The link between autoimmune and inflammatory disorders


FOTCM Member
Here is a very interesting post that reviews the intricacies of the immune system. Some might find it unreadable, but this author does a pretty nice synthesis while he connects some dots and clues on this difficult subject. First, some basic background on T-regs:

What are T-regs?

Regulatory T cells

Regulatory T cells (TReg cells) are a special subset of T cells [a type of lymphocyte] that prevent other immune cells from attacking the body’s own tissues and other harmless environmental materials, such as food and commensal organisms. Defects in regulatory T cells cause severe inflammatory disease.
The regulatory T cells (Tregs pronunciation: /ˈtiːrɛɡ/), formerly known as suppressor T cells, are a subpopulation of T cells which modulate the immune system, maintain tolerance to self-antigens, and prevent autoimmune disease.

Here is the article. The references marked as (R) are hyperlinked in the original article:

Tregs: The Missing Link To Cure Autoimmune and Inflammatory Disorders

If you are having a hard time reading the material, then just read the bolded parts.

Tregs comprise ∼5%–10% of T helper cells and can be identified by the DNA reading protein ‘Foxp3’ or a lot of CD25 proteins on its membrane/surface.

There are two types of Tregs: ‘natural’ (nTregs) or ‘induced’ (iTregs). Both types are anti-inflammatory. Natural means that they are part of the cells naturally found in our thymus gland. Induced means that they are created outside the thymus. (There are 2 kinds of induced Tregs: Tr1 and Th3) (R, R2).

Tregs produce TGF-B and interleukin IL-10, both of which mostly inhibit the immune system (R).

Tregs suppress the harmful/activated (effector) Th1, Th2, Th17 cells and their cytokines, eosinophils, mast cells, basophils, IgE’s (switches to IgG4) and the migration of inflammatory cells to tissues (R).

In addition, they suppress CD8+ T cells, dendritic cells (DCs), monocytes/macrophages, B cells, natural killer cells and natural killer T cells (R).

Tregs need to be ‘activated’ in order to have their suppressor functions (R).

Tregs inhibit immune activation by a direct cell to cell contact. This means that it doesn’t only work through cytokine intermediaries such as TGF-B and IL-10. These cells are directly anti-inflammatory (R). For some reason, this information excites me.

You can test your Treg Cell numbers by taking a blood test. This test doesn’t check for certain important aspects of Treg cells, to my knowledge (Foxp3 nor ‘high’ CD25). However, since these cells are mostly are good against autoimmunity, checking the absolute number of cells should have some value (R).

Checking TGF-B1 and IL-10 (checked in the Th1/Th2/Th17 dominance test) should give a clearer picture as to what your level of Tregs are like. This is because TGF-B1 increases Tregs and IL-10 is given off by Tregs. I’d recommend all three tests to get a decent picture.

Top 8 Picks to Increase Tregs

Probiotics (R) – must be this one. Great referenced article. {Referenced article mentions specifically: Lactobacillus casei (L. casei, Lactobacillus rhamnosus GG, L. casei Shirota, L. salivarius, L. reuteri, L. plantarum, L. paracasei}
Hi-maize /Resistant starch/Butyrate (R, R2, R3, R4)
DHA, vitamin A and vitamin D3 (R, R2)
EGCG/Tea (Jasmine) (R, R2), – DNMT inhibitor (R)
Curcumin (R, R2, R3) – Good for inducing oral tolerance by inducing gut Tregs in multiple ways. It does inhibit the suppressive activity of Tregs, though (R).
Black Cumin Seed Oil (R)
NAC (R) (Clinical Trial)
Cinnamon/Sodium Benzoate (R)

The Good

Treg cells help to restrain the immune system and prevent an excessive T Cell response (R).

Even is healthy people, immune cells can attack our own tissue. Tregs stop our immune cells from attacking our own tissue (R).

In particular, TGFb and IL-10 seem to be crucial for sustained tolerance induction by Treg. (R) On the other hand, TNF, IL-1 and IL-6 block the ability of Tregs to induce tolerance (R).

Tregs can also reverse food intolerances and allergies.

