The study, led by Soledad Bouquez and Paola López Campos under the direction of corresponding author Maite Duhalde-Vega, examined mice fed a high-fat diet, a model that reliably reproduces the metabolic disturbances seen in human obesity. High-fat diets have long been implicated in metabolic disorders through mechanisms involving hyperuricemia, gut dysbiosis, and intestinal barrier dysfunction, but the precise chain of cause and effect has remained elusive. The Argentine team set out to determine whether pharmacological reduction of uric acid could interrupt that chain, and if so, by what molecular route.

The results were striking. Mice on the high-fat diet developed hyperuricemia, and their gut microbial communities shifted into a dysbiotic state characterized by an expansion of Proteobacteria, a phylum widely regarded as a microbial signature of epithelial dysfunction, along with altered ratios of Firmicutes to Bacteroidetes, a compositional change repeatedly linked to obesity and type 2 diabetes in human studies. At the same time, the animals’ intestines mounted an inflammatory program: levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α rose, while the anti-inflammatory mediators IL-10 and IL-22 declined. The team also detected increased serum lipopolysaccharide, or LPS, indicating that bacterial products were leaking across a compromised intestinal wall into the circulation, fueling systemic inflammation marked by elevated IL-6 and C-reactive protein.

When the researchers added allopurinol to the high-fat diet, the picture changed dramatically. The drug, which inhibits xanthine oxidase and thereby blocks uric acid production, normalized serum uric acid levels and, with them, restored microbial balance. The dysbiotic expansion of Proteobacteria receded, the Firmicutes/Bacteroidetes ratio shifted back toward a healthier profile, and the inflammatory storm in the gut subsided. Pro-inflammatory cytokines fell, protective IL-10 and IL-22 recovered, serum LPS dropped, and markers of intestinal barrier dysfunction improved. Equally important, the systemic inflammatory signs, elevated circulating IL-6 and CRP, diminished, suggesting that repairing the gut wall had consequences well beyond the intestine itself.

The most mechanistically revealing part of the study concerned tryptophan metabolism, an increasingly central theme in gut immunology. Tryptophan, an essential amino acid obtained from the diet, can be metabolized along several competing routes. One route, driven by the enzyme indoleamine 2,3-dioxygenase 1, or IDO1, shunts tryptophan toward catabolites that are generally associated with inflammation and immune suppression. Another route, carried out by gut bacteria, produces indoles, small molecules that serve as ligands for the aryl hydrocarbon receptor, or AhR, a transcription factor expressed in immune and epithelial cells. When AhR is activated by these microbial indoles, it promotes the production of interleukin-22, a cytokine that strengthens epithelial barrier function, stimulates antimicrobial peptide release, and maintains mucosal homeostasis.

In the high-fat diet mice, this protective circuitry was broken. The animals showed increased IDO1 activity and diminished indole production, tilting tryptophan metabolism away from AhR-activating ligands and toward inflammatory catabolites. Allopurinol treatment reversed this shift: IDO1 activity decreased and indole production was restored, replenishing the supply of microbial metabolites capable of engaging AhR. The result was a reinvigorated AhR–IL-22 axis, which the authors identified as the key mediator of the drug’s gut-protective effects. Prior work, including landmark studies showing that tryptophan catabolites from the microbiota engage AhR and balance mucosal reactivity via interleukin-22, had established the plausibility of this pathway; the new study ties it directly to uric acid metabolism.

To prove that the AhR–IL-22 axis was not merely correlated with the improvements but actually required for them, the team employed CH-223191, a selective pharmacological antagonist of the aryl hydrocarbon receptor. When AhR signaling was blocked in allopurinol-treated mice, the drug’s anti-inflammatory and barrier-protective effects were reversed. Cytokine profiles deteriorated, barrier function declined, and the benefits of uric acid reduction evaporated. This loss-of-function experiment provides functional evidence, not just associative data, that the AhR/IL-22 axis mediates gut protection in this model, a level of mechanistic rigor that strengthens the study’s therapeutic implications considerably.

