Dear Sarah,

You want to think about the Impact of T Cell Polarization on SIgA Production. SigA is produced in the epithelia and mucosal linings of the sinuses and gut.

There are typical ways to support healthy GI mucosa, using glutamine, arabinogalactan, glutathione, butyric acid (Sunbutyrate), vitamin A, etc.

The question is, dysregulated GI epithelial function is associated with Th2 dominance, because inflamed epithelia make Th2-promoting cytokines that also drive mast cell activation, which drives neurogenic inflammation, which in turn drives more GI inflammation (loop). But Th2 cells also give help to B cells for the purposes of making antibodies, including IgA. So, if you need to dampen excessive Th2 response in a patient with dysbiosis who also has low SIgA, does lowering their Th2 response mean you’ll be pushing the patient into a situation in which they make even less SIgA, rather than the increased SIgA you were hoping for? Aren’t you stuck with two opposite agendas? The answer is no! If you are elevating SIgA while downregulating th2, you will have great gut support!

For completeness, it’s worth noting that low SIgA may also be a reflection of underlying disorders that are part of a conventional ddx, which can include agammaglobulinemias, hypoglobulinemia, selective IgG subclass deficiencies (2&4) with IgA deficiency, B or T cell disorders, common variable immunodeficiency (CVID), and Wiskott-Aldrich syndrome.