Probably the single most important reason we develop IgE-related allergies is because we aren’t creating Treg cells in the gut, but instead Th2 or Th17 cells (R).

This happens in 3 ways: by changing the type of dendritic cells that reside in our gut, by blocking Th2/mast cells/other immune cells, and by actually changing the tissue structure of our gut (R).

Our gut has dendritic cells that capture proteins from food and bring them to the lymph nodes. To produce Tregs, we need sufficient vitamin A, TGF-B, and the enzyme IDO (R).

If we produce Tregs, then they will tell the dendritic cells that the protein they carry is cool and there’s no need to ring the alarm bells (R).

For oral tolerance, immune cells (DCs) are told not to react to a protein in the gut tissue, and these cells circulate to other tissues, which trains the immune system (R).

Technical: Tregs produce inhibitory cytokines (eg, IL-10, TGFb, and IL-35), absorb inflammatory cytokines, kill target cells directly (secretion of granzymes, perforin), block important cellular functions (through CD25, 39, 73 and adenosine), increase cAMP (and therefore energy), decrease costimulatory molecules (CD80/CD86) and turn the dendritic cells off by activating surface proteins that inhibit immune function (CTLA-4, PD-1, or histamine receptor 2.)” (R, R2).

I’ve tried all different ways to induce tolerance, but I haven’t found this to be effective for lectin sensitivity at all. This works for probably most other food allergies.

Treg cells, surprisingly, can be important for clearing some infections. They are crucial for the establishment of a functional Th17 response after the infection in the gut (with the help of IL-2) (R).

Tregs can improve wound healing (R) and are neuroprotective in stroke models (R).

The Bottom Line: If you’ve got autoimmune or inflammatory problems, there’s a good chance that you’re deficient in Tregs or that they’re dysfunctional. Tregs can then be considered ‘good’.

The Bad

Unrestrained Treg-cell activity can lead to impaired immunity (R), which means high Tregs will make you will be less capable of fighting most infections.

For example, a high level of Tregs can theoretically make people with CFS and other disorders believed to be caused by viral infections worse. Indeed, not surprisingly, people with CFS have higher levels of Tregs. (R)

In my EBV/Mono post, I speak about how various autoimmune disorders can be caused by a viral infection that’s out of control.

Two significant factors that cause this is a low Th1 immune system/low INFy and low cytotoxic T cells (CD8+).

If you have high Tregs, it will decrease both of these immune system aspects, plus others that are involved with keeping viral infections at bay.

So any disorder caused or aggravated by a viral infection should become worse by having high Tregs.

However, if you have high Tregs, it will create tolerance to specific tissues and will, therefore, be overall beneficial when it comes to classical autoimmune disease. And we see this below in the list of diseases with low Tregs.

This may not be the case for something like CFS, though, which is more systemic rather than a specific tissue being attacked as is the case by a classical autoimmune disorder.

Tregs can have a dark side when it comes to cancer because they limit our ability to fight tumors, to a degree. They curtail the generation of Th1 responses. Part of these responses is the production of CD8+/Cytotoxic T cells and IFNy. Both of these fight tumors (R).

Tregs are also the main source of IL-10 in tumors, which I discussed inhibits our ability to kill tumors to some degree (R).

Tregs also inhibit the body’s ability to suppress the formation of cancerous cells (R), which means high Tregs will lead to cancer.

Patients with tumors have a local excess of Tregs (R).

Tregs can also increase inflammation in certain situations because they can become dysfunctional and start producing IL-17 (R).

Bottom Line: If you’ve got cancer, you might want to shift your immune system to decrease Tregs – at least in cancer tissue. However, systemic levels do likely influence levels in cancer tissues.

The Ideal Treg Scenario

The ideal scenario is to have a healthy Treg level throughout your body, but low Treg levels in cancer or precancerous tissue.

Also, ideally, Tregs would be decreased when we have an infection and increase when we get over it.

Why Can’t We Just Inject Tregs Into People?

Unfortunately, recent T cell biology investigations revealed that T cell nature is much more plastic than initially thought (R).

