Latest publication

Am J Physiol Gastrointest Liver Physiol. 2026 Feb 12. doi: 10.1152/ajpgi.00447.2025. Online ahead of print.

ABSTRACT

The intestinal epithelium is a key component of the intestinal barrier, which is the largest and most complex barrier of the human body, regulating nutrients absorption while restricting the entry of harmful antigens. Breakdown of this barrier facilitates microbial and dietary antigenic translocation, triggering local immune system activation and inflammation. Although barrier alterations alone may not be sufficient to initiate disease, accumulating evidence highlights its critical role in the pathogenesis and progression of a wide range of gastrointestinal and systemic disorders. Early identification of intestinal epithelium and barrier alterations could enable timely therapeutic approaches. This systematic review provides an overview of current in vivo (both non-invasive and invasive) and ex vivo/in vitro approaches used to assess intestinal epithelial barrier alterations. Non-invasive in vivo approaches rely mainly on urinary detection of orally ingested probes, but their clinical utility is limited by lack of standardization and specificity. Circulating and fecal constitutive markers derived from the intestinal barrier, which reflect epithelial alterations, together with indicators of microbial translocation, provide complementary insights but remain insufficiently validated. Advanced invasive endoscopic modalities such as confocal laser endomicroscopy enable near-histologic, real-time visualization but are costly and largely used as research tools in specialist centers. In vitro, transepithelial electrical resistance assessment remains the reference standard, though novel technologies (including impedance spectroscopy and organic electrochemical transistors) offer enhanced sensitivity and resolution. Despite progress, major gaps remain, including the absence of a standardized definition of epithelial barrier breakdown, the lack of a practical diagnostic tool, methodological heterogeneity, unvalidated thresholds, and limited prospective validation.

PMID:41677575 | DOI:10.1152/ajpgi.00447.2025

Nat Commun. 2026 Feb 3;17(1):714. doi: 10.1038/s41467-025-68264-5.

ABSTRACT

In Juvenile Idiopathic Arthritis (JIA), the most common childhood rheumatic disease, many patients also develop uveitis (JIA-uveitis), risking life-long vision loss. The mechanisms driving uveitis development in JIA remain understudied. Here, we demonstrate that peripheral blood CD19+IgD-CD27- double negative type 1 (DN1) B cells are elevated in JIA-uveitis compared to JIA patients without eye disease (JIA). The B cell receptor (BCR) repertoire was also more clonal and somatically hypermutated in JIA-uveitis and antigen-activated B cells infiltrated chronically inflamed JIA-uveitis eyes. Features of heightened B cell activation were recapitulated in experimental autoimmune uveoretinitis (EAU) and disrupting B and T cell interactions using monoclonal antibodies and transgenic mice suppresses uveitis. Together, these findings support a conceptual shift that uveitis is a primarily T cell driven disease and provide evidence for potential new therapeutic strategies that also consider B cells as drivers in disease pathology.

PMID:41633998 | DOI:10.1038/s41467-025-68264-5

bioRxiv [Preprint]. 2026 Jan 10:2022.10.19.512842. doi: 10.1101/2022.10.19.512842.

ABSTRACT

Innate lymphoid cells (ILCs) are rare, tissue-resident innate lymphocytes that functionally mirror CD4+ T helper cell lineages but lack antigen receptors. Type 3 ILCs (ILC3s) are enriched in the gut, airways, and mucosal lymphoid tissues, where they regulate inflammation and promote barrier integrity. To define the regulatory architecture of primary human ILC3s, we map promoter-anchored chromosomal contacts using high-resolution, low-input Promoter Capture Hi-C (PCHi-C) in these cells alongside CD4+ T cells. By combining statistical detection with a PCHi-C-adapted Activity-by-Contact approach, we link promoters to distal regulatory elements, identifying hundreds of ILC3-specific contacts. We use these maps to connect genome-wide association study (GWAS) risk variants for Crohn's disease to target genes using multiCOGS, a Bayesian framework that integrates PCHi-C with summary-statistic imputation and multivariate fine-mapping. This analysis highlights both known and unanticipated candidates, including CLN3, a causal gene for the neurodevelopmental Batten disease. Using a mouse ILC3-like cell line, we show that Cln3 is downregulated upon cytokine stimulation, and Cln3 overexpression alters stimulation-induced transcriptional programmes and cytokine secretion. Extending this approach, we generate a catalogue of ILC3-linked risk genes for five additional autoimmune conditions and show that they are enriched for regulators of the ILC3 inflammatory response identified in a CRISPR interference screen. Together, these findings illuminate long-range gene control in ILC3s and prioritise known and newly implicated autoimmune risk genes with potential roles in this clinically important cell type.

