
Q

How is Coeliac Disease recognized in biopsy? Morphology? Endoscopy?

A

Villi Atrophy

“Cracked-mud” appearance to mucosa

GBA Immunology (15 decks)

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