T helper 17 cell

And glutathione helps with the liver detoxification, helps with the intestinal lining, helps with the brain.

It decreases TH17 cells.

It does tons of stuff.

It increases regulatory T cells.

So, nevertheless, the researchers want to see if we can predict within patient groups populations, if there is a cell-type specific flux and metabolism that can be determined by using these new techniques.

For example, something very simple would be, what is the specific criterion for switching between fatty acid beta-oxidation to glycolysis in, say, Th17 cells? and whether or not those Th17 cells are functioning to be destructive of tumor cells or infected cells.

In other words, looking at the readout on Th17 cells, not just whether or not they're switching carbon source.

So this kind of study allows us to examine glucose versus fatty acid versus amino acids.

utilized in the bioenergetic system.

But I think that particularly when we're thinking about already often having a hypervigilant immune response that is more ready, fire, aim, that is not very discerning, that is autoimmune leaning, that a lot of times the immune system is a mix of underactive and overactive.

And I would suggest that we need to balance or modulate the immune system and look at Th1, Th2, Th17, Treg, those kinds of things to try to bring some balance back to the immune system and to be cautious if someone has an autoimmune disease that we don't want to then boost indiscriminately.

I do think that mold creates immune dysregulation such that then if someone subsequently encounters a tick or other vector, we call it vector-borne infections because ticks are not the only way that you can acquire Lyme disease and co-infections.

But then the mold has already impacted the immune system in such a way that then you're immune system cannot respond in a healthy way to Lyme and co-infections.

And it discusses how T cells can either directly or indirectly modulate bone health.

And four of these cells, so there's Th1, Th2, regulatory T cells, Th17, cells play a role in thyroid autoimmunity.

Again, it's the imbalance.

Not that all these cells cause autoimmunity, but if you have an imbalance of Th1, Th2, regulatory T cells, Th17 cells.

Again, I've spoken about these in other podcasts.

Regulatory T cells are important to keep autoimmunity in check.

It's got parts of the genetic code that are missing, which makes it a very reasonable vaccine.

If you look at the tuberculosis response and those who get this latent tuberculosis, those patients in general have less of a Th17 response.

And so that sets up this phase where the tuberculosis can hang out in the alveolar macrophages.

And again, that suggests it's this interaction of the macrophages and T cells where you're getting that interaction.

And so some of it is you'd love to look at biomarker testing to get a sense about that in some ways, whether that be urine or tissue.

One thing that we're very interested in is that the gut microbiome is really working along with a lot of this.

So we have a clinical trial here that we've developed where you could add a probiotic to be given with BCG for patients and see, does that help? If you have butyrate-producing species, can that help drive more Th17 response and affect the response to BCG? So that's a way where we're going to try and do that to see if we can improve the response.

But you would love to know at the precision level, how are patients likely to respond and do they need more? Or perhaps the surgery we do to get rid of the tumor is all people need.

Helper T cell 2 likes to make antibodies.

Then there's TH17.

Well, that's like a macrophage.

And then there's regulatory T cells, and there's memory T cells.

Right? So that was IL-12 to Th1 to interferon gamma to increase macrophage activity.

IL-23 takes the naive T cells and pushes them down a lineage of turning into Th17 cells, T helper 17 cells.

these release an interleukin called IL-17, and that increases neutrophils again to the area.

So the combination of all these things tends to present mostly as Crohn's disease, right? So I want everyone to remember the following.