PMID:41573945 | PMC:PMC12821085 | DOI:10.1101/2022.10.19.512842

Nat Commun. 2026 Jan 20;17(1):482. doi: 10.1038/s41467-026-68335-1.

ABSTRACT

The 2022 multi-country mpox (formerly monkeypox) outbreak, driven by mpox virus (MPXV) Clade IIb poses renewed threat to global public health. The cessation of smallpox vaccination has created large immunologically naïve cohorts, with uncertain implications for contemporary MPXV susceptibility. To assess whether residual vaccination-derived immunity influences exposure risk, we combine serological and phylodynamic analyses. Using a six-plex Luminex assay, we measure immunoglobulin G (IgG) binding to six MPXV antigens in 176 Nigerian adults comprising of 75 healthcare workers sampled in 2021 and 101 community volunteers sampled in 2023. At baseline, 24/176 (13.6%) were MPXV seropositive, predominantly born before 1980. Magnitude-breadth analysis scores were two-fold higher in pre-1980 cohort relative to post-1980 cohort. In 153 participants with follow-up samples (median 9 months), 5/153 (3%) showed evidence of exposure, with ≥2-fold increases in magnitude-breadth scores and antigen-specific responses against ≥4/6 antigens without reported clinical illness. Antigen-specific responses were strongest to B6R (11-fold), followed by M1R and A35R, with marked individual-level heterogeneity. Complementary phylodynamic reconstruction of 105 Nigerian MPXV genomes identified sporadic transmission against frequent dead-end infections. Together, these data show that residual smallpox immunity continues to shape mpox transmission and asymptomatic exposure contributes to under-detected spread, informing surveillance and targeted vaccination strategies.

PMID:41559051 | DOI:10.1038/s41467-026-68335-1

PLoS Pathog. 2026 Jan 16;22(1):e1013817. doi: 10.1371/journal.ppat.1013817. Online ahead of print.

ABSTRACT

Chronic HIV infection drives B cell dysfunction associated with the accumulation of tissue-like memory (TLMs) and activated memory B cells (MBCs) but decline in resting memory B cells. TLMs express multiple inhibitory receptors and lack response to soluble antigens. However, their origin and the mechanisms driving their expansion in HIV infection remain unclear. From bulk heavy chain BCR sequencing of MBC subsets from 5 PLWH with no detectable viremia, we hypothesized that TLMs (CD21- CD27- B cells) were significantly less mutated but also less diverse than other MBCs, suggesting an enrichment for innate-like B cells or that they belong to a less mature subset. Subsequent detailed multi-omics study of an immune response to a transient HIV viremia in an elite controller demonstrated a functional increase in Env-reactive IgG and MBCs with non-TLM phenotype. Single-cell RNA/BCR sequencing of PBMCs enriched for B cells revealed an orchestrated TNF-α response followed by interferon-α and -γresponses across all B cell subsets. This study provides new insights into multifaceted functional B cell response to transient HIV viremia and highlights TLM heterogeneity.

PMID:41544177 | DOI:10.1371/journal.ppat.1013817

Front Immunol. 2025 Dec 16;16:1707749. doi: 10.3389/fimmu.2025.1707749. eCollection 2025.

ABSTRACT

BACKGROUND: Schistosomiasis is caused by parasitic blood flukes of the genus Schistosoma. Despite ongoing mass drug administration efforts, the disease remains a major public health burden in endemic regions. A better understanding of early host responses to schistosomiasis is critical for developing effective vaccines and therapeutics.

METHODS: We conducted a longitudinal transcriptomic study of peripheral blood samples from 30 Schistosoma-naïve volunteers participating in two controlled human infection trials with male- or female-only S. mansoni cercariae. Blood was collected at six time points over 20 weeks post-infection. Whole-transcriptome RNA sequencing and integrative analyses, including differential gene expression, gene set enrichment, protein interaction networks, co-expression clustering, and immune module profiling, were employed to characterize temporal modulation of genes related to immune responses.