Treg cell therapy may be very risky, as the Treg cells transferred to the patient may reverse and become another proinflammatory Th17 cell (R). IL-10 is a cytokine that blocks this conversion from happening (R).

You see, in these cells, there are two proteins that read the DNA, which command the cell’s activities and produce products: Foxp3 and RORyt. When Foxp3 decreases relative to RORyt, the cell will start producing more IL-17. There’s no dividing line at which Tregs become dark villains; it’s on a continuum (R).

So it’s the level of Foxp3 in the Treg that matters most. In psoriasis, skin cells have lots of Tregs but reduced Foxp3 (R).

The good news is that HDAC inhibitors such as Hi-Maize/Resistant starch/Butyrate block the conversion of healthy Tregs to IL-17 producing Tregs (R).

Tregs are produced under the influence of solely TGF-β. Th17 cells are produced under the influence of TGF-β AND IL-6 or IL-21 (human studies point to IL-21, while mouse studies point to IL-6) (R).

Various cytokines such as IL-1b, IL-2 (Th1 cytokine), IL-23 and IL-15 turn Angelic Tregs to Villain Tregs.

What needs to be done then to heal yourself/prevent disease is to change the environment of these cells. This means to decrease systemic inflammation, ideally by getting to the root cause.

Diseases With Low/Dysfunctional Tregs

Heart Disease/Atherosclerosis (R)
Diabetes (R)
Sleep apnea (R)
Allergies (R, R2)
IBD (R): Colitis (R), Crohn’s (R).
Rheumatoid arthritis (R) – The function of Treg is known to be suppressed by TNF-α in RA (R)
Multiple sclerosis (R), Type I diabetes (R), SLE (R)
Hashimoto’s (R), Graves (R) – Dysfunctional Tregs, not lower numbers… In Thyroiditis patients, two studies showed no deficit in Treg number, while another study found that only untreated Graves’ patients had a significant decrease in Tregs (R).
Eczema (R), Psoriasis (R).
Gastritis, oophoritis, Prostatitis, Renal disease (R).

Increasing Tregs

Increasing Tregs is a way to benefit both Th1 and Th2 dominance (R). Tregs decrease Th1 cells and help create oral tolerance for Th1/Th2 type allergies.

Inhibiting mTOR results in increased Treg levels (R).

However, studies have found that having variations in mTOR is important for Treg development. So you don’t want to constantly inhibit it; instead, cycle with high and low mTOR activation (R).

The depletion of arginine, glutamine, and tryptophan increases Treg generation (via inhibiting mTOR) (R).

Increasing AMPK also increases Tregs (mTOR article has AMPK activators) (R).

Tregs prefer to burn fat for fuel and when you take this away from them, they are less likely to develop (R).

Oddly, gluten may increase Tregs. Tregs were significantly lower in patients who had abstained from gluten compared with individuals on a standard diet (R). However, I wouldn’t pay much attention to this, because Tregs probably went down as a result of less inflammation (so there needed to be less Tregs)…

Sun/UV (R)
Exercise (R)
Fall in love, have sex, nurse and have positive social encounters. All of these lead to increased oxytocin (R). Oxytocin increases Tregs and wound healing (R)
Circadian Rhythm – if you constantly break the rhythm, you will produce more Th17 instead of Tregs.
alpha-MSH (R)
Polyphenols in general (R)
Oxytocin (R)
L Reuteri – Increases oxytocin also (R)
IGF-1 (R)
Vit A adequacy/Cod liver (R)
Vitamin D3 adequacy/Cod liver (R)
THC/Pot (CB2) (R)
DHA (R, R2)
Grape Seed Extract (R)
Licorice (R)
Baicalin (R) (Increased Treg numbers, TGF-B, IL-10, and FOXP3) (R)
Honokiol (R) (TGF-B, IL-10, FOXP3)
Naringenin (R)
Astragalus (R, R2) – Increased Foxp3 and decreased that of RORγt. But it decreases TGF and Tregs when exposed to some viruses (R)
Lipoic Acid (R)
Cocoa (R) – prevented a decrease in Tregs…
Whey (R)
Cat’s claw (R)
Papain/Papaya (R)
Probiotics (R)–Lactobacilli (R), Probiotics (L casei, L Reuteri, Lactobacillus rhamnosus Goldin-Gorbach and L. casei Shirota, L. salivarius, IRT5L. plantarum, L. salivarius (R), and L. lactis (R)), B Fragilis (R).
Nicotine (R) (increases Foxp3, CTLA-4)
Nitric Oxide (R) – arginine, exercise
Exogenous ATP (R)
FOXO3a(+), IDO (R), DPP4 (-) (R), DNMT (-) (R), NFAT hyperactivation (R)….Some ingested immunoreactive proteins type I IFN, SIRS peptide 1–21, α-MSH, ACTH, SST…