The findings arrive amid growing interest in the interplay between purine metabolism, the microbiome, and intestinal health. Previous research has shown that hyperuricemia is associated with immune disorders and intestinal barrier dysfunction, that gut bacterial metabolism contributes to host purine homeostasis, and that hyperuricemia can influence tryptophan metabolism by inhibiting the transport proteins MRP4 and BCRP, which handle uric acid and metabolite trafficking across cell membranes. Uric acid itself is no innocent molecule: it was identified nearly two decades ago as a danger signal that alerts the immune system to dying cells, and elevated levels have been linked to metabolic syndrome through the activity of xanthine oxidoreductase. The new study weaves these threads into a coherent narrative in which dietary fat raises uric acid, uric acid disrupts the microbiome and tryptophan handling, and the resulting loss of AhR ligands starves the gut of the IL-22 signal it needs to maintain its barrier.

For clinicians, the appeal of the proposed strategy lies in its practicality. Allopurinol is inexpensive, generically available, and already used by millions of patients with gout and hyperuricemia, with a well-characterized safety profile. If the mechanisms observed in mice translate to humans, targeting hyperuricemia could offer a repurposable intervention for metabolic and inflammatory gut diseases, conditions that currently have limited therapeutic options. The authors suggest that uric acid modulation deserves consideration as a promising therapeutic strategy for these disorders, though they and outside observers alike will caution that mouse models of diet-induced disease do not always recapitulate human pathophysiology, and that clinical trials would be needed before uric acid lowering could be recommended for gut inflammation specifically.

The study also adds to a rapidly expanding literature on how diet reshapes the gut microbiome and, through it, systemic health. High-fat diets have been shown to alter microbial and metabolite profiles during obesity, to increase intestinal permeability, and to drive gut dysbiosis and inflammation that contribute to obesity-associated liver disease. Microbiota-targeted interventions, including washed microbiota transplantation in gout patients, have already shown hints of benefit on serum uric acid and intestinal barrier function in early pilot studies. What distinguishes the new work is its demonstration of a complete, mechanistically validated pathway, from dietary fat to uric acid to microbial composition to tryptophan-derived metabolites to AhR activation to IL-22-dependent barrier protection, with pharmacological confirmation at each critical node. That level of pathway resolution is rare, and it transforms a loose association between gout drugs and gut health into a testable therapeutic hypothesis.

The research, supported by grants from Argentina’s National Agency of Science and Technology and the Universidad de Buenos Aires, was conducted under approved animal care protocols and published as an original article in the Journal of Molecular Medicine. As obesity rates continue to climb worldwide and inflammatory bowel diseases grow more prevalent, the idea that a fifty-year-old gout medication might protect the gut by feeding the microbiome’s chemical conversation with the immune system is the kind of unexpected, cross-disciplinary insight that could reshape how clinicians think about the drugs they already prescribe. The next step will be determining whether lowering uric acid in people delivers the same tryptophan-centered, AhR-mediated protection that it does in mice, a question that the authors’ elegant mechanistic framework now makes far easier to ask.

Subject of Research: How anti-hyperuricemia therapy with allopurinol alleviates diet-induced gut inflammation in mice via the AhR–IL-22 signaling axis

Article Title: Anti-hyperuricemia therapy alleviates diet-induced gut inflammation via AhR-IL-22-signalling

Article References: Bouquez, S., Campos, P. L., Ottobre, M., & Duhalde-Vega, M. (2026). Anti-hyperuricemia therapy alleviates diet-induced gut inflammation via AhR-IL-22-signalling. Journal of Molecular Medicine, 104(1), Article 105. https://doi.org/10.1007/s00109-026-02713-6

Image Credits: AI Generated

DOI: 10.1007/s00109-026-02713-6

Keywords: hyperuricemia, allopurinol, uric acid, gut microbiota, gut inflammation, intestinal barrier, AhR, IL-22, tryptophan metabolism, indole, IDO1, high-fat diet

BSSG is a glucosylated sterol, a molecule built from a steroid backbone linked to a glucose moiety. It first attracted scientific attention decades ago in the Western Pacific, where an unusually high incidence of a disorder combining ALS-like motor neuron loss, parkinsonism and dementia was documented among the indigenous Chamorro population of Guam, and later in the Kii peninsula of Japan and Western New Guinea. The common thread turned out to be dietary: communities in these regions traditionally consumed flour made from cycad seeds, which contain considerable concentrations of BSSG. When Western dietary habits spread and cycad consumption declined after World War II, the incidence of ALS-PDC fell sharply. Previous work has shown that BSSG is neurotoxic in cell culture and in animals, driving glutamate-mediated excitotoxicity, promoting the accumulation of hyperphosphorylated tau in neurons and exacerbating apoptosis in astrocytes. Mice fed BSSG develop a pre-symptomatic ALS-PDC-like phenotype, but the earliest steps of the molecule’s path through the body have remained poorly charted.