RESULTS: Robust and highly time-dependent transcriptional responses were observed, peaking at Week 4 post-infection. Differential gene expression and pathway analyses revealed activation of immune responses, including type I and II interferon signaling, chemokine-mediated pathways, and antigen presentation. Notably, both Th1 and Th2 signatures were evident at Week 4. Key immune hubs included IFNG, TNF, and IL1B, along with transcriptional regulators such as STAT1 and IRF7. Blood transcription module analysis further highlighted transient activation of interferon and plasma cell-related responses.

CONCLUSIONS: This study provides a comprehensive transcriptional map of early host responses to S. mansoni infection in humans. The findings underscore the central role of interferon pathways, early mixed Th1/Th2 polarization, and inflammation-associated gene signatures in shaping host response to S. mansoni infection. These insights may inform the rational design of vaccines and biomarkers for schistosomiasis.

PMID:41476985 | PMC:PMC12748245 | DOI:10.3389/fimmu.2025.1707749

Clin Microbiol Infect. 2025 Dec 20:S1198-743X(25)00625-1. doi: 10.1016/j.cmi.2025.12.015. Online ahead of print.

ABSTRACT

OBJECTIVES: In sub-Saharan African children under-five, non-typhoidal Salmonella (NTS) frequently cause fatal bloodstream infections. Antimicrobial resistance and absence of antibiotic treatment efficacy data challenge effective treatment. In this prospective observational study, we provide treatment efficacy data of susceptibility-matched antibiotic regimens from the treatment of NTS bloodstream infections in children in Kisantu district hospital (DR Congo).

METHODS: Children (>28 days-<5 years) admitted with severe febrile illness were enrolled after blood culture sampling. Clinical and microbiological data of children with NTS bloodstream infection were collected in-hospital and at 1-month post-discharge.

RESULTS: NTS bloodstream infection was diagnosed in 12.7% (239/1867) of enrolled children. Extensive drug-resistance (concurrent ampicillin, cotrimoxazole, chloramphenicol, third generation cephalosporin and fluoroquinolone non-susceptibility) occurred in 60% (144/236), i.e. 69% (71/103) in O5-antigen positive Typhimurium, 85% (72/85) in O5-antigen negative Typhimurium but only 2% (1/48) in Enteritidis serovars. Only 64% (146/228) of children received susceptibility-matched antibiotics and overall in-hospital case fatality was 25.1% (60/239). Compared to susceptibility-mismatched antibiotic treatment, susceptibility-matched third generation cephalosporin treatment on hospital day 0-1 had better 14-day in-hospital survival (hazard ratio at death (HRdeath): 0.37 [0.16-0.88]). Similarly, susceptibility-matched third generation cephalosporin, ciprofloxacin, or azithromycin treatment on hospital day 2-6 had better 28-day in-hospital survival (HRdeath: 0.21 [0.06-0.68], 0.15 [0.02-1.10] and 0.26 [0.08-0.84], respectively). After ≥5 days of susceptibility-matched antibiotics, NTS persisted in control blood cultures in 15% (13/88).

CONCLUSION: NTS bloodstream infections were often extensively drug-resistant, leading to susceptibility-mismatched antibiotic treatment. When NTS were susceptible, third generation cephalosporin, ciprofloxacin and azithromycin treatment appeared to be effective.

PMID:41429348 | DOI:10.1016/j.cmi.2025.12.015

PLoS Comput Biol. 2025 Dec 15;21(12):e1013799. doi: 10.1371/journal.pcbi.1013799. Online ahead of print.

ABSTRACT

The subcellular localisation of proteins is a key determinant of their function. High-throughput analyses of these localisations can be performed using mass spectrometry-based spatial proteomics, which enables us to examine the localisation and relocalisation of proteins. Furthermore, complementary data sources can provide additional sources of functional or localisation information. Examples include protein annotations and other high-throughput 'omic assays. Integrating these modalities can provide new insights as well as additional confidence in results, but existing approaches for integrative analyses of spatial proteomics datasets, such as concatenation-based methods and transfer learning approaches like KNN-TL, are limited in the types of data they can integrate and do not quantify uncertainty in their predictions. Here we propose a semi-supervised Bayesian approach (wherein model parameters are inferred from both labeled marker proteins and unlabeled data while quantifying prediction uncertainty) to integrate spatial proteomics datasets with other data sources, to improve the inference of protein sub-cellular localisation. We demonstrate our approach outperforms other transfer-learning methods and has greater flexibility in the data it can model - including categorical annotations (e.g., Gene Ontology terms), continuous measurements (e.g., protein abundance), and temporal profiles (e.g., time-series expression data). To demonstrate the flexibility of our approach, we apply our method to integrate spatial proteomics data generated for the parasite Toxoplasma gondii with time-series gene expression data generated over its cell cycle. Our findings suggest that proteins linked to invasion organelles are associated with expression programs that peak at the end of the first cell-cycle. Furthermore, this integrative analysis divides the dense granule proteins into heterogeneous populations suggestive of potentially different functions. Our method is disseminated via the mdir R package available on the lead author's Github.

