Lec14Food Allergy Flashcards Preview

Immunology > Lec14Food Allergy > Flashcards

Flashcards in Lec14Food Allergy Deck (33):

What are some things often confused with allergies?

toxic/pharmacologic causes
- bacterial food poisoning
- scromboid fish poisoning
- caffeine
intolerance: lactase deficiency


What is the pathogenesis of food allergy

Ingest food into gut, instead of getting Treg stimulation to produce regulatory cytokines [TGF-B, IL-10] ---> either IgE or non IgE mediated response

-- TH2 cells generated and direct IgE antibodies
----- IgE antibodies specific to epitope on food protein bind mast cells [that have high affinity IgE receptors] and mast cells
----- Re-expsorue causes IgE cross linking --> mediators [ie histamine] released
----- IgE mediated response

-- OR T cells produce cytokines that cause allergic [eosinophilic] inflammation [IL-5]
----- non-IgE mediated response


What is IgG response in gut?

- when soluble proteins pass through barriers [glycocalyx, epithelial cells, etc] they are processed in lamina propria


What is IgA response in gut?

When viruses or bacteria processed by M cells overlying Peyer's patches


What allergy reactions traditionally IgE mediated?

- urticaria angioedema
- ashtma
- rhinitis
- GI anaphylaxis
- oral allergy
- system anaphylaxis or food associated/exercise induced anaphylaxis


What allergy rxns traditionally non-IgE mediated

- enterocolitis
- enteropathy
- celiac


What allergies mixed?

- eosinophilic esophagus
- atopic dermatitis


Symptoms of allergy

- hives, sweeling itchy
- vomit, diarrhea, pain, mouth symptoms
- altered consciousness, poor pulse, low BP
- throat closing, coughing, hoarse wheeze


Are IgE or non IgE faster rxn



Prick skin test

- rapid, sensitive test to detect specific IgE
- get wheal [bump] and flare [surrounding red]
- histamine = positive control [makes blood vessels leaky]
- salt water = negative control
- must be off antihistamines
- positive test does not prove symptomatic sensitivity just suggests likelihood


Serum Food-Specific IgE "RAST" Test

- blood test to measure specific IgE
- put protein of interest on matrix
- add patient serum
- wash
- used secondary anti-IgE labeled antibody with marker
- Measure fluoresence to see amount of IgE specific to protein [ex. almond]
- less sensitive than prick skin test
- not affected by antihistamine use
- report level, class, percent of antibodies
- if nevative means there is no IgE mediated allergy
- if positive still not proof of symptomatic allergy


Why do some people with IgE positive RAST or skin test have no allergic symptoms? What factors involved

- if cell mediated: may get positive skin but negative IgE test

- Different amount of Ig: more Ig = more likely to have symptoms to allergy

- Different affinity: if lower affinity Ig may not stick well to almond, don't get symptoms

- Different binding pattern: Ig that binds one part of protein may have bigger effect than Ig that binds another part

- binds to protein that breaks down easily: then antibody might not really have time to see and interact with the antigen


How does digestion of protein antigen [ex peanut] affect allergic response?

- antibody might bind to an epitope in its normal conformation
- when antigen digested --> if epitope destroyed then antibody may no longer be able to bind properly


oral food challenge

- food eaten gradually in increasing amount with physician supervising and emergency treatment on hand
- open, single-blind, or double-blind/placebo controlled challenge
- allows you to verify allergy/tolerance AND diagnose non-IgE mediated food allergy


Oral allergy syndrome [pollen-food syndrome]

- oral syndrome of mouth itch
- related to pollen allergy
- usually no symptoms beyond mouth
- cooking destroys protein
--- do commercial skin test [cooked] vs fresh skin test
- may be concentrated in peel
- birch allergy: apple, plum, cherry, apricot
- ragweed allergy: watermelon, melon
- type of IgE mediated


