The investigators used disproportionality analysis to assess whether skin cancer appeared more often than expected among reports involving particular medicines. This approach generated reporting odds ratios (RORs) and information components (ICs) from the spontaneous-reporting data. Risankizumab had the strongest measured signal, with an ROR of 8.01, a 95% confidence interval of 7.62–8.42 and an IC025 of 2.88. Tildrakizumab had an ROR of 5.81, with a 95% confidence interval of 4.13–8.19 and an IC025 of 1.84. Ustekinumab had an ROR of 5.53, with a 95% confidence interval of 5.23–5.85 and an IC025 of 2.35. These measures quantify disproportionate reporting within FAERS; they do not establish that the medicines caused skin cancer or show the magnitude of any absolute increase in incidence.

Subgroup analyses indicated that the reporting association was more pronounced among older patients, particularly those older than 75 years. The researchers also performed time-to-onset analysis and Weibull modelling to examine reporting patterns after treatment initiation. The modelling identified a “wear-out” failure pattern for ustekinumab and risankizumab, indicating that the frequency of reports increased over time in the dataset. This pattern describes when reports accumulated; it does not demonstrate that cancer risk itself rises with longer treatment. Additional analyses of interactions with co-medications did not identify significant synergistic reporting signals for skin cancer.

The findings are best understood as signal detection from a spontaneous-reporting database rather than a comparison of cancer incidence among treated and untreated groups. The study’s population comprised individual safety reports entered into FAERS, and its results concern reporting associations for IL-12/23, IL-23 and IL-17 inhibitors during the specified period. The authors concluded that disproportionate skin-cancer reporting warrants further prospective investigation to establish its clinical significance, particularly for risankizumab and ustekinumab. Their results do not demonstrate that the medicines cause skin cancer, quantify absolute risk or establish that the observed reporting pattern reflects a change in the incidence of skin cancer. The findings also do not support treating the weaker IL-17 inhibitor signals as causally established, especially after they disappeared in the psoriasis-restricted sensitivity analysis.

Subject of Research: FAERS disproportionality analysis of skin-cancer reporting involving IL-12/23, IL-23 and IL-17 inhibitors.

Article Title: Potential association between IL-12/23, IL-23, and IL-17 inhibitors and skin cancer: a pharmacovigilance study based on the FAERS database

Article References: Jiang, X., Huang, Y., Xie, M., Peng, L., Xu, M., Qi, Z., Wang, G., & Pu, X. (2026). Potential association between IL-12/23, IL-23, and IL-17 inhibitors and skin cancer: a pharmacovigilance study based on the FAERS database. Frontiers in Pharmacology, 17, Article 1944368. https://doi.org/10.3389/fphar.2026.1944368

Image Credits: AI Generated

DOI: 10.3389/fphar.2026.1944368

Keywords: FAERS, pharmacovigilance, skin cancer, disproportionality analysis, IL-23 inhibitors, IL-17 inhibitors, risankizumab, ustekinumab, tildrakizumab, adverse-event reporting, Potential, association

The researchers recruited 60 patients with SLE and thrombocytopenia, 40 patients with SLE without thrombocytopenia and 40 healthy controls, then collected blood samples from the three groups. They measured PVT1, miR-181a, FOXP3 and RORγt gene expression using reverse-transcription polymerase chain reaction. Serum concentrations of IL-23, IL-10, lipocalin2 and matrix metalloproteinase 9 (MMP9) were measured with enzyme-linked immunosorbent assays.

Among patients with thrombocytopenic SLE, serum IL-23, lipocalin2 and MMP9 concentrations were higher and IL-10 concentrations were lower than in the non-thrombocytopenic SLE and healthy control groups. The abstract also reports increased miR-181a and RORγt expression, decreased PVT1 and FOXP3 expression, a higher IL-23 level and a lower IL-10 level among thrombocytopenic SLE patients with positive antiphospholipid antibodies. It does not identify the comparison group for that subgroup result or provide complete numerical data.

The authors interpret PVT1/miR-181a as a possible upstream regulator of the RORγt/FOXP3 balance and its associated IL-23 and IL-10 markers, linking these patterns to the possible pathogenesis of SLE-associated thrombocytopenia. The findings are observational associations and do not establish that the measured RNA or cytokine patterns cause thrombocytopenia, antiphospholipid antibodies, bleeding or thrombosis. The abstract reports no effect sizes, confidence intervals, longitudinal outcomes or diagnostic-performance measures. Because only the abstract was available, the full methods, statistical analyses and results could not be assessed; the results identify candidate markers for further investigation but do not establish diagnostic accuracy, predict future complications or demonstrate a clinical benefit from targeting these pathways.

Subject of Research: Molecular marker differences in systemic lupus erythematosus-associated thrombocytopenia

Article Title: Unravelling the role of the non-coding RNAs PVT1/miR-181a in orchestrating IL-23/RORγt and FOXP3/IL-10 axes in thrombocytopenia associated with systemic lupus erythematosus: insights into the clinical paradox of antiphospholipid syndrome

Article References: Abd-Elmawla, M. A., Shaker, O. G., Mamdouh, M., Zekry, S. S., Ibrahim, S. G., Hegazy, G. A., & Ayeldeen, G. (2026). Unravelling the role of the non-coding RNAs PVT1/miR-181a in orchestrating IL-23/RORγt and FOXP3/IL-10 axes in thrombocytopenia associated with systemic lupus erythematosus: insights into the clinical paradox of antiphospholipid syndrome. Molecular Biology Reports, 53(1), Article 1576. https://doi.org/10.1007/s11033-026-12551-x

Image Credits: AI Generated

DOI: 10.1007/s11033-026-12551-x

Keywords: systemic lupus erythematosus, thrombocytopenia, PVT1, miR-181a, RORγt, FOXP3, IL-23, IL-10, antiphospholipid antibodies, biomarkers, Unravelling, role

The patient was a 47-year-old man whose psoriasis vulgaris had been diagnosed 15 years earlier. After topical treatment of his psoriatic plaques, something striking happened: depigmented patches, the hallmark of vitiligo, emerged at sites that overlapped with the psoriatic lesions and then expanded in step with his overall psoriasis disease activity. When he first presented to the Nagasaki team eight years ago, he received a dual diagnosis of psoriasis and vitiligo. Oral cyclosporine, an immunosuppressant that dampens T-cell activation, was tried at a dose of 2.5 mg/kg/day, later tapered to 1 mg/kg/day, but it failed to control the psoriasis and, notably, the vitiligo continued to spread. At that point his psoriasis was severe, with a Psoriasis Area and Severity Index score of 23.2 and 20 percent of his body surface area affected, while he showed no joint symptoms suggestive of psoriatic arthritis.

