Quote from Dr. Garrett Smith on May 30, 2019, 2:06 am

This is pretty straightforward.  Retinoic acid (Poison/"Vitamin A") increase the inflammatory responses to potential allergens in the gut.  Retinoic acid is also known for being a "chemical peel" that dissolves skin, and thus would be a direct cause of increased intestinal permeability, aka "leaky gut".

Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens

[that is the most GARBAGE, misleading, and outright WRONG title of a study I've ever seen, but it fits in the cover-up of Poison/"Vitamin A" toxicity, see below]

Under physiological conditions the gut-associated lymphoid tissues not only prevent the induction of a local inflammatory immune response, but also induce systemic tolerance to fed antigens. A notable exception is coeliac disease, where genetically susceptible individuals expressing human leukocyte antigen (HLA) HLA-DQ2 or HLA-DQ8 molecules develop inflammatory T-cell and antibody responses against dietary gluten, a protein present in wheat. The mechanisms underlying this dysregulated mucosal immune response to a soluble antigen have not been identified. Retinoic acid, a metabolite of vitamin A, has been shown to have a critical role in the induction of intestinal regulatory responses. Here we find in mice that in conjunction with IL-15, a cytokine greatly upregulated in the gut of coeliac disease patients, retinoic acid rapidly activates dendritic cells to induce JNK (also known as MAPK8) phosphorylation and release the proinflammatory cytokines IL-12p70 and IL-23. As a result, in a stressed intestinal environment, retinoic acid acted as an adjuvant that promoted rather than prevented inflammatory cellular and humoral responses to fed antigen. Altogether, these findings reveal an unexpected role for retinoic acid and IL-15 in the abrogation of tolerance to dietary antigens.

What did retinoic acid do?  Hint: it had to do with "inducing inflammation" and nothing to do with "immunity"...

1. First, "release the proinflammatory cytokines".  That's bad.
2. It promoted inflammatory responses to the fed antigens.  That's bad too.
3. It "abrogated" (unnecessarily obscure word used for "withdraw, rescind, revoke, or cancel", aka REMOVED) tolerance of dietary antigens.  That means that things were now causing reactions when they didn't before!  New food allergies / hypersenstivities / intolerances!  GOOOOO science!  [/sarcasm]

Here's another very important part of the paper.  The scientists were proud of their "new model" for replicating celiac disease in lab rats.  They could not do it without including Poison/"Vitamin A" retinoic acid.  Here's their own wording on it:

To test this hypothesis, D^d-IL-15tg mice that have levels of IL-15 in the Lp comparable to those observed in the Lp of CD patients⁹ (compare Fig. S3 and Fig. 4e), were crossed onto humanized HLA-DQ8tg mice¹⁹ (DQ8-D^d-IL-15tg). As observed in CD patients^20,21, anti-gluten CD4⁺ and CD8⁺ IFN-γ-producing T cells were induced in the MLN (Fig. S9a and Fig. S10) and Lp (Fig. 4a) of gliadin-fed DQ8-D^d-IL-15tg mice. Furthermore, this induction was dependent on the presence of RA (Fig. S11).

The creation of the celiac disease model in the mice REQUIRED THE PRESENCE OF POISON/"VITAMIN A" AS RETINOIC ACID.

The slight induction in IFN-γ producing T cells in DQ8tg mice fed gluten may be related to the reported innate effects of gluten³. In accordance with human studies^22,23, IL-17-producing T cells were detected (Fig. S9b, S9c, S10c) only at very low frequency (compare Fig. S10b to Fig. S10c). As observed with OVA, feeding RA further enhanced inflammatory T_H1 and T_H17 responses to dietary gluten in the MLN (Fig. S9a and Fig. S9b) and the Lp (Fig. 4a and Fig. S9c).

Feeding Poison/"Vitamin A" increased the inflammatory response to dietary gluten!

