ArticleDiabetes2026
Activation of Intestinal Type 3 Innate Lymphoid Cells and Regulatory T Cells Through Free Fatty Acid Receptor 2 Ameliorates Type 1 Diabetes in Mice.
Article in Diabetes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Reduction in intestinal type 3 innate lymphoid cells (ILC3) frequency is associated with type 1 diabetes (T1D) pathogenesis in humans and in animal models. The current study showed that, after T1D induction by multiple-low-dose streptozotocin in male C57BL/6 mice, ILC3 were reduced in both blood and pancreas and produced less IL-22 and IL-2, and a decreased proportion expressed the gut-homing α4β7 integrin in the pancreas. Additionally, T1D induction in ILC3-impaired mice produced exacerbated hyperglycemia. To activate ILC3, Compound 1 (Cpd1), a synthetic selective free fatty acid receptor 2 (FFAR2) agonist, was administered orally in a prophylactic regimen, at early therapeutic stages, or during established disease, resulting in significant amelioration of T1D symptoms. Cpd1 upregulated ILC3 and activated regulatory T cells (Treg) within the small intestine lamina propria and the pancreas, enhanced intestinal barrier integrity, and increased microbial diversity. Cpd1 also reduced α4β7-expressing inflammatory cells in the pancreas while promoting the accumulation of gut-imprinted ILC3. IL-22 was important for this anti-inflammatory response, as treatment efficacy was inhibited when mice were additionally given neutralizing anti-IL-22 antibodies. Of note, NOD mice receiving Cpd1 exhibited postponed disease initiation, but the incidence of disease was similar to that of the control group. Overall, activation of intestinal ILC3 and Treg via FFAR2 engagement, and translation of these anti-inflammatory effects to the pancreas, provided significant benefit in a mouse T1D model. ARTICLE HIGHLIGHTS: Modulating the adaptive immune response alone is insufficient for effective type 1 diabetes treatment. This study investigates targeting intestinal type 3 innate lymphoid cells as a novel therapeutic approach for type 1 diabetes. A synthetic free fatty acid receptor 2 agonist, Compound 1, activates intestinal IL-2+ and IL-22+ type 3 innate lymphoid cells and thereby reduces pancreatic inflammation, stabilizes intestinal barrier, and improves clinical outcomes in a type 1 diabetes mouse model. Compound 1 demonstrates therapeutic potential and may serve as a candidate for future clinical trials in type 1 diabetes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.