With conventional immunosuppression failing, the clinicians turned to a more targeted weapon: risankizumab, an antibody that blocks the p19 subunit of interleukin-23, a cytokine central to the psoriatic inflammatory cascade. The patient received 150 mg subcutaneously at baseline, again one month later, and then every three months. The response was dramatic on the psoriatic side of the ledger. Within four months of treatment, his psoriasis improved markedly, and over five years of continuous therapy he experienced no new psoriatic lesions. The vitiligo, however, told a different story. It persisted and even expanded mildly despite the sustained IL-23 blockade, a dissociation that carries important biological and therapeutic implications.

Before starting the antibody therapy, the team obtained skin biopsies from two carefully chosen sites: one lesion containing both psoriasis and vitiligo, which the authors designate PVL, and a purely vitiliginous lesion without psoriatic features, designated VL. Under the microscope, the difference was unmistakable. The co-localized lesion displayed the textbook architecture of psoriasis: parakeratosis, the retention of nuclei in the stratum corneum; elongated rete ridges plunging deep into the dermis; Munro’s microabscesses, clusters of neutrophils trapped within the horny layer; and a dense inflammatory infiltrate in the dermis. The pure vitiligo lesion, by contrast, showed only mild epidermal hyperplasia with a limited superficial dermal infiltrate. Critically, neither lesion contained any detectable melanin or melanocytes when stained with Fontana-Masson and Melan-A, confirming complete melanocyte loss in both territories.

The immunological deep-dive focused on a panel of inflammatory cell markers: CD3 for total T cells, CD4 for helper T cells, CD8 for cytotoxic T cells, CD123 for plasmacytoid dendritic cells, and Foxp3 for regulatory T cells. In the co-localized lesion, the dermis was packed with CD3-positive and CD4-positive cells, while CD8-positive cells appeared in both the dermis and, more sparsely, in the epidermis. CD123-positive cells were distributed throughout the dermis, and Foxp3-positive regulatory T cells were present in small numbers. The pure vitiligo lesion showed only scant numbers of all five cell types in both epidermis and dermis, a picture of relative immunological quiet.

Quantitative analysis sharpened the contrast. Counting positively stained cells in three representative microscopic fields, the researchers found roughly eight times more CD3-positive T cells in the co-localized lesion than in the pure vitiligo lesion, 335 plus or minus 211 versus 42 plus or minus 36 cells per 100-times field. Plasmacytoid dendritic cells, identified by CD123, were nearly six times more abundant in the psoriasis-containing lesion, at 32 plus or minus 19.2 versus 5.6 plus or minus 4.6 cells per field. Interestingly, when the authors calculated the proportion of regulatory T cells as the Foxp3-to-CD3 ratio, the two lesions looked broadly similar: 45.4 percent in the co-localized lesion versus 37.0 percent in the pure vitiligo lesion. The message, the authors argue, is that the co-localized site simply hosted far more inflammation, while the overall cellular composition remained comparable between the two, likely reflecting the intrinsic inflammatory nature of psoriasis rather than a disease-specific interaction between the two conditions.

Several threads of prior research help make sense of these numbers. A earlier report by Ono and colleagues examined coexisting vitiligo and psoriasis lesions and found that the proportion of regulatory T cells among CD3-positive T cells increased from vitiliginous to psoriatic tissue, a pattern consistent with the Nagasaki findings. The abundance of CD123-positive cells in the co-localized lesion also points to plasmacytoid dendritic cells as players in psoriatic inflammation, echoing a landmark study showing that these cells can initiate psoriasis through production of interferon-alpha. But here lies the biological irony: plasmacytoid dendritic cells and type I interferons have also been implicated in driving progressive vitiligo. The same innate immune pathway that helps ignite psoriasis may simultaneously fuel the destruction of melanocytes, potentially explaining how the two diseases can coexist in one patch of skin and why blocking IL-23 alone left the depigmentation untouched.

The clinical course raises the question of causality. Psoriasis preceded the vitiligo in this patient, and the absence of melanocytes within the inflamed areas supports the idea that chronic psoriatic inflammation may have inflicted secondary damage on melanocytes. Yet the picture is not that simple. The psoriatic changes were concentrated mainly in the central regions of the vitiligo patches rather than at their actively expanding edges, which does not fully fit a straightforward Köbner phenomenon, the process by which trauma or inflammation triggers psoriatic lesions in previously unaffected skin. The authors also note a sobering precedent: a separate case report described de novo vitiligo emerging during IL-23p19 inhibitor therapy, suggesting that this drug class may not suppress vitiligo-associated inflammation and may, in some patients, even contribute to its development.

The authors are candid about the limits of their evidence. This is a single case report, with biopsy sampling restricted to two sites and without detailed functional immunological analyses such as cytokine profiling or single-cell sequencing. The findings neither confirm nor exclude a Köbner phenomenon as the mechanism linking the two diseases. Still, the case carries practical weight for clinicians. It demonstrates that a highly effective IL-23 pathway blockade can clear psoriasis while leaving vitiligo to pursue its own course, reinforcing the concept that these diseases, though both immune-mediated, run on partly separable molecular circuits. It also adds to a small but growing literature on co-localized psoriasis and vitiligo, a phenomenon rare enough that each well-documented case meaningfully expands the field’s understanding.

What makes the report resonate beyond dermatology is the broader immunological lesson it encodes. The skin can simultaneously host a Th17-driven, IL-23-dependent inflammatory program and a cytotoxic, interferon-influenced attack on pigment cells, with regulatory T cells present in similar proportions in both settings. Dissecting which signals are shared and which are disease-specific, particularly the ambiguous role of plasmacytoid dendritic cells and type I interferons, may inform future therapies aimed at calming one autoimmune process without unleashing another. For now, the Nagasaki case stands as a vivid reminder that the immune system’s battles in the skin are not always mutually exclusive, and that the same patch of skin can be a battlefield for two wars at once.