What the following is about to say is that Poison/"Vitamin A" retinoic acid is inflammatory in multiple ways:

In sharp contrast to previous studies suggesting that RA blocks the induction of inflammatory intestinal T cell responses⁶, RA promoted (Fig. 2a, Fig. 2b, Fig. S6a-c) and was also critical for T_H1 polarization (Fig. 2d and Fig. 2e). In addition to its ability to promote IL-12 in DC, RA also acted at the level of T cells to amplify IL-12p70-mediated T_H1 T cell differentiation (Fig. S5 and Fig. S6b). Surprisingly, RA also enhanced T_H17 cell responses in vitro in the presence of IL-6 (Fig. S7a) and in vivo (Fig. S7b-d). Finally, the critical role of IL-15 in the induction of inflammatory T cell responses to dietary antigen was demonstrated by blocking IL-15 signaling in vivo using either a neutralizing anti-IL-15 or IL-15/IL-2Rβ antibody¹³ (Fig. 2f, Fig. 2g, Fig. S6d, Fig. S7e, and Fig. S7f). Altogether these observations suggest a sequential model (Fig. 4f) whereby IL-15 first acts in concert with RA to induce IL-12 and IL-23 in MLN DC (Fig. 2d and data not shown). Along with RA, these inflammatory mediators then operate at the level of T cells to promote T_H1 cell differentiation and, when IL-6 is present¹⁴, T_H17 cell differentiation. While our finding of the adjuvant effect of RA is unexpected within the field of mucosal immunity, it is consistent with its usage as a beneficial proinflammatory adjuvant in anti-tumor immunity^15,16.

If you can't see the scientific CYA going on above, please read again.  Everything is being done to save the reputation of Poison/"Vitamin A", because to admit the opposite would be unthinkable (and unFUNDable).

These observations caution against the use of vitamin A and RA for the treatment of autoimmunity and inflammatory intestinal disorders associated with high levels of IL-15. Indeed, a causal relationship between retinoids used for the treatment of acne and inflammatory bowel disease was suggested in a subset of patients²⁷.

Gosh, so they're seeing a connection between Poison/"Vitamin A" and autoimmunity and inflammation?  That's because AUTOIMMUNITY IS BUILT UPON A FOUNDATION OF POISON/"VITAMIN A" TOXICITY.

One final aspect of our study is that we may have in hand a long-awaited physiopathologically relevant murine model mimicking the early stages of CD. This model is unique in that development of inflammatory anti-gluten immunity develops without microbial adjuvant or systemic immunization in immunologically competent mice with a polyclonal T cell receptor repertoire.

They're very proud of their new model, that REQUIRED Poison/"Vitamin A" to be present as the non-microbial/pathogenic, non-immunization/vaccination trigger of autoimmune disease in mice!  Hey guys, I think you proved something, but it wasn't what you were aiming for!

There's one last thing I want to cover from this paper.  Pay attention to the bolded part below.

Mucosal tolerance has important fail-safe mechanisms that prevent the initiation of unnecessarily destructive inflammatory immune responses to harmless antigens contacted at mucosal surfaces. These mechanisms include induction of regulatory T cells (iTreg) expressing the transcription factor forkhead box P3 (Foxp3) and deletion of T cells specific to the ingested antigen^1,2.

The induction (increase) of iTreg cells helps to reduce "unnecessarily destructive inflammatory immune responses to harmless antigens contacted at mucosal surfaces".  In a nutshell, we want more of the iTreg induction, so we can have less gut inflammation caused by harmless FOODS.

In accordance with its ability to further block iTreg generation in the presence of IL-15 (Fig. 1a), RA significantly amplified the release of all proinflammatory cytokines (Fig. S4a).

Poison/"Vitamin A" blocked iTreg generation/induction, and significantly increased ALL proinflammatory cytokines.

Poison/"Vitamin A" toxicity causes gut diseases of all types, and most people notice that increased food sensitivities happen early on in their downward health spiral (before they know about how to fix it with Nutritional Restoration and the Poison/"Vitamin A" and Glyphosate Detox approaches, that is).