The complexities of the above antibodies are explained further below:
IgE – blood draw (serum only)
IgE antibodies are found primarily in mucous secretions. In serum it is present in very low concentrations and elevated in atopic diseases such as allergic asthma, hay fever and atopic dermatitis. IgE is a type 1 or immediate onset, hypersensitivity reaction. An IgE reaction occurs immediately or soon after exposure to the allergen; food or inhalant.
An IgE immune mediated reaction may occur within seconds to 1 hour of exposure and symptoms may include anaphylaxis, swelling or itching of the throat, eyelids, face mouth or tongue, hives, atopic dermatitis, nasal congestion, wheezing or asthma, bloating, stomach, abdominal pain or abrupt diarrhoea. A ‘late phase’ reaction can occur 4 – 6 hours after the initial reaction and persist for days causing oedema and inflammation.
IgE antibodies that are specific for the allergen, bind onto immune cells called mast cells and basophils. The allergen latches onto the mast cell-bound IgE antibodies in a cross-linking manner. This initiates the release of histamine and other inflammatory mediators from these cells. This is how the allergic reaction occurs.
IgG – blood spot (or serum)
IgG antibodies represent the most prevalent class found in the blood. It is the primary mediator of the memory immune response.
IgG is a type III or delayed onset, hypersensitivity reaction produced after a secondary response to an antigen. It is delayed in that it may take several hours or days for a reaction to occur and it can persist for weeks, therefore IgG sensitivities are often termed “hidden” as people are often unaware of which food has caused their reaction.
This antibody/antigen complex activates complement (a group of small proteins found circulating in the blood stream that are involved in the release of inflammatory mediators)
The reaction is caused when IgG anti-bodies form complexes with food antigens. These food-immune complexes can deposit in any tissue or organ and activate the complement cascade of inflammation by degranulation and release of inflammatory metabolites. Although immune cells called macrophages dispose of these immune complexes immediately, they only have a finite capacity to do so. Excess antigen may saturate the macrophages capacity resulting in the prolonged circulation of complexes and their deposition into the body tissues.
Depending on which tissues are involved, it is thought that these complexes may be implicated in many different conditions / symptoms including but not limited to: Arthritis, Asthma, Eczema, Fibromyalgia, Psoriasis, headaches, sinus conditions, low energy. IgG is the most common cause of an adverse reaction to food and the most commonly under diagnosed. US Biotek assays for all 4 sub-classes of IgG anti-bodies (as each can contribute to the inflammation precipitating symptoms).
IgA – blood spot (or serum)
US Biotek Laboratory’s IgA Antibody Assessment testing provides additional information to identify possible suspect food triggers. IgA may be ordered independently, or with any IgG panel or any combined IgG/IgE panels.
IgA may be elevated where IgG is not:
US BioTek’s in-house studies show that of 90-95% of blood samples negative for specific-IgE, 70-85% of these test positive for specific-IgG. Of blood samples negative for both specific-IgE and IgG, 30-40% test positive for specific-IgA.
Research studies suggest elevated serum antibodies, IgE, IgG or IgA to food proteins are markers of this immune intolerance.
The immunological trigger effects of specific-IgA antibodies merit close consideration for the screening and management of chronic inflammatory disease conditions where there is a suspected loss of oral tolerance.
IgA represents a primary immune reaction. The half-life is about 5-6 days, compared to IgG which is about 20-24 days, and indicative of an ongoing immune reaction. The assessment of both these antibodies offers a comprehensive picture.
It is generally thought that serum of IgA- deficient individuals may contain increased amounts of IgG subclass antibodies in the form of immune complexes to a wide variety of food antigens (casein, bovine immunoglobulin, bovine albumin, a-lactalbumin, chicken ovalbumin, gliadin) simply because of the potential compromised first line of defense that secretory IgA offers.
On the other side of the coin, serum of IgA excess subjects may contain increased amount of IgA subclass antibodies in the form of immune complexes to a wide variety of food antigens, also suggesting globally increased antigen absorption from compromised mucosal integrity.
“Unfortunately there is no hard and fast rule on when to order IgG vs. IgA or both. Both IgA and IgG may be present in a variety of chronic inflammatory disorders.”