Peanuts and IgA production in stool... vs IgE production in serum!

Antibodies come in 5 different types, with many different subtypes. IgE is classically known to associate with allergies, IgG is known to help stop infections, and IgM is the primary antibody produced when specificity first starts developing. IgD is not well studied but can be found with the IgM antibodies.

IgA (the 5th type) is known to help stop infections within mucosal areas (lungs/intestinal lining), but we aren’t fully sure of its role and how its development correlates to allergies. This paper tries to clarify IgA development and its correlation to classical IgE production.

This team aims to clarify the development of food-reactive IgA and how it may correlate to IgE production. They collected stool samples from healthy (non-peanut allergy) human individuals to get an idea of what the antibody population and groupings are like in the digestive tract. Yes, I know... the thought of stool samples is kind of gross but it is a non-invasive way of looking into antibody production within the intestines. Healthy individuals had high concentrations of IgA and some IgG and IgM that were all very specific for peanuts and no other legumes.

After gaining this baseline of antibodies within human stool, the researches created a peanut-exposure mouse model to replicate this phenomenon. Despite not creating a fully accurate model (the mice had high and stable IgA production that was peanut-specific, but there was also IgE production within the serum) they were able to take advantage of this induction of both IgA and IgE to understand what cell types (if different) could be controlling their production.

By using genetically modified mice they were able to discern that IgA production needs CD4+T-cells, but they did not need two specific subsets of this cell type. These two subsets are the follicular helper T-cell and the follicular regulatory T-cell. These cells are generally necessary for pathogen-antibody production, so this was an interesting find. Additionally, they were able to discern that an immune stimulator known as CD40L was necessary for this IgA production.

A lot more needs to be deciphered from the results that this paper brings out, but some do need to be taken with a grain of salt. As they pointed out, this model is interesting since the concentration of IgE was also increased when IgA was increased with the cholera toxin. We think that IgA is supposed to be an antibody that mitigates allergic responses, but then there would be an inverse or opposite correlation. Instead of both antibodies having high concentrations, the high concentration of IgA should have paired with a low concentration of IgE, and vice versa.

This is a good paper to take some results from:

1) peanuts on their own are not able to induce a highly-specific IgA concentration within the stool of mice

2) peanuts paired with the cholera toxin will produce this specific IgA concentration, but also induce a high IgE concentration in the serum

3) when both IgA and IgE are induced (in the stool and serum respectively) the IgE production needs follicular helper T-cells and follicular regulatory T-cells, which are both also found to be necessary for pathogen IgA induction. Contrastingly, IgA induction needs a different T-cell subset and CD40L stimulation from this subset. There is no knowledge yet of what this subset may be according to the researchers.

4) IgA induction was seen, though at a slightly lower concentration, within the stool when the peanuts were paired with a different adjuvant that is also a common fungus within plants. IgE induction was not found when using this adjuvant.

Therefore, another round of experiments should be done using this other adjuvant instead. Since this one did not induce IgE and seems to more closely replicate the antibody concoction found within human stool samples.

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