Subject of Research: Co-localized psoriasis and vitiligo in a single patient, with immunohistochemical analysis of immune cell infiltration and the differential response to IL-23 blockade

Article Title: A coexistence case of psoriasis and vitiligo: insights into possible pathomechanisms

Article References: Koike, Y., Shimono, M., Kuwatsuka, S., & Murota, H. (2026). A coexistence case of psoriasis and vitiligo: insights into possible pathomechanisms. Journal of Cutaneous Immunology and Allergy, 9, Article 17495. https://doi.org/10.3389/jcia.2026.17495

Image Credits: AI Generated

DOI: 10.3389/jcia.2026.17495

Keywords: psoriasis, vitiligo, IL-23, risankizumab, plasmacytoid dendritic cells, Köbner phenomenon, regulatory T cells, interferon, melanocytes, immunohistochemistry, case report, dermatology

Inflammatory bowel disease, which encompasses ulcerative colitis and Crohn’s disease, affects millions of people worldwide and is characterized by chronic, relapsing inflammation of the gastrointestinal tract. Current therapies, including corticosteroids, immunosuppressants, and biologics targeting tumor necrosis factor alpha, can be effective but often carry substantial side effects, high costs, and loss of efficacy over time. This therapeutic gap has driven intense interest in natural products, particularly polyphenol-rich plant extracts, that might modulate inflammation with fewer adverse consequences. Grapevine leaves have been used in traditional medicine across the Mediterranean for centuries, valued for their astringent and anti-inflammatory properties, but their potential in intestinal inflammation had remained largely unexplored in rigorous preclinical models.

The research team, led by Houssam Shaib with collaborators including Laura Dosh, Lara Diab, Rana Bou Khalil, and Abdo Jurjus, began by characterizing the phytochemical profile of grapevine leaves collected from Mount Lebanon. Using hydroethanolic extraction, a method that efficiently captures both water-soluble and alcohol-soluble compounds, they quantified the extract’s total phenolic content, condensed tannin levels, and antioxidant reducing power. The results were striking: the extract contained 63.3 milligrams of gallic acid equivalents per gram for total phenolics and 60.8 milligrams of catechin equivalents per gram for condensed tannins, both indicating a densely polyphenol-rich preparation. Reducing power activity, a measure of the extract’s capacity to donate electrons and neutralize reactive species, yielded an EC50 of 121.4 micrograms per milliliter, confirming substantial antioxidant capacity.

These measurements matter because oxidative stress is a central driver of intestinal inflammation. In colitis, infiltrating immune cells generate reactive oxygen species that damage epithelial cells lining the colon, breach the mucosal barrier, and allow luminal bacteria to trigger further immune activation. Polyphenols and condensed tannins can interrupt this cascade at multiple points, scavenging free radicals, chelating pro-oxidant metal ions, and modulating intracellular signaling pathways such as nuclear factor kappa B and mitogen-activated protein kinase, which orchestrate the transcription of inflammatory genes. The chemical profile of the Lebanese grapevine leaf extract therefore suggested it was well equipped to counter the oxidative and inflammatory damage characteristic of colitis.

To test this hypothesis, the researchers induced acute colitis in BALB/c mice using intrarectal administration of 2,4,6-trinitrobenzenesulfonic acid, or TNBS, a widely used haptenizing agent that provokes a T helper cell type 1 and type 17 driven inflammatory response closely mimicking aspects of human Crohn’s disease. TNBS damages the colonic epithelium and renders it immunogenic, unleashing a wave of inflammatory cytokines that recruit immune cells into the gut wall. Following induction, the mice received oral doses of the grapevine leaf extract at different concentrations, allowing the team to assess both efficacy and dose-response relationships.

The disease model performed as expected. TNBS-treated mice displayed marked intestinal inflammation, with increased colon weight reflecting edema and tissue thickening, dense infiltration of inflammatory cells, and visible epithelial damage. At the molecular level, the researchers observed significant upregulation of the genes encoding interleukin-17, interleukin-23, interferon gamma, and transforming growth factor beta, a cytokine signature that maps directly onto the IL-23/IL-17 axis now recognized as a pivotal pathway in inflammatory bowel disease. Biologic drugs targeting IL-17 and IL-23 have shown clinical benefit in patients, underscoring the relevance of this signaling axis as a therapeutic target.

Treatment with the grapevine leaf extract changed the picture dramatically. Mice receiving the extract showed significantly improved clinical signs and attenuated histopathological lesions, with reduced inflammatory cell infiltration and less epithelial injury compared with untreated colitic animals. Most notably, the 300 milligram per kilogram body weight dose demonstrated the strongest immunomodulatory effect, restoring inflammatory cytokine gene expression toward basal levels comparable to those of healthy control mice. This dose-dependent normalization of the IL-17, IL-23, IFN-gamma, and TGF-beta signature suggests that the extract does not merely mask symptoms but actively recalibrates the immune signaling underlying the disease process.

The authors analyzed parametric data using one-way analysis of variance with Tukey’s post hoc test, while non-parametric data such as disease scores and gene expression were evaluated with the Kruskal-Wallis test, providing statistical rigor appropriate to the mixed data types. All animal procedures were approved by the Institutional Animal Care and Use Committee of the American University of Beirut, and plant samples were collected from private land with the landowner’s explicit permission. The work was funded by the Farouk Jabre Grant at the American University of Beirut, and the authors declare no competing interests.

The implications extend beyond the laboratory. Grapevine leaves are an abundant agricultural residue generated in enormous quantities by the wine industry each pruning season, which means a therapeutic extract could be sourced sustainably and inexpensively from material that would otherwise be discarded. This aligns with growing interest in circular economy approaches to nutraceutical and pharmaceutical development, particularly in Mediterranean countries where both viticulture and inflammatory bowel disease intersect. A standardized grapevine leaf extract could, in principle, be developed as a complementary therapy for maintaining remission in inflammatory bowel disease patients or as a preventive agent in at-risk populations, though considerable work remains before such applications.

Important caveats temper the excitement. The study was conducted in an acute mouse model of chemically induced colitis, which, while valuable for dissecting inflammatory mechanisms, does not fully recapitulate the chronic, relapsing nature of human inflammatory bowel disease. Bioavailability of polyphenols and tannins in humans is often limited by poor absorption and rapid metabolism, and effective doses in mice do not translate directly to human dosing. Human clinical trials, chronic disease models, and detailed mechanistic studies identifying the specific active compounds within the extract will all be necessary. Nevertheless, the demonstration that a simple, traditionally used plant extract can restore a disease-driving cytokine profile to healthy baseline levels in vivo is a compelling proof of concept, and it adds grapevine leaves to the expanding pharmacopoeia of natural products under investigation for inflammatory disorders.