Decreasing Tregs

The mTOR–Akt pathway suppresses Treg cell production and activity (R). So you want to inhibit mTOR.

High-fat diet (R) (in mouse livers)
Leptin (R)
Marathons/Excess exercise (R)
Artemisinin (R) – in cancer cells
NAD+? (R)
Melatonin (R) – in tumor tissues

Contradictory/Doesn’t Alter Tregs

Resveratrol (R) – By activating SIRT1, it may block Tregs (R). Prevents high-fat diet decrease in Tregs (R).
Bromelain (R) (Decreases CD25 though)
Berberine (R)


Stevia, Blueberry

Oxidative Stress Helps Tolerance…What To Do?

Oxidative stress/ROS actually helps Tregs suppress immune activation. Particularly, NADPH oxidase is important (produces superoxide). In fact, Tregs are able to suppress the secretion of cysteine into the microenvironment by dendritic cells to indirectly suppress T effector proliferation via cysteine depletion (R).

First, there’s no need to worry about molecular hydrogen because that doesn’t affect the free radical superoxide, which is what the study is concerned with.

However, this puts a damper on NAC and Spirulina, both of which inhibit the oxidant in question.

However, I’ve done well on NAC and most clients report positive results.

In addition, many benefits have been reported in a clinical trial: NAC increased mitochondrial membrane potential in all T cells, profoundly reduced mTOR activity, enhanced apoptosis, reversed expansion of CD4−CD8− T cells, stimulated FoxP3 expression in CD4+CD25+ T cells, and reduced anti-DNA production (R). Increased mitochondrial membrane potential leads to the destruction of activated T cells (R).

I think what might be happening here is NAC may briefly decrease the induction of tolerance for a couple of hours. Since it’s brief, it’s not an issue. Otherwise, NAC may behave differently when people ingest it. Whatever the case, I think the benefits outweigh this potential negative.


FOTCM Member
I found another useful post by the same author on Natural Killer Cells. Those who are low in these cells might find it easy to catch seasonal viruses. The following post has some tips on how to increase your NK cells. In a different context, there might be inflammation when a person is high on NK cells, hence the tips for also decreasing them. Some people have easy access to lab tests that measure all these parameters, but reviewing this material might also give clues for those who use clinical signs and symptoms as the main guides as well.

All About Natural Killer Cells and How to Increase and Decrease Them

Natural Killer Cells are high and low in a variety of conditions. They can contribute and prevent disease. Do YOU have low or high Natural Killer Cells?

Intro to Natural Killer (NK) Cells

Natural Killer (NK) cells are a type of toxic lymphocytes that are critical to the immune system (R).

NK cells are produced in the bone marrow, lymph nodes, spleen, tonsils, and thymus, where they then enter into the circulation (R).

They control several types of tumors and microbial infections by limiting their spread and future tissue damage that can occur (R).

The cells become active around 3 days after infection and respond to tumor formation in the body (R).

NK cells monitor tumors that may grow by directly triggering the death of tumor cells(R).

They have the ability to recognize stressed cells without having to have a previous exposure to the pathogens (R), allowing for a fast immune reaction (R).

NK cells can develop long-lived and highly specific memories to a variety of targets (R).

Extreme genetic diversity is present in both mice and humans coding for NK cells (R).

What Function Do Natural Killer Cells Have?

Individuals lacking NK cells have regular viral infections and die prematurely (R).

Individuals deficient in NK cells are prone to early phases of herpes virus infection (R) and NK cells help fight HIV (R).