To trace those steps, the team administered BSSG to zebrafish larvae and adults, either directly in the water at 10 micromolar or through customized BSSG-enriched food pellets, and to mice receiving 1 milligram per day, five days a week, for fifteen weeks. Mass spectrometry of lipid extracts confirmed that the compound accumulated in the trunk region of treated larvae, which contains the intestine. What happened next was unexpected: rather than an immediate neurological signature, the first visible target was the gut. Nearly all BSSG-exposed larvae developed dark aggregates in the intestine, prompting the researchers to look more closely at intestinal physiology.

The evidence of inflammation was striking and multi-layered. In vivo staining with neutral red revealed a reduction in lysosome-rich enterocytes, a well-established marker of intestinal injury in zebrafish models. The number of mucus-secreting goblet cells, which shield the intestinal wall from digestive enzymes and pathogens, dropped significantly, and the expression of agr2, a gene essential for mucus production, fell in parallel. At the same time, fluorescent neutrophils infiltrated the mid-intestine in dramatically higher numbers in a transgenic reporter line, and a separate NF-κB reporter line lit up along the gut wall, indicating activation of a central inflammatory signaling pathway. Acridine Orange staining revealed increased cell death, while a Stat3 reporter suggested depletion of the stem-like cells at the bases of intestinal folds, the zebrafish counterparts of mammalian crypt base columnar cells that normally replenish the epithelial lining.

Crucially, the effect was specific to the glucosylated form. β-sitosterol, which shares BSSG’s steroid structure but lacks the glucose moiety, produced none of these intestinal changes, pointing to the sugar group as the molecular feature responsible for the damage. That distinction matters beyond the aquarium: elevated levels of glucosyl-β-d-cholesterol, an endogenous human glucosylated sterol, are found in patients carrying GBA1 mutations, a major genetic risk factor for Parkinson’s disease, while glucosyl-α-d-cholesterol is produced by Helicobacter pylori during gastric infections, itself linked to increased lifetime risk of Parkinson’s. The mechanisms connecting these sterols to nervous system damage have remained obscure, and the new results suggest the intestine may be where the story begins.

Gut inflammation was only the opening act. Treated zebrafish larvae showed a marked reduction in peristaltic contractions and significantly delayed gastrointestinal transit, hallmarks of disturbed intestinal motility that in humans often precede the motor symptoms of Parkinson’s disease and ALS by years. Notably, counts of enteric neurons and their progenitors were unchanged, suggesting that BSSG impairs the function of the enteric nervous system rather than its structure. The team then performed what they describe as the first ex vivo analysis of neuromuscular contractility in isolated adult zebrafish intestines, mounting whole guts in oxygenated organ baths and measuring tension with isometric force transducers. Treated intestines contracted more forcefully in response to potassium chloride depolarization, to the cholinergic agonist carbachol, and to electrical field stimulation of enteric neurons, while relaxation in response to a β-adrenergic agonist was unaffected. The pattern points to hypercontractility of both the muscular and neuronal components of the gut wall, a profile reminiscent of inflammatory bowel disease.

Molecular profiling deepened the picture. RNA sequencing of chronically treated larvae identified 261 differentially expressed genes, with upregulated genes concentrated in acute inflammatory response, defense against bacteria and response to reactive oxygen species. Markers such as mmp9, pept1, saa and s100a10a, which mirrors human calprotectin, an established inflammatory bowel disease marker also elevated in Parkinson’s and Alzheimer’s patients, were all increased. The entire suite of hemoglobin genes was downregulated, a change recently associated with the pathophysiology of several neurodegenerative diseases. In the brains of adult treated zebrafish, autophagy-related genes including atg5, lc3b and p62 were reduced, hinting at a possible impairment of the cellular waste-clearance process whose failure promotes neurotoxic protein aggregates.