Subject of Research: Anti-inflammatory effects of grapevine leaf extract in a mouse model of TNBS-induced colitis

Article Title: Protective anti-inflammatory effects of Vitis vinifera leaf extract against TNBS-induced colitis in mice

Article References: Shaib, H., Dosh, L., Diab, L., Khalil, R. B., Salloum, F., Jaber, L., Amo, M., Haidar, A., Hamadeh, S., & Jurjus, A. (2026). Protective anti-inflammatory effects of Vitis vinifera leaf extract against TNBS-induced colitis in mice. BMC Complementary Medicine and Therapies. https://doi.org/10.1186/s12906-026-05639-1

Image Credits: AI Generated

DOI: 10.1186/s12906-026-05639-1

Keywords: Vitis vinifera, grapevine leaf extract, colitis, TNBS, inflammatory bowel disease, cytokines, IL-17, IL-23, antioxidants, polyphenols, natural products, mouse model

The central argument is provocative: periodontitis should be understood not as a bacterial infection with an immune side effect, but as an immunopathological condition rooted in impaired immune homeostasis. While a dysbiotic microbiome — dominated by organisms such as Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans — initiates the disease, the sustained destruction of connective tissue and alveolar bone is driven primarily by dysregulated host immune responses rather than direct bacterial toxicity. Environmental factors like smoking and stress compound the problem, but the tissue damage ultimately flows from chronic activation of inflammatory and osteoclastogenic networks within the periodontal microenvironment.

At the heart of this network are CD4+ T cells, which upon activation by antigen-presenting cells differentiate into specialized subsets: Th1, Th2, Th9, Th17, Th22, and regulatory T (Treg) cells. Each subset carries a distinct transcription factor and cytokine signature. For decades, researchers interpreted periodontal disease through the simplified Th1–Th2 paradigm, in which Th1 responses were cast as pro-inflammatory destroyers and Th2 responses as protective regulators. The new review dismantles that dichotomy. Th1 and Th2 cytokines are simultaneously detected in periodontal lesions, and their relative dominance fluctuates with disease stage, microbial burden, and the local cytokine milieu — evidence that the disease is not governed by any single, unidirectional T helper response.

The Th1 compartment illustrates this complexity. Driven by signals such as bacterial lipopolysaccharide and the cytokine IL-12, Th1 cells produce interferon-γ (IFNγ), which activates macrophages and amplifies pro-inflammatory signaling. Patients with periodontitis show elevated proportions of circulating and local Th1 cells and increased IFNγ expression compared with healthy controls. Yet IFNγ plays a genuinely context-dependent role: some evidence shows it can directly suppress osteoclast differentiation in vitro, potentially protecting against bone loss, while other studies link Th1-biased responses to increased inflammatory bone resorption. The net effect depends on the balance between antimicrobial defense, inflammatory amplification, and regulation of bone remodeling.

A parallel player, the cytokine IL-18, adds another layer to the Th1 story. Originally identified as an IFNγ-inducing factor, IL-18 is consistently elevated in the serum, saliva, and gingival crevicular fluid of periodontitis patients. It acts synergistically with IL-12 to sustain IFNγ production, and it may also directly participate in tissue destruction: IL-18 reportedly stimulates the activation of matrix metalloproteinases, enzymes that degrade the extracellular matrix, driving inflammatory bone loss after oral infection with P. gingivalis. The IL-18–Th1 axis, the review suggests, may be an important immunological link connecting adaptive immunity to alveolar bone destruction.

On the regulatory side, Th2 cells — defined by the transcription factor GATA3 and secretion of IL-4 and IL-13 — appear to restrain rather than fuel the disease. IL-4 can inhibit expression of key pro-inflammatory cytokines including IL-1, TNFα, and IL-6, and concentrations of IL-4 in gingival crevicular fluid are notably lower at periodontitis sites than in healthy gingiva, suggesting an association with inflammation resolution. IL-13, meanwhile, can upregulate transforming growth factor-β and downregulate the collagen-degrading enzyme MMP1 in gingival fibroblasts. The alarmin IL-33, released from gingival epithelial cells, further shapes a Th2-skewed microenvironment — though it too is double-edged, with some studies showing it can amplify early inflammatory responses and exacerbate bone loss depending on whether it is released in controlled or necrotic contexts.

The most dramatic character in this story, however, is the Th17 cell. Defined by the master transcription factor RORγt and production of IL-17A, IL-17F, IL-21, and IL-22, Th17 cells have been established as central pathogenic drivers of inflammatory bone loss. Elevated levels of RORC2 and IL-17A are documented in periodontal lesions, localized within the lamina propria, and their expression positively correlates with clinical attachment loss and bone destruction. Mechanistically, IL-17 acts on osteoblasts and periodontal ligament cells to upregulate RANKL — the key osteoclast-promoting signal — while downregulating its decoy receptor osteoprotegerin, tipping the RANKL–OPG balance toward resorption. IL-17 also recruits neutrophils via chemokines such as CXCL1 and CXCL2, and excessive neutrophil accumulation produces matrix metalloproteinases, reactive oxygen species, and neutrophil extracellular traps that compound tissue breakdown. The cytokine IL-23, produced in response to dysbiotic microbial stimulation, is critical for stabilizing and amplifying these pathogenic Th17 responses. Yet even IL-17 is not simply villainous: at controlled physiological levels it maintains mucosal barrier homeostasis and clears extracellular microbes without destructive inflammation.

The review’s most striking claim concerns what happens when the system’s own brakes fail. Treg cells, characterized by Foxp3 expression, are supposed to suppress excessive inflammation through TGFβ, IL-10, and IL-35, restraining Th1, Th17, and B cell responses and shifting the RANKL–OPG balance toward a bone-protective state. Experimental models support this: expanding or transferring Treg cells reduces inflammatory cytokine production and alveolar bone loss, while depleting them worsens disease. But under chronic inflammatory conditions, Treg cells undergo functional instability. Persistent IL-6–STAT3 signaling destabilizes Foxp3 expression by altering methylation of the TSDR regulatory region, predisposing Treg cells to convert into IL-17-producing ex-Treg cells. These hybrid populations — IL-17+ Tregs and Foxp3+ Th17 cells — display markedly enhanced osteoclastogenic potential compared with conventional Th17 cells and are implicated as key contributors to pathological bone resorption. In other words, the immune system’s peacekeepers are being conscripted into the destruction they were meant to prevent.