Mice with less NK cell function are more prone to cancers (R).

Activation of NK Cells

Circulating NK cells remain in their resting phase. NK cells activated by cytokines lead to the invasion of these cells into tissues with pathogen-infected cells (R).

When activated, they secrete cytokines such as interferons (R) and TNF-a (R).

NK cells release a membrane-disrupting protein, perforin, which causes cell death of the target cell (R).

So perforin perforates the “skin” of the pathogen (R).

Conditions With Elevated Natural Killer Cells

Obesity promotes the expression of inflammatory genes in the abdominal fat.

It elevates the number and activity of NK cells in only the stomach fat (R).

When NK cells are removed, inflammation in abdominal fat is suppressed and insulin resistance is improved (R).

NK cells control insulin resistance by transmitting proteins that affect macrophages(R).

In Asthma, NK cells contribute to IgE mediated immune-responses and may exacerbate the condition (R).

In Type 1 diabetes, NK cells increase the destruction of the pancreas (R).

Higher NK cells form in women who have reoccurring miscarriages (R).

Th1 Dominance and NK Cells

Th1 dominance (IL-12, IL-2) increases NK Cell activity (R).

On the other hand, NK cells may, in turn, destroy and suppress Th1 cells (R).

I actually don’t do very well with the more potent stimulators of NK Cells. This could either be because I don’t do well with NK cell stimulants, or because NK Cell stimulators have other immune boosting properties – or both.

Conditions That Have Low Natural Killer Cells

Cancer (low activity) (R) – NK cells ‘eat’ cancer cells.
Viral infections (low number and activity) (R) – NK cells fight off viruses.
CFS (low activity) (R)
Multiple Sclerosis (low activity) (R)
Rheumatoid Arthritis (low number and activity) (R)
Lupus (low number and activity) (R)

Impairment of Natural Killer cells is also associated with advanced aging (R).

Natural Ways to Increase Natural Killer Cells

These strategies lead to increased natural killer cells.


Exercise (R)
Massage therapy (R)


Curcumin (R)
Zinc (R)
Selenium (R)
Garlic (R)
Astaxanthin (R)
Melatonin (R)
Astragalus (R)
Amla or Amla/Gallic acid – Must be one of these. Not for Th1 dominant (R).
Spirulina (R).
Eleuthero – Should be this one…at night (R).
Danshen/Salvia Miltiorrhiza – A-glucosidase inhibitor. Slows carb absorption. Great for heart health (R).
Blueberry (R)
Echinacea (Should be this one) or Cichoric acid (from Echinacea) (R).
Spleen (R)
Thymus Peptides – for weakened immunity (R)


Dopamine (through ACh) (R)
Thyroid Hormones/T3 (R, R2)
Prolactin (R)
Substance P (R)

Natural Ways to Enhance Natural Killer Cell Function

These strategies lead to increased function or cytotoxicity of Natural Killer Cells.


Exercise (R)
Strength training (R)
Antioxidants (R)
Massage therapy (R)
White button mushrooms (R)

Supplements (if overactive immune system)

These supplements are safe if you are Th1 dominant and have an overactive immune system, but you’d still like to stimulate NK Cells.

Curcumin (R)
Resveratrol (R)
Andrographis (R)
Ashwagandha (R)
Magnesium (R)
Cardamom (R)
Probiotics: S Boulardii (IHERB) (R), L casei (R), L bulgaricus (R)
Vitamin B12 (R)
Garlic (allicin) (R)

Supplements (if underactive immune system)

Thymus -immune deficiency (R)
Astragalus (R)
Beta Glucans (R)
Goji Berries (AMZN)-should be this one or Goji Berries (IHERB) (R)
Reishi – night time (R)
Gynostemma (R)
Amla or Amla/Gallic acid (R)
Ginseng (R)
Lion’s Mane (R, R2).
Echinacea (Should be this one), Cichoric acid (from Echinacea) (R).
Chlorella Tablets (R)
GOS (galacto-oligosaccharides) (R)
Germanium (R)
Cocoacalm – nice relaxer (R)
CoQ10 – in older women, but not men (R).
Vitamin E – in older women, but not men (R).
Low dose naltrexone (LDN) (drug) (R)
Arabinogalactan (R, R2)