The mouse experiments confirmed that the phenomenon crosses species. After fifteen weeks on the BSSG diet, mice showed increased macrophages in the lamina propria of the small intestine, fewer goblet cells, and significantly shortened microvilli under electron microscopy, suggesting impaired absorptive capacity. Treated mice weighed less than controls despite eating the same amount. RNA sequencing of mouse gut tissue revealed 1,835 differentially expressed genes dominated by immune response categories, with upregulation of Toll-like receptors 2, 4 and 6, the inflammasome component Nlrp3, the pro-inflammatory cytokines IL-1β and IFN-γ, and, notably, Lrrk2, one of the most significant genetic risk factors for Parkinson’s disease, whose protein promotes NF-κB signaling in the gut. The antimicrobial peptide Reg3-γ was downregulated, mirroring the goblet cell loss. Preliminary fecal microbiota sequencing also suggested early dysbiosis, with an expansion of potentially pathogenic families such as Bacteroidaceae and Helicobacteraceae and a reduction of anti-inflammatory Lachnospiraceae.

Perhaps the most intriguing mechanistic clue came from BSSG’s structural kinship with steroid hormones. In a radioligand binding assay, BSSG displaced about 12.5 percent of radiolabeled dexamethasone from the glucocorticoid receptor, while leaving estrogen, mineralocorticoid and progesterone receptors untouched. To test this in living animals, the researchers exploited zebrafish mutants unable to synthesize active glucocorticoids, crossed with a transgenic line whose intestines glow green when the glucocorticoid receptor is activated. BSSG treatment significantly increased intestinal fluorescence in these receptor-reporter animals, indicating that the molecule can engage the receptor in vivo. Even more tellingly, zebrafish engineered to lack the glucocorticoid receptor entirely were largely protected: their goblet cell numbers, inflammatory gene expression, gut contractility and microbiota composition barely changed with BSSG exposure. Because the glucocorticoid receptor normally suppresses inflammation in the intestine, the results suggest BSSG may sabotage this built-in anti-inflammatory brake.

The authors propose a model in which dietary BSSG first inflames the gut, weakening the epithelial barrier, disturbing motility and shifting the microbiome, and then, through disruption of the gut–brain axis, predisposes the nervous system to degeneration, ultimately culminating in ALS-PDC. While the glucocorticoid receptor interaction still requires in vitro validation, altered glucocorticoid signaling has already been implicated in ALS, Parkinson’s and Alzheimer’s disease. If the model holds, restoring intestinal homeostasis could become an early intervention strategy, targeting the disease at its apparent point of origin rather than its neurological endpoint.

The mammalian gastrointestinal tract is a heavily immunocompetent organ, hosting an intricate network of immune cells finely tuned to balance tolerance and defense. Among these, T lymphocytes stand out for their antigen-specific surveillance and regulatory roles. Canonical T cells typically express either the CD4 or CD8αβ co-receptors, facilitating their well-characterized helper or cytotoxic functionalities. However, DNT cells defy this paradigm: they lack both CD4 and CD8αβ markers but express the T-cell receptor alpha-beta (TCRαβ), prompting questions about their lineage and immunological roles.

Led by Associate Professor Yasuhiro Nemoto and Professor Ryuichi Okamoto of the Institute of Science Tokyo, the research team focused on these double negative populations in the murine small intestine, leveraging advanced intravital imaging—a technique enabling real-time observation of cellular interactions within living organisms. This breakthrough allowed observation of DNT cells migrating autonomously through the intestinal lamina propria, an area densely populated by immune and epithelial cells.

Perhaps most startling was the elucidation of a novel immune function: DNT cells act as tolerogenic antigen-presenting cells. Traditionally, professional APCs such as dendritic cells, macrophages, and B cells capture and process antigens to prime naïve T cells, initiating adaptive immune responses. The discovery that DNT cells themselves internalize intestinal antigens and migrate to secondary lymphoid sites to present these antigens to naïve CD4⁺ T cells challenges existing immunological dogma. Unlike classical APCs, however, DNT cells conspicuously lack co-stimulatory molecules—such as CD80 and CD86—which are essential for the full activation of T cells.

This absence of co-stimulation imparts a critical functional twist. When DNT cells present antigens, they induce a state of anergy—or non-responsiveness—in CD4⁺ T cells rather than activation. Anergy is a fundamental mechanism to maintain immune tolerance and prevent aberrant inflammation. Thus, DNT cells act not as elicitors of immune attack but as regulators that suppress excessive immune responses, particularly in the immunologically complex environment of the gut where tolerance to dietary and commensal antigens must be preserved.

