Allergy Flashcards
- Define allergic disorder.
Immunological process that results in immediate and reproducible symptoms after exposure to an allergen. Usually involves an IgE-mediated type 1 hypersensitivity reaction.
- Define sensitisation.
Detection of specific IgE either by skin prick testing or in vivo blood test
NOTE: this does NOT define allergic disease
- Describe the difference between immune responses mediated by Th1 and Th2 cells.
Pathogens that have conserved structures (PAMPs) such as bacteria are recognised by Th1 and Th17 cells Multicellular organisms (e.g. helminths) and allergens don’t have conserved structured but they release mediators that damage epithelial cells. Disturbance of epithelial cells is recognised by the Th2 cells
- Outline the Th2-mediated immune response.
Damages epithelium releases signalling molecules (e.g. TSLP)
These cytokines will act on Th2, Th9 and ILC2 cells, which then produce IL4, IL5 and IL13
These cytokines act on basophils and eosinophils which play a major role in the expulsion of allergens and parasites
TSLP and other cytokines can also activate follicular Th2 cells which release IL4
IL4 stimulates B cells to produce IgE and IgG4
- What other allergic response can be initiated by parasites and allergens which is not mediated by Th2 cells?
Allergens can cross-link IgE leading to mast cell degranulation and the release of histamines, prostaglandins and leukotrienes
These mediators act on the epithelium causing increasing permeability, smooth muscle contraction and neuronal irritability (itching)
This response aims to expel the parasite/allergen and is implicated in asthma, eczema and hay fever
- Describe the relationship between Langerhans cells and Th2 cells.
Langerhans cells promote the secretion of Th2 cytokines
- What induces the production of IL4?
Peptide presentation via MHC to TCR or Th2 cells
- How is oral allergen exposure different from respiratory or skin exposure with regards to developing an allergic response?
Oral exposure promotes immune tolerance whereas skin and respiratory exposure promotes IgE sensitisation
When an allergen is ingested orally, Tregs in the GI mucosa will inhibit IgE synthesis to keep the immune system in balance
- List some theories behind the increasing prevalence of allergic disorders.
Hygiene hypothesis
Lack of vitamin D in infancy (leads to food allergy)
Dietary factors (reduced omega and linoleic fatty acids)
High concentration of dietary advanced glycation end-products and pro-glycating sugars which the immune system mistakenly recognises as causing tissue damage (e.g. soda)
- List some clinical features of IgE-mediated allergic responses.
Angioedema Urticaria Flushing Itching Cough SOB Wheeze
- State some examples of co-factors that could trigger an allergic response.
Exercise
Alcohol
- List some elective investigations for allergic disease.
Skin prick and intradermal tests Specific IgE measurement Component resolved diagnostics Basophil activation test Challenge test
- List some investigations that may be conducted during an acute allergic episode.
Serial mast cell tryptase
Blood/urine histamine
- What features of the specific IgE test are used to predict risk and likelihood of symptoms?
Concentration - higher levels means more symptoms
Affinity to the target – higher affinity means increased risk
Capacity of IgE antibody to induce mast cell degranulation
- Describe how specific IgE tests work.
Allergen is bound to a sponge and mixed with the patient’s serum
Specific IgE will bind to the allergens on the sponge (if present)
This is washed with anti-IgE antibody which is fluorescently labelled
Higher values are associated with allergic disorders
NOTE: good negative predictive value