Other: LSD (R)


T3 (R)
Growth hormone (R)
IGF-1 (R)
Prolactin (R)
Th1 dominance: IL-12, IL-2 (CD56bright nk cells) (R)

NK Cell Inhibitors

Lectins initiate excess polyamine production, which may be the result of an effort to repair the damage to intestinal microvilli caused by lectins (R). A high polyamine level may decrease NK cell populations (R).
Lipoic Acid (R)
CRH/ACTH/Cortisol (R) – from stress or other causes
Indoleamine 2,3-Dioxygenase (IDO) – activated from cortisol and inflammation (R)
Folic acid (synthetic form) (R)
Somatostatin (Growth Hormone–Inhibiting Hormone) (R)

NK Cell Cytotoxicity Inhibitors

Acetylcholine (R)
Estradiol (R)
Marijauna: THC (R), CBD (R)
Opioids (R)
Folic acid (R)
Fish oil/DHA (R)
Testosterone + Strength training (R)

Testing For Natural Killer Cells and Their Function/Activity

These tests check for absolute NK cells, their activity and a particularly important subset of NK Cells (CD57 NK Cells).

Natural Killer Cell Activity
Natural Killer Cells (CD16+CD56)– also tests CD3 (T Lymphocytes), CD4 (Th cells),CD8 (Cytotoxic T cells), CD19 (B cells)…Ratio should be less than 2.4 (R). Low CD8+ cells are implicated as an underlying cause of autoimmunity (R)
CD57 (Natural Killer Cell Subset) and CD8 Cells – CD57 cells are a subset of natural killer cells that are important to getting rid of infections. Studies have shown that natural killer cells play a major role in chronic Lyme disease. Many of those who have chronic Lyme disease have suppressed levels of natural killer cells. CD57 T cells are generated in response to chronic antigen stimulation. Progression to CD57 reflects a maturation pathway for NK cells and represents a shift toward a more deadly NK cell, greater responsiveness and decreased responsiveness to cytokines (R). CD57 is increased by CMV infection (R), and it presumably helps ward it off.


FOTCM Member
Thank you Gaby! Very interesting. I recently had a blood test done, and some of the markers mentioned in the articles you quoted were a bit high, some low. I´ll experiment with some of the natural options suggested, and see what happens.


Jedi Council Member
FOTCM Member
Yes, thank you very much Gaby for this articles!! And his entire site ( looks very interesting and full of information.


FOTCM Member
Tregs: The Missing Link To Cure Autoimmune and Inflammatory Disorders

[...] To produce Tregs, we need sufficient vitamin A.
I was thinking that often there is a vitamin D deficiency in autoimmune and inflammatory conditions and when supplementing vitamin D3, vitamin K is suggested. However, vitamin A has a very important role. If we supplement only vitamin D3, there could be an artificial deficiency in vitamin A.

Here is a post on vitamin A from the same blog:

The Importance of Real Vitamin A


It reminds me of the importance of cod liver oil. Here is the relevant quote:

I still recommend you consume foods like Cod liver, regular liver or supplement with Vitamin A/Retinol.

I recommend first experimenting with a higher dosage and seeing how you feel – say 30,000iu. Then cut back to taking 2000iu daily. If you buy 8000iu, you can take it once every four days. Make sure to take extra K2 and D3.
A tablespoon of cod liver oil may contain between 10000-14000 units of vitamin A:


Cod liver oil contains a high amount of vitamin A in the form of retinol. This form of the vitamin is stored in your body and can accumulate to toxic levels if you consume excessive amounts. One tablespoon of cod liver oil may contain as much as 14,000 international units of vitamin A. The upper tolerable intake, or the maximum amount you should consume in one day, is 10,000 international units.
One teaspoon of regular cod liver oil has about 5000 UI of vitamin A.