The physiological significance of these findings was underscored in murine models of intestinal inflammation. DNT cell activity correlated negatively with inflammation severity, supporting their role as anti-inflammatory mediators. More importantly, the team extended their observations to human disease, investigating samples derived from patients afflicted with Crohn’s disease, a chronic inflammatory condition of the gastrointestinal tract characterized by dysregulated immune responses. Here, DNT cells exhibited marked deficits in antigen uptake and presentation abilities, implying that impaired DNT cell function may contribute substantially to the pathogenesis of this debilitating disorder.

These insights open exciting new avenues in the pursuit of targeted immunotherapies for inflammatory bowel diseases (IBD). By harnessing or restoring the tolerogenic functions of DNT cells, therapeutic strategies could be designed to recalibrate intestinal immune responses, potentially offering relief and remission for patients suffering from Crohn’s disease and related disorders. This approach offers a stark contrast to broad-spectrum immunosuppressants currently in use, promising more precise modulation of immune pathways with fewer side effects.

The identification of DNT cells as a unique class of antigen-presenting cells also enriches the broader immunological framework by adding complexity to the cellular crosstalk within mucosal tissues. These findings underscore the dynamic plasticity of immune cells and suggest that immune cell specialization extends beyond traditional categorizations, particularly in tissue-specific contexts such as the gut.

Central to this discovery was intravital microscopy’s unparalleled ability to capture immune cell behavior in vivo. This technology combines advanced optics with sophisticated imaging software to permit longitudinal studies of cell motility, interaction, and function in their native microenvironment—insights impossible to glean from ex vivo or fixed samples. The visualization of DNT cell migration and antigen processing represents a methodological leap with broad applications across immunology.

Associate Professor Nemoto highlighted the novelty of the research, emphasizing the global first: “Our study is the inaugural report demonstrating that intestinal DNT cells serve as tolerogenic antigen-presenting cells. This challenges the longstanding paradigm that only classical APCs mediate antigen presentation and immune activation. The unique behavior of DNT cells positions them as key regulators of intestinal immune tolerance.”

Furthermore, the study suggests that immune regulation by DNT cells hinges not merely on antigen presentation but crucially depends on the absence of co-stimulation, delineating a mechanism by which these cells dampen inflammation rather than triggering it. This enhances our understanding of how immune tolerance is meticulously maintained in the gut despite constant exposure to foreign antigens.

Future directions include exploring the molecular signals governing DNT cell differentiation and antigen presentation, their interactions with other intestinal immune populations, and their potential alterations in various gastrointestinal diseases. Investigating ways to potentiate DNT cell regulatory functions or repair their dysfunction could revolutionize therapies for autoimmune and inflammatory conditions beyond Crohn’s disease.

In conclusion, the Institute of Science Tokyo’s landmark work not only elucidates a previously hidden facet of intestinal immunity but also paves the way for innovations in clinical immunology. The revelation that double negative T cells act as natural suppressors of intestinal inflammation, employing antigen presentation without activating co-stimulatory signals, provides a fresh blueprint for immunoregulatory mechanisms in the mucosa and highlights new therapeutic targets for inflammatory diseases. This study exemplifies the power of cutting-edge technology and collaborative science in unearthing the sophisticated balance of immune function within the human body.

Subject of Research: Animals

Article Title: Intestinal CD4−CD8αβ−TCRαβ+ T cells function as tolerogenic antigen presenting cells in mice

News Publication Date: 1-Aug-2025

Web References: https://doi.org/10.1038/s41467-025-62089-y

Image Credits: Institute of Science Tokyo

Keywords: Immune cells, Double negative T cells, Intestine, Antigen presentation, TCRαβ, Crohn’s disease, Intravital microscopy, Inflammatory bowel disease, Gut immunity, Tolerance, Anergy, Antigen-presenting cells

The research, conducted in murine models, focuses on a specialized subset of CD4+ T cells that are specific for gut-colonizing segmented filamentous bacteria (SFB). These T cells, referred to as gut commensal-specific T cells (T_comm), undergo dysregulation during episodes of intestinal inflammation, such as those observed in inflammatory bowel disease and related pathologies. Remarkably, this dysfunction endows them with the ability to migrate into the CNS, an organ previously thought insulated from direct microbial influence, where they contribute to neuroinflammatory cascades.