3 Food Protein-Induced Enteric syndromes

non-IgE mediated
- food induced enterocolitis syndrome
- food induced enteropathy/malabsorption
- benign eosinophilic proctitis


food induced enterocolitis syndrome

- age onset: 1 day - 9 months
- duration: 9-18 months
- features: diarrhea, bloody stool, injury to villi, edema, vomiting, failure to thrive
- get high WBC count
- cause: milk, soy, rice, oat
- mech: reduced TGF beta receptor expression, increased TNF-alpha


food induced enteropathy/malabsorption

- onset: 2-18 months
- duration: 18-36 months
- failure to thrive emesis [vommitting], edema, diarrhea, blood stool, injury to villi
- cause: milk, soy


Benign eosinophilic proctitis

- onset: 4 day - 4 months
- duration: 6-9 months
- features: maybe edema, diarrhea, blood stool
no villous injury, no emesis/vommitting, resolves in a few months on its own
- cause: breast feeding [milk]


Atopic dermatitis

- chronic, itchy skin rash
- classic distribution on body
- waxes and wanes
- triggers: allergies, temp, emotion, irritants, infection
- about 1/3 of kids have food allergy: egg, milk, wheat soy
- mix of IgE and non-IgE mediated


Allergic eosinophilic esophagitis [EOE]

- mix of IgE and non-IgE mediated
- onset: infancy to adulthood
- symptoms: reflux esophagitis, vomiting, food refusal, abdominal pain, chest pain, sleep disturbance
- foods implicated: milk, wheat, soy, egg, beef
- diagnosis
--- fails to respond to reflux meds
--- endoscopy and biopsy of esophagus
--- response to food elimination or steroids
- furrows in esophagus, rings, white plaques that represent dead cells and eosinophils


Hygiene hypothesis

- we make the environment super clean
- this tips the balance because the immune system doesn't have enough to react to thus get immune attacking non-pathogens


6 theories of food allergies

- hygiene
- delaying ingestion of allergens
- exposures by non-ingestion routes
- not enough vitamin D
- obesity, unhealthy fats in diet, etc
- how food is processed [ex oil in peanut butter at adjuvant for peanut allergy]



- engineered protein
- attaches to IgE Fc region [if it was the variable region would induce anaphylaxis, thus can only bind free floating IgE because receptor IgE Fc is not available for binding]
- inactivates IgE as long as it is being taken [need to keep administering it]
- has shown to raise threshold of peanut allergy maybe
- mech: anti IgE binds IgE and blocks it from reaching and binding mast cell to initiate inflammation


Traditional chinese medicine methods

- herbal remedies used for centuries
- FAHF2: stops peanut-induced anaphylaxis in sensitized mice


What is FAHF-2

herbal chinese medicine remedy that stops peanut-induced anaphylaxis in sensitized mice


2 main goals of food immunotherapy

- provide protection from anaphylaxis
- restore permanent oral tolerance


What is desensitization

- temporarily increased threshold for food allergic reaction
- protection from life-threatening anaphylaxis
- affected by illness, exercise, menstruation, pollen season
- dependent on regular intake of food [if you stop giving treatment will stop being desensitized]


What is tolerance

- permanent or long-term
- independent of regular food intake or therapeutic agent
- unaffected by illness, exercise, menstruation, pollen season


Typical food challenge study routine

- initial food challenge and escalation until desensitization
- after 12 months stop treatment for 4-6 wks then challenge again and see if tolerance has developed


Mechanistic studies during exposure therapy

- skin tests get smaller
- specific IgG increases
- specific IgE increases then decreases
- basophil activation decreases
- T regulatory cells more active


Epicutaneous Immunotherapy [EPIT]

- skin exposure not likely to result in serious side effects
- epithelial langerhands cells may cause some regulatory or TH1 like response with chronic exposure


Milk oral immunotherapy + Xolair [anti -IgE]

- evaluatemilk OIT alone and together with xolair