FOTCM Member
Here is another clue that healing your gut flora might be the one factor that can protect you against viral infections:

Gut microbiome emerges as new target for controlling viral infections

In the review, researchers highlight several ways in which gut microbes influence viral infection and transmission. By using germ-free and antibiotic-treated mice infected with human and murine viruses, particular focus has been placed on mechanisms by which bacteria and other components of the microbiome promote enteric virus replication and transmission. For instance, gut bacteria are required for efficient mouse mammary tumour virus (MMTV) transmission from mother to offspring. Interestingly, the effects of microbiota on enteric viruses depend on the virus' route of transmission, with the natural oral route the most appropriate. In addition, several enteric viruses may induce host immune tolerance through attachment to bacterial constituents such as lipopolysaccharide, resulting in viral replication and transmission.

Furthermore, the authors note that bacterial microbiota has an essential role in maintaining antiviral intestinal immune responses. In this context, the presence of an innate immunity in the gut environment contributes to viral clearance. As a result, strategies that enhance these innate immune mechanisms may be useful in controlling viral infections.


Jedi Council Member
I am going to add some articles to this interesting and practical thread:
Scientists have shown that chewing your food properly can boost your mouth's immune system to protect you against illness.

The study led by teams at The University of Manchester and National Institutes of Health in the USA, revealed that a specific type of immune cell, the Th17 cell, can be stimulated when you chew.

The immune cell is important in protecting against bacterial and fungal infections that are commonly found in the mouth .

Although it has long been known that the nutrients from food can support a healthy immune system the findings establish that the action of eating itself is important too.

In other parts of the body, such as the gut and skin, Th17 cells are stimulated by the presence of friendly bacteria; it was previously assumed this was the case in the mouth.

However, the team found that damage caused by the abrasion of chewing induced factors from the gums that could activate the same pathways as friendly bacteria and act upon Th17 cells.

However, stimulation of Th17 cells for immune protection can be a double-edged sword: too many Th17 cells can contribute to periodontitis – a common gum disease that is linked to complications in lots of diseases including diabetes, rheumatoid arthritis, heart problems and pre-term birth.

The research was funded by the BBSRC and National Institute of Dental and Craniofacial Research in the United States

Lead researcher and biologist Dr Joanne Konkel, from The University of Manchester, said: "The immune system performs a remarkable balancing act at barrier sites such as the skin, mouth and gut by fighting off harmful pathogens while tolerating the presence of normal friendly bacteria.

"Our research shows that, unlike at other barriers, the mouth has a different way of stimulating Th17 cells: not by bacteria but by mastication. Therefore mastication can induce a protective immune response in our gums".

In the journal Immunity, the team show that they were able to stimulate increases in Th17 cells in mice by merely changing the hardness of their food, proving that mastication was the critical factor.

But these Th17 cells also had a bad side; "We were also able to show that increased damage from mastication could also exacerbate bone loss in periodontitis".

She added: "Importantly, because inflammation in the mouth is linked to development of diseases all around the body understanding the tissue-specific factors that regulate immunity at the oral barrier could eventually lead to new ways to treat multiple inflammatory conditions."
Researchers from Schepens Eye Research Institute of Massachusetts Eye and Ear have uncovered two factors responsible for the chronic, lifelong nature of autoimmune disorders, which tend to "flare up" intermittently in affected patients. These two factors are cell-signaling proteins called cytokines—specifically Interleukin-7 and -15 (IL-7 and IL-15)—that are secreted by cells of the immune system and help modulate memory Th17 cells, a subset of T cells which are known to contribute to autoimmune disorders. Until now, it was unclear how Th17 cells maintained memory; the study results show that IL-7 and IL-15 signal the Th17 cells to chronically reside in the body. These findings, published online in the Journal of Autoimmunity, may lead to the development of new therapies to address a variety of chronic autoimmune disorders.

"We wanted to know the precise factors that maintain memory in Th17 cells so that we can better understand what is causing chronic autoimmune disorders," said senior author Reza Dana, M.D., M.Sc., MPH, Director of the Cornea and Refractive Surgery Service at Mass. Eye and Ear and the Claes H. Dohlman Professor of Ophthalmology at Harvard Medical School. "By selectively targeting the production and expression of IL-7 and IL-15, we may be able to prevent the development of chronic autoimmune disorders."

