Interleukin 10

So while this adaptive immune response is pushing forward, eradicating the virus, causing some damage to our tissues as well, including lung damage, you need something to switch that off.

And they discovered that this little pulse of IL-6 at the right time stimulates the release of IL-10.

IL-10 stimulates these particular type of white cells called Treg cells, and in turn, they switch off interferon gamma.

And it's that standing down of interferon gamma that allows you to progress from Th1, which is this very aggressive type of adaptive immunity, towards a much more tolerogenic, gentler Th2 response.

But guess what?

So vitamin D attaches to two specific gene promoter regions, and it pushes that IL-6.

It's all dependent on that.

So if you can't have sufficient vitamin D to switch on those genes, you fail to switch on your IL-10, you fail to switch on the Treg cells, and you get this persisting Th1, this very aggressive, uh, immune response.

In terms of atopic dermatitis, there was a 2025 study in pediatric allergy and immunology that measured urinary levels of phthalates in children and found that higher levels of phthalates in their urine increased the risk of atopic dermatitis.

They were able to link that to showing that phthalate exposure resulted in higher levels of IL-5 and decreased levels of IL-10.

So again, basically you're increasing Th2 inflammation and kind of decreasing the amount of anti-inflammatory cytokines.

In terms of hydradenitis suppurativa, there was a 2025 study in the Journal of Investigative Dermatology showing a link between the severity of a patient's disease being linked to the amount of plastic exposure they had from food through packaging or eating out.

but they do seem to reprogram.

And so what you're gonna see with the B cells is they're gonna move into more of an IL-10 responsive, um, IL-8 capable.

So they're gonna have the ability to, uh, neutrophil recruit.

They're gonna remain relatively non-inflammatory.

And when this particular switch gets turned on, you get these very inflammatory molecules.

It's like pouring gasoline on a fire with TNF alpha, interleukin-1 beta, IL-6, IL-8, IL-10.

All these inflammatory molecules come out from these very small cells in the brain called microglial cells.

Now, what causes the microglial activation? Well, infections can cause it.

But a family came to him in the first weeks of life where a child had very severe inflammatory bowel disease within a month of life.

And they're now coming to a hematologist, right? And Christoph discovered that this patient actually had a mutation in a new gene or an old gene, but new in humans, identified in humans, called the IL-10 receptor.

And if you lack the IL-10 receptor, like if you lack the Wiskott-Aldrich syndrome protein gene, actually your presentation is with inflammatory bowel disease.

And first of all, it was remarkable that standard genetic approaches identified this new immune deficiency.

But IL-10 and IL-10 receptor, people have been studying, this is a hormone in the blood that suppresses the immune system.

So if you don't have this hormone that suppresses the immune system, you have an overactive immune system.

People had been studying this in mice and humans for quite some time.

And even there were a mouse model of inflammatory bowel disease that was discovered in the 1990s that if you lacked IL-10, people knew mice would get inflammatory bowel disease.

And when this particular switch gets turned on, you get these very inflammatory molecules.

It's like pouring gasoline on a fire with TNF alpha, interleukin-1 beta, IL-6, IL-8, IL-10.

All these inflammatory molecules come out from these very small cells in the brain called microglial cells.

Now, what causes the microglial activation? Well, infections can cause it.

They're all present, but so are the signals that will actively suppress the immune system.

So IL-10, um, TGF-beta.

So the body is inflamed, but also immune suppressed at the same time, which is part of the reason why that tissue survives so well instead of being cleared.

There's also lesion-devised extracellular vesicles.

Those promote and amplify the inflammatory response.

They also measured interleukin 10, or IL-10, which acts as an anti-inflammatory cytokine.

So IL-10 is the peacekeeper that tries to cool the inflammation down.

Precisely.

So the hypothesis going into the blood analysis is pretty obvious.

What exactly did the ELISA tests show?

Well, in the placebo group, as expected, the cytokine levels remained stagnant.

In the probiotic group, the researchers did observe a slight numerical reduction in the pro-inflammatory cytokines and a slight increase in the anti-inflammatory IL-10.

Older mutant mice developed increased hepatic B-cell and macrophage infiltration and fibrosis while simultaneously showing improved glucose metabolism and liver insulin action.

The authors suggest that increased IL-10 production in peripheral tissues, including visceral adipose tissue and spleen, may contribute to preserve metabolic homeostasis despite progressive liver abnormalities.

These findings illustrate how partial SHP1 dysfunction can produce different effects depending on cell and tissue context.

Reduced SHP1 activity can enhance inflammatory responses in immune cells while relieving inhibitory control over insulin signaling in insulin-responsive tissues.