One of the central findings is that T_comm cells lose their stringent antigen specificity once licensed to infiltrate the CNS. This permits them to be reactivated by host-derived protein antigens via a process known as molecular mimicry. Essentially, peptides expressed within the CNS share structural similarities to bacterial antigens, tricking these T cells into mounting an immune response against self-tissues. The consequent production of potent cytokines such as GM-CSF, IFNγ, and IL-17A by the infiltrated T_comm cells serves as a key trigger for neuroinflammatory damage.

Delving deeper into the molecular underpinnings, the study elucidates that T_comm cells instigate CNS inflammation through both IL-23 receptor (IL-23R)-dependent and independent pathways. The IL-23R-dependent mechanism involves the activation of an encephalitogenic program within T cells, driving their pathogenic potential. Concurrently, the production of GM-CSF proceeds independently of IL-23R signaling, underscoring the multifaceted nature of T_comm-mediated neuroinflammation.

A crucial effector population targeted by these dysregulated T_comm cells are microglia, the resident immune cells of the brain and spinal cord. Upon activation by currents of inflammatory cytokines, microglia adopt pro-inflammatory phenotypes that exacerbate neuronal injury and propagate CNS inflammation. This microglial activation represents a tipping point where peripheral immune dysregulation translates into central nervous system pathology.

The implications of these findings are profound. They challenge the prevailing paradigm that microbial influences on the CNS are limited to indirect modulation via metabolic products or systemic inflammation. Instead, they propose an immune cell-centric mechanism by which gut microbial dysbiosis can have direct ramifications on neurological health, placing T_comm cells at the crossroads of gut-brain immunology.

Emerging from this work is a nuanced appreciation of how regulatory T cells, which normally suppress excessive immune responses, play a crucial restraining role. In the absence of functional regulatory T cells, T_comm cells escape immune checkpoints, gaining access to the CNS and unleashing inflammatory responses. This highlights the intricate balance between immune tolerance and activation in maintaining both intestinal and neurological homeostasis.

Moreover, the concept of molecular mimicry within the CNS adds a compelling layer to autoimmune disease models. It provides a mechanistic basis for how infections or microbial exposure in the periphery might precipitate autoreactive immune responses against central nervous system components, echoing theories proposed in diseases such as multiple sclerosis.

The study’s detailed interrogation of T_comm cell behavior also reveals potential therapeutic targets. Modulating IL-23R signaling or intervening in GM-CSF production pathways could offer strategies to stifle neuroinflammation initiated by gut-derived immune cells. Such interventions might benefit patients suffering from neuroinflammatory conditions that currently lack effective treatments.

From a broader perspective, these findings emphasize the significance of the gut microbiota as not merely a collection of commensals but as an active player orchestrating immune responses with far-reaching systemic consequences. As microbiome research continues to unravel complex host-microbe interplays, the delineation of immune cell trafficking and activation patterns provides vital insights into disease etiology.

The study also prompts a reevaluation of neurological disease pathogenesis, advocating for integrative approaches that consider the gut-brain axis as a dynamic immunological interface. Identifying early markers of T_comm cell dysregulation might enable preemptive strategies to mitigate or prevent neuroinflammatory damage.

This paradigm shift underscores the importance of maintaining intestinal immune equilibrium, where perturbations can ripple into severe consequences for distant organ systems. It opens the door to exploring microbiota-targeted therapies not only for gastrointestinal disorders but also for neuroimmune diseases.

In summary, this cutting-edge research delineates a novel mechanism through which gut-resident microbes indirectly provoke CNS inflammation by shaping T cell repertoires and functions. It bridges long-standing gaps in understanding how peripheral immune disturbances translate into central autoimmune pathology, paving the way for innovative clinical approaches.

As the scientific community delves deeper into the complexities of immune-microbiota interactions, these insights strengthen the notion that health and disease are inseparable from the microbial world within us. The study stands as a testament to the power of multidisciplinary research in unraveling the hidden connections that define human biology.

Subject of Research: The interplay between gut microbiota-specific CD4+ T cells and neuroinflammation in the central nervous system.

Article Title: Gut inflammation promotes microbiota-specific CD4 T cell-mediated neuroinflammation.

Article References:
White, Z., Cabrera, I., Mei, L. et al. Gut inflammation promotes microbiota-specific CD4 T cell-mediated neuroinflammation. Nature (2025). https://doi.org/10.1038/s41586-025-09120-w

Image Credits: AI Generated