Affecting up to 50 million Americans, autoimmune disorders develop when the body's immune system attacks its own healthy tissue. Many autoimmune disorders are chronic, and patients may experience "flare-ups," in which symptoms worsen temporarily and then enter a period of remission.

Previous research studies have linked Th17 cells to a variety of autoimmune disorders, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, and chronic inflammatory eye disorders such as uveitis and dry eye disease. When Th17 cells are activated, a subset of them become memory cells, causing them to reside in the body for long periods of time. These memory Th17 cells can become reactivated and cause flare-ups of the autoimmune condition. However, the underlying mechanisms that promote the maintenance of Th17 memory were previously unknown.

Using a mouse model for dry eye disease, an autoimmune condition affecting the surface of the eye, the study authors set out to determine what molecular factors are critical for the maintenance of Th17 memory. They identified IL-7 and -15 as playing a crucial role in the survival and homeostatic proliferation of memory Th17 cells, and when they neutralized IL-7 and IL-15, they saw a substantial reduction of memory Th17 cells.

While further studies are needed to determine ways to block these factors, the findings suggest that targeting IL-7 and IL-15 in order to remove the memory Th17 cells may be an effective treatment strategy for autoimmune diseases.

"In the case of dry eye disease, many of the treatments are showing limited efficacy in patients that do not have a highly inflamed eye," said Dr. Dana. "Targeting the chronic, immune nature of autoimmune diseases may be a better strategy for controlling these conditions."
The hardening of the arteries, also called atherosclerosis, that can lead to heart attack or stroke. has also been linked to autoimmune disorders. It has not been clear why these diseases are related, but a study published January 9th by Cell Press in the journal Immunity reveals that a molecule that causes atherosclerosis also activates white blood cells called T cells, causing clinical symptoms of autoimmune disease to worsen in mice. The findings shed light on the tight link between autoimmunity and atherosclerosis, opening new avenues for the treatment of autoimmune disorders.

"The lesson from this study is that immune diseases are not always a matter of immune system alone," says senior study author Yeonseok Chung of the University of Texas Health Science Center at Houston. "With our findings, we have just started to understand how factors in the circulatory system impact the immune system."

Atherosclerosis is a chronic inflammatory disease and the leading cause of death in developed countries. Patients with this vascular disease have elevated levels of a molecule called oxidized low-density lipoprotein (oxLDL), which is known to activate the immune system. Because patients with T cell-mediated autoimmune disorders such as psoriasis and rheumatoid arthritis have a much higher risk of developing atherosclerosis, Chung and his team speculated that the tight link between these disorders could be explained by oxLDL-mediated activation of T cells.

In the new study, the researchers found that oxLDL increases the number of T helper 17 (Th17) cells in a mouse model of atherosclerosis. To examine the relationship between atherosclerosis and autoimmunity, the researchers exposed the atherosclerotic mice to a molecule that causes autoimmune disease. When these mice were treated with an agent that inhibits the activity of Th17 cells, clinical symptoms of autoimmune disease improved. Taken together, these findings suggest that a molecule that causes atherosclerosis also activates T cells responsible for autoimmune disorders.

"Our study suggests that we should consider circulatory factors in current therapeutic approaches for the treatment of autoimmune diseases," Chung says. "For instance, we expect that controlling oxLDL levels in circulation could greatly improve the therapeutic efficacy of immunological or pharmacological treatment of autoimmune diseases."

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Thanks for this thread Gaby. Our immune systems are intricate systems indeed.

This recent article may also be interesting in this context, it's about the health risks of getting your tonsils and/or adenoids removed. Seems to fit into the picture.

Findings In this population-based cohort study of almost 1.2 million children, removal of adenoids or tonsils in childhood was associated with significantly increased relative risk of later respiratory, allergic, and infectious diseases. Increases in long-term absolute disease risks were considerably larger than changes in risk for the disorders these surgeries aim to treat.
from _Association of Respiratory, Allergic, and Infectious Diseases With Removal of Adenoids and Tonsils

Oh how I wish I still had my tonsils ;-)
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