Adding a further dimension, recent spatial transcriptomic and single-cell studies reveal that the periodontal immune landscape is highly organized. Periodontitis lesions contain immune cell aggregates resembling tertiary lymphoid structures — localized hubs that sustain antigen presentation, T cell activation, and B cell maturation directly within chronically inflamed gingival tissue. The close spatial proximity of antigen-presenting cells, T helper cells, and B cell-rich compartments may facilitate sustained exposure to IL-6 and IL-23, promoting Th17 expansion and Treg instability while stabilizing chronic inflammatory circuits that resist systemic immune regulation. Along the Th17–Tfh axis, Th17 cells can even acquire T follicular helper-like features during chronic inflammation, reshaping local humoral responses, though the functional consequences remain incompletely understood.

The therapeutic implications are profound. If periodontitis reflects immune imbalance and phenotypic instability rather than the dominance of a single lineage, then selectively suppressing individual cytokines or discrete T cell subsets may be insufficient as long as the underlying dysregulation persists. The review argues that future interventions should instead reinforce regulatory stability, preserve protective T cell phenotypes, and restore a balanced cytokine environment supporting controlled host–microbe equilibrium. Emerging subsets such as Th9 and Th22 cells — whose contributions remain largely correlative and require loss-of-function studies to resolve — may offer additional targets. Ultimately, the authors contend, understanding T cell plasticity and immune adaptation within the periodontal microenvironment will be essential for designing next-generation precision host-modulatory therapies: treatments that restore durable immune homeostasis, prevent pathological osteoclastogenesis, and protect the bone that anchors our teeth — all without compromising the antimicrobial defenses we cannot afford to lose.

Subject of Research: T helper cell plasticity and Th17–Treg instability in the immunopathogenesis of periodontitis

Article Title: The dynamic landscape of T helper cell plasticity and Th17–Treg instability in periodontitis

Article References: Lim, Y.-J., & Kim, T. S. (2026). The dynamic landscape of T helper cell plasticity and Th17–Treg instability in periodontitis. Experimental & Molecular Medicine. https://doi.org/10.1038/s12276-026-01847-4

Image Credits: AI Generated

DOI: 10.1038/s12276-026-01847-4

Keywords: periodontitis, T helper cells, Th17, Treg cells, immune plasticity, IL-17, IL-23, osteoclastogenesis, alveolar bone loss, Foxp3, oral mucosal immunity, cytokines

The research focuses on a family of CD4-positive helper T cells known as Th17 cells, which have occupied an ambiguous position in cystic fibrosis immunology for over a decade. Elevated levels of interleukin-17, the signature cytokine of this lineage, were initially interpreted as a hallmark of pathology, since IL-17 drives neutrophil recruitment and tissue-destructive inflammation. Later work complicated that picture by showing that Th17 cells are functionally heterogeneous. Conventional Th17 cells, which co-produce IL-17 alongside the anti-inflammatory cytokine IL-10 and the epithelial-supporting IL-22, actually promote mucosal homeostasis and barrier integrity. By contrast, a distinct pro-inflammatory population, termed Th1/17 for its co-expression of interferon-gamma and IL-17 in the absence of IL-10, has been implicated in chronic inflammatory diseases ranging from multiple sclerosis to Crohn’s disease. Which of these faces Th17 presents in the cystic fibrosis lung remained an open question.

To resolve it, the team analysed T cells isolated from explanted lungs and blood of people with cystic fibrosis, alongside non-CF lung tissue and healthy donor blood. Using high-dimensional flow cytometry and unsupervised clustering based on chemokine receptor expression, they identified two pathogenic subsets, CCR5-positive Th1/17 cells and pro-inflammatory CCR5-positive Th17 cells, that were markedly enriched in cystic fibrosis lungs compared with both patient blood and non-CF lungs. Critically, this enrichment was not a general feature of the disease. The pathogenic subsets expanded selectively in lungs chronically colonized by Pseudomonas aeruginosa, irrespective of whether other pathogens such as Staphylococcus aureus were also present. In Pseudomonas-negative patients, protective conventional Th17 cells predominated instead, pointing to the bacterium itself as the upstream driver of the pathological shift.

The functional consequences of this shift were striking. In an air-liquid interface model of primary human bronchial epithelium, a laboratory system that recapitulates the differentiated, ciliated airway lining, activated Th1/17 and pro-inflammatory Th17 cells caused extensive disruption of epithelial integrity. Immunofluorescence staining for zonula occludens-1, a core component of tight junctions, revealed discontinuous, fragmented junctional patterns in cultures exposed to these subsets, while conventional Th17 cells left the barrier largely intact. Quantitative artificial intelligence-assisted image analysis confirmed the selective loss of junctional continuity. The pathogenic subsets also provoked a significantly stronger inflammatory response from epithelial cells, which released elevated amounts of cytokines and chemokines including IL-8, IL-6, CCL20 and RANTES, molecules that in turn recruit further immune cells to the airway wall.

Transcriptomic profiling by RNA sequencing deepened the picture. Pulmonary Th1/17 and pro-inflammatory Th17 cells from Pseudomonas-infected cystic fibrosis lungs displayed a distinctive signature of 210 upregulated and 40 downregulated genes compared with the same subsets in blood and non-CF lungs. Gene set enrichment analysis showed that lung-resident pathogenic cells upregulated 21 pathways linked to bacterial response, inflammation and tissue remodelling, with high-ranking genes including PPARG, CEBPD and IRAK2, transcriptional regulators known to shape Th17 differentiation and function. Peripheral counterparts of the same subsets showed a largely repressed programme, indicating that the lung environment itself actively reconfigures these cells rather than merely recruiting pre-formed effectors from the circulation.

T cell receptor sequencing added a crucial layer of evidence. The researchers found a significant expansion of private clonotypes, receptor sequences unique to individual patients, within cystic fibrosis lungs, accounting for 45.8 percent of the Th1/17 repertoire compared with roughly 22 percent in non-CF lungs. Among the most expanded clonotypes, some were shared between Th1/17 and pro-inflammatory Th17 cells but minimally represented in Th1 or conventional Th17 populations, suggesting a common antigenic experience driving functional convergence. Partial overlap between the receptor repertoires of pathogenic subsets and conventional Th17 cells, but not Th1 cells, provided a molecular fingerprint of lineage relationships that the team then tested experimentally.

