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I wrote here on the balance between the different types of T-helper cells, with emphasis on Th1 and Th2. In general, Th1 helps guide the body’s fight against intracellular organisms like viruses and certain types of intracellular bacteria, while Th2 focuses more on extracellular organisms such as parasites. The balance of T helper cells is important to keep the immune system on the straight and narrow: veering too far into Th2 dominance can lead to allergies and atopy, while too much to the Th1 side can lead to tissue-specific autoimmunity (though more systemic autoimmune conditions tend to be Th2 dominant).
There are two other types of helper T cells, though: Th17 and T regulatory cells, also known as T suppressor cells. The article above touched on Th17 a bit, which in general gets more involved with fighting against fungi and extracellular bacteria (such as many of the tick-borne illnesses. Overstimulation of Th17 can lead to autoimmunity also.
All of these immune cells do their jobs by releasing inflammatory cytokines which act as signaling molecules. As I said here, inflammation in its place is a good thing. The problem comes in when the process becomes chronic.
The T regulatory cells, or Tregs, do what their name suggests: they help to regulate the function of both T and B cells in general. This has a modulating effect upon out-of-control immune responses, such as autoimmune disease.
Formation of Tregs
T regulatory cells are produced by the thymus gland, or they can be produced from naive T cells by stimulation from TGFb1 elsewhere in the body, particularly in the ileum, to help induce tolerance to food and otherwise harmless environmental factors. (This is one of the potential benefits of TGFb1 and why you don’t want the levels to be too low: TGFb1 helps produce immune tolerance via the production of Tregs).
But, when the signal from TGFb1 is combined with the inflammatory cytokine interleukin-6, these nascent T cells instead differentiate into more Th17. The problem here with respect to driving autoimmunity is less about the increase in Th17 and more about the decrease in the Tregs, though the increase of Th17 can itself be responsible as well.
Supporting Treg Formation and Function
While autoimmune treatment should always focus on treating the cause whenever possible—which would include addressing the trigger that shifted the T helper balance in the wrong direction in the first place—it’s also helpful to support the Treg cells to assist in inducing immune tolerance. Here are some natural ways to do this.
- Vitamin D. Often chronic infections will hijack the Vitamin D receptor so that they can get away with their sinister intentions: vitamin D is that important to immune function. It’s also been specifically proven to increase Treg levels in patients with autoimmunity.
- Vitamin A. Another favorite for acute immune support, Vitamin A also specifically blocks the signaling from IL-6 which encourages differentiation of naive T cells to Th17 rather than to Tregs, thereby increasing Treg production.
- Butyrate. One of the short chain fatty acids that acts as food for the colon, butyrate is produced by healthy gut flora. It can also encourage differentiation of naive T cells into Tregs—suggestive (once again) that a healthy microbiome is important for immune health.
- Glutathione. The body’s master antioxidant, glutathione not only assists with cleaning up oxidative damage and assisting with Phase 2 detoxification, it also helps to induce immune tolerance by preserving Treg function.
- Astragalus. An adaptogen that helps modulate the stress response, astragalus not only lowers excessively high TGFb1, but (probably as part of the same mechanism) also helps to balance the Treg/Th17 ratio.
- Green tea. Well known for antioxidant function in its own right, green tea also is high in EGCG, the zinc ionophore that helps zinc to get into the cells more efficiently and thus supports immune function. It also apparently helps to modulate Tregs.
- Berberine. A fantastic antimicrobial, often useful for SIBO protocols as well as for lowering lipids and glucose, berberine also specifically regulates the Treg/Th17 balance in the colon.
- Curcumin. The highly anti-inflammatory extract of turmeric also decreases differentiation of T cells into Th17, thereby increasing Treg differentiation instead.