PMID:41396985 | DOI:10.1371/journal.pcbi.1013799

Clin Rheumatol. 2025 Dec 11. doi: 10.1007/s10067-025-07845-7. Online ahead of print.

NO ABSTRACT

PMID:41379361 | DOI:10.1007/s10067-025-07845-7

Nat Immunol. 2025 Dec 1. doi: 10.1038/s41590-025-02380-8. Online ahead of print.

NO ABSTRACT

PMID:41326670 | DOI:10.1038/s41590-025-02380-8

J Gen Virol. 2025 Dec;106(12):002172. doi: 10.1099/jgv.0.002172.

ABSTRACT

After severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, a minority of patients experience persistent or emerging symptoms, termed 'long coronavirus disease (COVID)' or post-acute sequelae of COVID-19. The molecular causes of long COVID remain unclear, but disrupted immune functions, such as inflammation and immune deficit, have been posited as factors. In this retrospective cohort study, we measured markers of immune function in a group of patients with long COVID up to 40 months post infection. As proxies for immune function, we measured serum antibody levels, antibody neutralizing capability and production of IFN gamma (IFN-γ) and IL-2 against SARS-CoV-2 and other viral peptides. As expected, serum antibody levels increased over time with vaccinations and reinfections with later variants of SARS-CoV-2. Patients also showed corresponding increasing SARS-CoV-2-specific IL-2 responses and stable IFN-γ responses. We observed no significant differences in immune responses among patients with ongoing long COVID, those who had recovered from it or individuals who recovered from acute COVID-19. Overall, we found no indication of a reduction in these aspects of immune function after SARS-CoV-2 infection. This study provides a valuable foundation for further research aimed at understanding the causes of long COVID.

PMID:41324571 | PMC:PMC12668617 | DOI:10.1099/jgv.0.002172

Science. 2025 Nov 27;390(6776):eadq4691. doi: 10.1126/science.adq4691. Epub 2025 Nov 27.

ABSTRACT

Host body temperature can define a virus's replicative profile-influenza A viruses (IAVs) adapted to 40° to 42°C in birds are less temperature sensitive in vitro compared with human isolates adapted to 33° to 37°C. In this work, we show that avian-origin PB1 polymerase subunits enable IAV replication at elevated temperatures, including avian-origin PB1s from the 1918, 1957, and 1968 pandemic viruses. Using a model system to ensure biosafety, we show that a small increase in body temperature protects against severe disease in mice and that this protection is overcome by a febrile temperature-resistant PB1. These findings indicate that although elevated temperature itself can be a potent antiviral defense, it may not be effective against all influenza strains. These data inform both the clinical use of antipyretics and IAV surveillance efforts.

PMID:41308154 | DOI:10.1126/science.adq4691

Viruses. 2025 Oct 22;17(11):1405. doi: 10.3390/v17111405.

ABSTRACT

Early studies on the evolution of SARS-CoV-2 revealed mutations that favored host transmission of the virus and more efficient viral entry. However, cell-free virus spread is vulnerable to host-neutralizing antibodies. As population immunity developed, mutations that confer escape from neutralization were selected. Notably, cell syncytia formation wherein an infected cell fuses with a noninfected cell is a more efficient route of transmission that bypasses humoral immunity. Cell syncytia formation has been implicated in the pathogenicity of SARS-CoV-2 infection whilst compromising host transmission due to impaired whole virion release. Therefore, understanding the mechanisms of virus-mediated cell-cell fusion will aid in identifying and targeting more pathogenic strains of SARS-CoV-2. Whilst the general kinetics of cell-cell fusion have been known for decades, the specific mechanisms by which SARS-CoV-2 induces fusion are beginning to be elucidated. This is partially due to emergence of more reliable, high throughput methods of quantifying and comparing fusion efficiency in experimental models. Moreover, the ongoing inflammatory response and emerging health burden of long COVID may point to cell-cell fusion in the pathogenesis. In this review, we synthesize current understanding of SARS-CoV-2-mediated cell-cell fusion and its consequences on immune escape, viral persistence, and the innate immune response.