That experimental work centred on dendritic cells, the antigen-presenting sentinels that instruct T cell fate. The team exposed human monocyte-derived dendritic cells to 26 clinical Pseudomonas aeruginosa strains isolated longitudinally from Danish cystic fibrosis patients, spanning early isolates taken at disease onset and late isolates collected after years of chronic colonization. Late strains were internalized more efficiently and persisted longer inside dendritic cells than the reference laboratory strain PAO1. More importantly, clinical isolates skewed the dendritic cell cytokine output toward a polarizing cocktail of IL-1β and IL-23, the two cytokines known to drive interferon-gamma-producing Th17 differentiation, while relatively suppressing IL-12, the canonical Th1-polarizing signal. IL-1β secretion correlated with intracellular bacterial persistence, and clinical strains also triggered strong release of CCL20, the chemokine that recruits CCR6-positive Th17 cells to sites of infection.

In antigen-specific co-culture assays, the researchers then demonstrated that conventional Th17 cells, not Th1 cells, are the precursors of the pathogenic populations. After ten days of co-culture with Pseudomonas-infected dendritic cells, sorted conventional Th17 cells acquired robust interferon-gamma and IL-17 co-expression, whereas Th1 cells never converted. Unexpectedly, early clinical isolates lacking the classic adaptations of chronic infection, such as reduced motility and biofilm formation, were at least as effective as late isolates at inducing this conversion, and some strains exceeded the levels seen with PAO1. The reprogramming extended to transcription factors: converted cells upregulated C/EBPδ and PPARγ, and in some cases BATF3, mirroring the profile of lung-resident pathogenic Th17 cells from patients. This indicates that the immunostimulatory virulence determinants responsible are present from the earliest stages of colonization and retained throughout bacterial adaptation to the cystic fibrosis lung.

The study thereby rewrites a long-standing paradigm. Adaptive immune dysfunction in cystic fibrosis was widely assumed to emerge only in late-stage disease, but the new data show that Pseudomonas aeruginosa can corrupt protective Th17 immunity from the moment it establishes infection, creating a self-sustaining immunopathological loop in which reprogrammed T cells damage the epithelium, epithelial cells release chemokines that recruit more Th17 cells, and the resulting inflammation further impairs bacterial clearance. The findings carry direct therapeutic implications. IL-1 receptor blockade with anakinra has already been shown to mitigate Pseudomonas-driven airway inflammation in cystic fibrosis, and IL-23 inhibitors are clinically established in other chronic inflammatory diseases, although safety concerns about prolonged IL-1β blockade and the need to preserve protective mucosal immunity remain. The authors caution that their lung cohort reflects advanced disease and that the specific bacterial or host antigens driving the T cell skewing are still unknown. Even so, selectively depleting Th1/17 and pro-inflammatory Th17 cells, or blocking their generation from conventional Th17 precursors, now stands as a credible precision immunomodulatory strategy, one that could address the inflammation that persists even in patients receiving CFTR modulator therapy.

Subject of Research: Pseudomonas aeruginosa-driven reprogramming of Th17 cells in cystic fibrosis lung immunopathology

Article Title: Pseudomonas aeruginosa induces the generation of pathogenic IFNγ+Th17 cells that promote lung damage and chronic inflammation in cystic fibrosis

Article References: Dusetti, I., Conte, G., Chiara, M., Puccio, S., Guidone, D., Ricciardelli, E., Cibella, J., Ronzio, M., Dolfini, D., Rossi, E., Landini, P., Ascagni, M., Orlandi, R., Damarco, F., Palleschi, A., Gramegna, A., Blasi, F., Lugli, E., Galietta, L. J., … Paroni, M. (2026). Pseudomonas aeruginosa induces the generation of pathogenic IFNγ+Th17 cells that promote lung damage and chronic inflammation in cystic fibrosis. Nature Microbiology. https://doi.org/10.1038/s41564-026-02469-2

Image Credits: AI Generated

DOI: 10.1038/s41564-026-02469-2

Keywords: cystic fibrosis, Pseudomonas aeruginosa, Th17 cells, interferon-gamma, dendritic cells, IL-23, IL-1β, epithelial barrier, T cell receptor, mucosal immunity, chronic inflammation, immunotherapy

The first node is the intestinal epithelium, the single-cell-thick lining that decides what passes from the gut lumen into the body. Its integrity depends on tight junctions built from proteins such as claudins and occludins, on a protective mucus layer, and on antimicrobial peptides secreted into the lumen. In Crohn’s disease, disruption of these tight junctions produces the phenomenon known as leaky gut: paracellular leakage that allows microbial antigens to cross into the lamina propria, where they encounter the immune system. Pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 can worsen the damage, and a decline in Wnt/beta-catenin signaling, a pathway essential for epithelial proliferation and differentiation, may impair mucus synthesis and tissue repair. The result is a barrier that fails precisely when the tissue needs regeneration most.

The review emphasizes that epithelial cells are not passive bricks in a wall. They actively participate in immune surveillance, secreting cytokines and chemokines such as interleukin-8 that recruit neutrophils to inflammatory sites. When pathobionts such as adherent-invasive Escherichia coli remodel this crosstalk, the recruitment and activation of immune cells becomes distorted, protective pathogen-clearance responses falter, and inflammation deepens. Meanwhile, intracellular signaling systems including NF-kappaB, Notch and PI3K/Akt govern how epithelial cells proliferate, differentiate and respond to stress; NF-kappaB activation during inflammatory interactions can remodel cytokine production and downregulate tight-junction expression, compounding the very barrier defect that triggered it.

The second node is the immune system. In Crohn’s disease, the balance between pro-inflammatory cytokines such as TNF-alpha and interleukin-6 and anti-inflammatory mediators such as interleukin-10 and transforming growth factor-beta tips sharply toward inflammation. T helper 17 cells expand, interleukin-17 mediates tissue injury, and regulatory T cells, the custodians of immune tolerance, lose ground. Chemokines such as CCL2 and CXCL10, which normally direct monocytes and T cells to sites of infection, instead orchestrate a chronic influx of activated immune cells into the gut wall. The review stresses that restoring inflammatory balance without disabling the immune system’s ability to fight infection remains one of the central therapeutic challenges in the field.

