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Inflammation > Hypersensitivity Type 1 > Flashcards

Hypersensitivity Type 1 Flashcards

1
Q

What is a sensitisation phase?

A

Primary antigen exposure to develop an adaptive immune response

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2
Q

What is an effector phase?

A

Late primary, chronic, or recall of an adaptive immune response that leads to pathology

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3
Q

What mediates a Type 1 reaction?

A

IgE ab

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4
Q

What mediates a type II reaction?

A

IgG or IgM ab

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5
Q

What mediates a type III reaction?

A

Ag/Ab complexes (IgG OR IgM)

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6
Q

What mediates a type IV reaction?

A

Ag specific T cells and macrophages

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7
Q

What responses does TH2 coordinate?

A

High IgE levels
M2 Macrophages
Recruitment + Activation of mast cells, eosinophils, basophils

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8
Q

Where are Eosinophils located?

A

Tissues, esp CT under mucosa
Circulation
Inflammation sites

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9
Q

How are Eosinophils activated?

A

Cytokines
Complement
Ab opsonized Ag

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10
Q

Where are Mast Cells located?

A

Tissue, esp at mucosa

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11
Q

How are mast cells activated?

A

Cytokines
Major basic protien
FceR1

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12
Q

Where are Basophils located?

A

Circulation
Sites of inflammation

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13
Q

How are basophils activated?

A

Cytokines
Major basic protein
FceR1

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14
Q

What is type I hypersensitivity?

A

Antigen crosslinking of mast cell and basophil bound IgE, resulting in degranulation and histamine response

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15
Q

What are some of the most common allergens?

A

Pollen, insect bite/sting/feces, hair, egg, shellfish, milk products

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16
Q

What are some clinical presentations?

A

GI tract - vomiting, diarrhea
Eyes, airways - rhinitis, conjunctivitis, asthma
Skin - dermatitis
Generalised - anaphylaxis, urticaria, bronchospasms

17
Q

What leads to the sensitisation phase of a Type I Hypersensitivity reaction?

A

Induction of an IR favouring IgE production
Th2 env - IL4 IL5 IL9 IL13
Sensitized immune cells at skin barrier
Environmental antigens normally don’t promote IR due to Treg presence

18
Q

What is Atopy

A

Predisposition to suffer IgE mediated allergic responses
Associated with high IgE, IL3 +IL 5 levels and Eosinophilia
Not responsible for all IgE hypersensitivities

19
Q

Describe the genetic effects on Atopy

A

High genetic component
Many susceptibility genes where IgE response cytokines, receptors, PG rec and proteinases are overexpressed or made more sensitive
Breed and lineage predisposition

20
Q

What is the hygiene hypothesis in reference to environmental effects on atopy?

A

Early exposure to infectious agents inhibit atopy development by developing a more directed immune response
Likely through promotion of Treg function

21
Q

How does pollution contribute to the environmental effects on atopy?

A

Possibly contributes to development or simply exacerbates the clinical symptoms of atopic dermatitis

22
Q

What is anaphylaxis?

A

Allergen is distributed systemically through blood circulation/response is systemic

23
Q

Describe an anaphylactic situation

A

Rapid onset of an acute IgE mediated reaction
Mild to severe
Local to generalized

24
Q

What is anaphylactic shock?

A

Generalized and severe iGe mediated response

25
Q

What is typically seen in anaphylaxis?

A

Systemic histamine release from mast cells and basophils - Widespread increase in vascular permeability + smooth muscle contraction
-> drop in BP - Hypotonic shock
->Resp failure

26
Q

Common treatment option for anaphylaxis

A

Epinephrine
Relaxation of sm mcl
Reverse cardiovascular effects

27
Q

NON TESTED
Series of allergy treatments

A

1.AntiInflammatory Mediators
2.Allergen Reduction
3.Improve Physical Barrier Function
4.Remove other causes of inflammation

28
Q

NON TESTED
What are some anti-inflammatory mediators

A

AntiHistamines - block H1 receptors
Corticosteroids - last response for general immune response suppression
NSAIDS - inhibit PG formation by COX

29
Q

NON TESTED
What is allergy desensitisation?

A

Immunotherapy designed to restore normal allergen response via regular allergen administration
Associated with IgE to IgG class switch and induction of Treg
50% success rate

30
Q

NON TESTED
What are some immunomodulatory antibodies?

A

Anti-IgE - Block mast cell triggering
Anti- IL5/CCR4 - reduces eosinophil generation/recruitment
Anti-IL31 - Reduces Th2 driven inflammation, anti-pruritic,

Inflammation (2 decks)

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