Hypersensitivity Type 1 Flashcards
What is a sensitisation phase?
Primary antigen exposure to develop an adaptive immune response
What is an effector phase?
Late primary, chronic, or recall of an adaptive immune response that leads to pathology
What mediates a Type 1 reaction?
IgE ab
What mediates a type II reaction?
IgG or IgM ab
What mediates a type III reaction?
Ag/Ab complexes (IgG OR IgM)
What mediates a type IV reaction?
Ag specific T cells and macrophages
What responses does TH2 coordinate?
High IgE levels
M2 Macrophages
Recruitment + Activation of mast cells, eosinophils, basophils
Where are Eosinophils located?
Tissues, esp CT under mucosa
Circulation
Inflammation sites
How are Eosinophils activated?
Cytokines
Complement
Ab opsonized Ag
Where are Mast Cells located?
Tissue, esp at mucosa
How are mast cells activated?
Cytokines
Major basic protien
FceR1
Where are Basophils located?
Circulation
Sites of inflammation
How are basophils activated?
Cytokines
Major basic protein
FceR1
What is type I hypersensitivity?
Antigen crosslinking of mast cell and basophil bound IgE, resulting in degranulation and histamine response
What are some of the most common allergens?
Pollen, insect bite/sting/feces, hair, egg, shellfish, milk products
What are some clinical presentations?
GI tract - vomiting, diarrhea
Eyes, airways - rhinitis, conjunctivitis, asthma
Skin - dermatitis
Generalised - anaphylaxis, urticaria, bronchospasms
What leads to the sensitisation phase of a Type I Hypersensitivity reaction?
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
What is Atopy
Predisposition to suffer IgE mediated allergic responses
Associated with high IgE, IL3 +IL 5 levels and Eosinophilia
Not responsible for all IgE hypersensitivities
Describe the genetic effects on Atopy
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
What is the hygiene hypothesis in reference to environmental effects on atopy?
Early exposure to infectious agents inhibit atopy development by developing a more directed immune response
Likely through promotion of Treg function
How does pollution contribute to the environmental effects on atopy?
Possibly contributes to development or simply exacerbates the clinical symptoms of atopic dermatitis
What is anaphylaxis?
Allergen is distributed systemically through blood circulation/response is systemic
Describe an anaphylactic situation
Rapid onset of an acute IgE mediated reaction
Mild to severe
Local to generalized
What is anaphylactic shock?
Generalized and severe iGe mediated response
What is typically seen in anaphylaxis?
Systemic histamine release from mast cells and basophils - Widespread increase in vascular permeability + smooth muscle contraction
-> drop in BP - Hypotonic shock
->Resp failure
Common treatment option for anaphylaxis
Epinephrine
Relaxation of sm mcl
Reverse cardiovascular effects
NON TESTED
Series of allergy treatments
1.AntiInflammatory Mediators
2.Allergen Reduction
3.Improve Physical Barrier Function
4.Remove other causes of inflammation
NON TESTED
What are some anti-inflammatory mediators
AntiHistamines - block H1 receptors
Corticosteroids - last response for general immune response suppression
NSAIDS - inhibit PG formation by COX
NON TESTED
What is allergy desensitisation?
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
NON TESTED
What are some immunomodulatory antibodies?
Anti-IgE - Block mast cell triggering
Anti- IL5/CCR4 - reduces eosinophil generation/recruitment
Anti-IL31 - Reduces Th2 driven inflammation, anti-pruritic,