The third node is the gut microbiota. In Crohn’s disease, microbial diversity falls, beneficial short-chain fatty acid-producing members of the phylum Firmicutes are depleted, and potential pathobionts, most notably adherent-invasive E. coli, expand. This matters because microbial metabolites are among the most important chemical messengers between the microbiota and the host. Short-chain fatty acids such as acetate, propionate and butyrate, produced by the fermentation of dietary fiber, serve as the primary energy source for colonic epithelial cells, upregulate tight-junction expression, and promote the differentiation of regulatory T cells while suppressing pro-inflammatory Th17 responses through histone deacetylase-dependent mechanisms. When butyrate-producing taxa vanish, the epithelium loses fuel, the immune system loses a brake, and tolerance gives way to activation.

The heart of the review is its description of three positive feedback loops that weld these nodes together. In the IL-23/Th17 axis, interleukin-23 drives Th17 polarization, leading to interleukin-17 secretion, epithelial barrier disruption, microbial translocation and sustained IL-23 release. In the TNF-alpha-driven pathway, TNF-alpha disrupts epithelial tight junctions, enabling pathobiont translocation, TLR4/NF-kappaB activation and amplified TNF-alpha production. In the SCFA depletion cycle, reduced short-chain fatty acid levels impair regulatory T cell differentiation, promoting Th17 dominance, inflammation and further depletion of the very microbes that produce these metabolites. Each loop can, in principle, start anywhere, and once running, any one of them can keep the others alive.

This circuit model carries a pointed therapeutic implication: single-pathway drugs can be highly effective in selected patients, yet persistent activity in other compartments of the circuit may explain why some responses are incomplete or not durable. The clinical evidence reviewed supports this reading. The IL-23 inhibitor risankizumab produced greater endoscopic response than placebo at week 52 in patients with moderate-to-severe Crohn’s disease, including those who had failed anti-TNF therapy, with a relative risk of 3.40 in the ADVANCE/CD-101 program. The oral JAK1 inhibitor upadacitinib demonstrated efficacy for both induction and maintenance in phase 3 trials. For perianal fistulizing disease, darvadstrocel, an adipose-derived stromal-cell therapy, achieved fistula resolution in 56 percent of patients at 24 weeks in the ADMIRE-CD II trial and has been authorized in the European Union and Japan.

Non-drug strategies fit the same framework. The Crohn’s Disease Exclusion Diet, which removes specific food components, has shown efficacy for inducing and sustaining remission in randomized trials of patients with mild-to-moderate disease over 12 to 24 weeks, plausibly by reshaping the microbial and metabolic arm of the circuit. Fiber-rich diets that promote Bifidobacterium and Lactobacillus, SCFA supplementation, and probiotics targeting butyrate-producing taxa all aim to restore the microbial node. The review also flags a broader metabolic dimension: shared pathways involving dysbiosis, barrier impairment and chronic low-grade inflammation suggest that conditions such as Type 2 diabetes and metabolic syndrome should be viewed as potential modifiers of the epithelial-immune-microbiota axis rather than incidental comorbidities.

The framework is explicitly hypothesis-generating rather than a clinical guideline, and the authors are candid about its limits. Animal models such as TNF-delta-ARE mice and AIEC-colonized rodents capture fragments of the disease but none reproduces the full polygenic susceptibility, transmural inflammation and relapsing course seen in patients. A long-standing controversy remains over whether dysbiosis is a primary cause or a secondary consequence of inflammation; the review’s integrative position is that dysbiosis may act as a primary driver in young-onset or treatment-naive disease while functioning mainly as a disease-perpetuating amplifier once inflammation has established a permissive microbial niche. Environmental factors, including high-fat diets and psychological stress, can push the network in either direction by reshaping microbial composition and mucosal immune competence.

Where the framework becomes actionable is in measurement and stratification. Each node of the circuit can be paired with observable indicators: intestinal permeability markers, endoscopic and transmural healing, fecal calprotectin, cytokine profiles, microbial diversity, pathobiont enrichment and metabolite levels. Longitudinal profiling of these measures could, in principle, sort patients into barrier-dominant, immune-dominant, microbiota-dominant or mixed phenotypes, each pointing toward a different therapeutic priority. Multi-omics platforms combining shotgun metagenomics, metabolomics and proteomics, together with machine-learning models such as those predicting endoscopic response to ustekinumab from genomic and transcriptomic data, and AI-assisted endoscopy systems like EndoBrain and CAD-EYE, are already moving in this direction, though the authors caution that most current biomarkers capture only one dimension of disease biology and that cross-sectional observations cannot reliably distinguish primary drivers from secondary consequences. The STRIDE-II treat-to-target recommendations, which emphasize endoscopic healing and, in selected settings, transmural assessment by intestinal ultrasound or MRI, provide the monitoring backbone. What remains to be proven, through longitudinal validation and controlled trials, is whether treatments chosen by mechanism rather than by convention genuinely deliver more durable mucosal healing, lower relapse risk and better lives for people with Crohn’s disease.

Subject of Research: The interplay of epithelial barrier dysfunction, immune dysregulation and gut microbiota dysbiosis in Crohn's disease pathogenesis and therapy

Article Title: Tripartite Interplay of Epithelial, Immune, and Microbiota Dysregulation in Crohn's Disease: Mechanisms and Translational Strategies

Article References: Lai, Q., Zhang, Q.-Y., Yang, W.-P., & Luo, C.-Y. (2026). Tripartite Interplay of Epithelial, Immune, and Microbiota Dysregulation in Crohn's Disease: Mechanisms and Translational Strategies. Immunity, Inflammation and Disease, 14(10), Article e70538. https://doi.org/10.1002/iid3.70538

Image Credits: AI Generated

DOI: 10.1002/iid3.70538

Keywords: Crohn's disease, intestinal epithelial barrier, gut microbiota, Th17 cells, IL-23, TNF-alpha, short-chain fatty acids, AIEC, JAK inhibitors, risankizumab, dysbiosis, precision medicine

Non-tuberculous mycobacteria, often abbreviated NTM, are environmental organisms that increasingly cause chronic and debilitating lung disease worldwide. Among them, Mycobacterium abscessus stands out as particularly menacing. It is naturally resistant to many standard antibiotics, it can form ropelike cords that shield it from engulfment by immune cells, and it thrives in patients with pre-existing lung damage such as bronchiectasis, cystic fibrosis, or pulmonary fibrosis. Treatment regimens typically stretch for many months, involve multiple toxic drugs, and frequently fail to eradicate the infection. Against this grim clinical backdrop, the question of how the immune system naturally fights M. abscessus has remained surprisingly underexplored, particularly with respect to γδ T cells, an unconventional lymphocyte population whose role in NTM infection had never been systematically characterized.

γδ T cells differ from the conventional αβ T cells that dominate textbook immunology. Rather than recognizing peptide fragments presented by major histocompatibility molecules, they respond rapidly to a wide range of stress signals and microbial products, earning them a reputation as a bridge between innate and adaptive immunity. A major subset of these cells produces interleukin-17A, a powerful inflammatory cytokine best known for recruiting neutrophils and shaping defenses at body surfaces. To determine whether these cells matter in M. abscessus infection, the researchers built a mouse model of pulmonary infection and mapped the immune landscape of lung tissue over the early days of disease using single-cell RNA sequencing, a technique that captures the gene expression profile of thousands of individual cells simultaneously.

The single-cell atlas revealed a striking pattern. As infection took hold, γδ T cells accumulated in the lung and expanded a population that expressed high levels of IL-17A. When the team removed γδ T cells entirely, using mice genetically engineered to lack them, the consequences were dramatic: bacteria persisted at far higher levels in the lungs and spleens, and lung inflammation worsened. Conversely, when γδ T cells were depleted in animals that had already cleared a first infection and were then re-challenged, the protective advantage of prior exposure evaporated. These experiments established γδ T cells as indispensable players in the early defense against M. abscessus, a finding that had not been demonstrated before for any non-tuberculous mycobacterial pathogen.

Delving deeper, the investigators identified IL-17A itself as the linchpin of this protective response. Mice unable to produce IL-17A lost much of their capacity to control the infection, and importantly, the defect traced back to the γδ T cells themselves. Without IL-17A signaling, the cells became less adept at recognizing the bacterium and lost much of their cytotoxic firepower. In an elegant series of transfer experiments, IL-17A-deficient γδ T cells failed to protect infected animals, whereas their normal counterparts succeeded. This revealed something unusual: IL-17A was not merely acting as a broadcast signal to other immune players but was required within the γδ T cells themselves, a cell-intrinsic requirement that underscores how tightly the cytokine and its producer are wired together during this infection.

The mechanism by which these cells actually kill the bacterium proved to be equally instructive. M. abscessus is an extracellular pathogen during key phases of infection, residing outside host cells in the airways and tissue spaces. The researchers found that IL-17A-positive γδ T cells eliminated extracellular bacteria through a granzyme B-dependent cytotoxic pathway. Granzyme B is a serine protease classically associated with the destruction of virus-infected or malignant cells, delivered through pore-forming perforin or other release mechanisms. Its deployment against free-living bacteria adds a new dimension to the antimicrobial portfolio of γδ T cells and explains how a lymphocyte population usually discussed in the context of autoimmunity and inflammation can act as a direct bactericidal weapon.

How, then, does the immune system know to mobilize these cells in the first place? The answer lies in a cascade that begins with Toll-like receptor 2, a pattern-recognition receptor on macrophages that detects components of the bacterial cell wall. When M. abscessus engaged TLR2 on lung macrophages, the macrophages responded by secreting two cytokines, interleukin-1β and interleukin-23. This cytokine pair is a well-known stimulus for IL-17 production in T cells, and in this context it drove both the expansion and the activation of the IL-17A-positive γδ T cell population. Blocking either IL-1β or IL-23 in infected mice diminished the γδ T cell response and impaired bacterial control, mapping out a complete signaling axis that runs from bacterial recognition through macrophage activation to lymphocyte mobilization and, ultimately, bacterial killing.

Perhaps the most clinically resonant aspect of the study concerns patients whose immunity depends on interferon-gamma, the canonical cytokine for defense against mycobacteria. A subset of individuals, particularly in Southeast Asia, develops autoantibodies that neutralize their own interferon-gamma, leaving them exquisitely vulnerable to disseminated NTM infections. Using single-cell RNA sequencing of peripheral blood cells from NTM patients, the researchers found evidence that anti-interferon-gamma autoantibodies compromise γδ T cell function in humans, mirroring what they observed in mice lacking the interferon-gamma receptor. Crucially, in mice engineered without functional interferon-gamma signaling, IL-17A-positive γδ T cells still conferred protection, and the same held true in a model combining M. abscessus infection with bleomycin-induced pulmonary fibrosis. In other words, this arm of immunity operates independently of the interferon-gamma axis and remains effective even in scarred, damaged lungs.

The implications for therapy are considerable. Current treatment of NTM disease relies almost entirely on antibiotics that the pathogen is adept at resisting, and there are no licensed immunotherapies that bolster host defenses. If the pathways defined in this study can be harnessed in patients, whether by stimulating IL-1β and IL-23 signaling, expanding protective γδ T cell populations, or delivering IL-17A-driven cytotoxic activity directly, clinicians could gain a means of strengthening the lung’s own antimicrobial machinery. Such approaches would be especially valuable for the growing population of patients with anti-interferon-gamma autoantibodies or structural lung disease, for whom conventional regimens offer diminishing returns. The researchers caution that translating mouse findings to the clinic will require careful work, particularly because IL-17A is also implicated in inflammatory conditions such as psoriasis and could carry safety risks if induced systemically. Nevertheless, the identification of a concrete, mechanistically defined cell type that can clear M. abscessus marks a genuine advance. It transforms γδ T cells from immunological bystanders into a promising therapeutic target, and it reframes the fight against antibiotic-resistant mycobacteria as a battle that the immune system, with the right encouragement, may be able to win on its own terms.

Subject of Research: The role of IL-17A-producing γδ T cells in controlling pulmonary Mycobacterium abscessus infection in mice.

Article Title: IL-17A-producing γδ T cells control pulmonary Mycobacterium abscessus infection in mice

Article References: Hu, X., Lin, S., Meng, W., Liu, H., Qin, Z., Wu, Z., Wan, Y., Ma, S., Yang, X., Yin, Z., Chu, Y., Zhang, W., Shao, L., & Lin, Y. (2026). IL-17A-producing γδ T cells control pulmonary Mycobacterium abscessus infection in mice. Nature Microbiology. https://doi.org/10.1038/s41564-026-02466-5

Image Credits: AI Generated

DOI: 10.1038/s41564-026-02466-5

Keywords: Mycobacterium abscessus, non-tuberculous mycobacteria, γδ T cells, IL-17A, interferon-gamma, granzyme B, TLR2, IL-1β, IL-23, pulmonary infection, immunology, antibiotic resistance