PMID:41305428 | DOI:10.3390/v17111405

Gastroenterology. 2025 Nov 26:S0016-5085(25)05987-6. doi: 10.1053/j.gastro.2025.08.040. Online ahead of print.

ABSTRACT

BACKGROUND & AIMS: Quantification of the human S100A8/S100A9 tetrameric protein complex in stool, referred to as fecal calprotectin, is an extensively validated biomarker supporting the diagnosis and management of gastrointestinal diseases. Here, we studied the quaternary protein structures (termed configuration) of S100A8 and S100A9 and their biological function in inflammatory bowel diseases (IBD).

METHODS: We dissected fecal S100A8 and S100A9 configurations in patients with IBD by size-exclusion chromatography coupled with tandem mass spectrometry and systematically defined human S100A8 and S100A9 homodimer functions compared with the calprotectin heterotetramer (CP) in the intestine of mice and in human epithelium and T cells. Moreover, we report a protein interaction network of fecal S100A8 and S100A9 in IBD.

RESULTS: Stool from patients with active IBD contained abundant S100A8 and S100A9 dimers besides CP. Fecal S100A9 detection associated with clinical and endoscopic disease activity in IBD patients with low CP concentration. Oral exposure to human recombinant S100A8 and S100A9 homodimers, but not to CP, worsened intestinal inflammation in toxic and genetic mouse models. Functional profiling revealed that human S100A8 and S100A9 homodimers enhanced activation of cluster of differentiation 4+ and 8+ T cells, which promoted experimental colitis. In turn, genetic inactivation of S100a9 protected against experimental enteritis and colitis, and pharmacologic inhibition of S100A9 ameliorated chronic colitis.

CONCLUSIONS: Collectively, this study links the detection of fecal S100A9 dimers with clinical and endoscopic disease activity in IBD and identifies inflammatory actions of S100A8 and S100A9 homodimers in the intestine. Our findings pave the way for novel diagnostic and therapeutic approaches in patients with inflammatory diseases of the intestine.

PMID:41295942 | DOI:10.1053/j.gastro.2025.08.040

STAR Protoc. 2025 Nov 20;6(4):104218. doi: 10.1016/j.xpro.2025.104218. Online ahead of print.

ABSTRACT

MDA5 is one of the primary eukaryotic innate immune sensors of viruses, recognizing long double-stranded RNA (dsRNA). Here, we present procedures for the recombinant expression and purification of murine MDA5 from E. coli. We describe the steps to purify MDA5 in high yields for downstream experiments and procedures to determine the ATPase activity and RNA-binding properties of purified MDA5. These approaches can be used to produce disease-associated mutants of MDA5, to uncover the biochemical mechanisms underpinning known disease phenotypes. For complete details on the use and execution of this protocol, please refer to Singh et al.1.

PMID:41269861 | DOI:10.1016/j.xpro.2025.104218

Nat Commun. 2025 Nov 20;16(1):10222. doi: 10.1038/s41467-025-65023-4.

ABSTRACT

Impaired mitochondrial bioenergetics in macrophages promotes hyperinflammatory cytokine responses, but whether inherited mtDNA mutations drive similar phenotypes is unknown. Here, we profiled macrophages harbouring a heteroplasmic mitochondrial tRNAAla mutation (m.5019A>G) to address this question. These macrophages exhibit combined respiratory chain defects, reduced oxidative phosphorylation, disrupted cristae architecture, and compensatory metabolic adaptations in central carbon metabolism. Upon inflammatory activation, m.5019A>G macrophages produce elevated type I interferon (IFN), while exhibiting reduced pro-inflammatory cytokines and oxylipins. Mechanistically, suppression of pro-IL-1β and COX2 requires autocrine IFN-β signalling. IFN-β induction is biphasic: an early TLR4-IRF3 driven phase, and a later response involving mitochondrial nucleic acids and the cGAS-STING pathway. In vivo, lipopolysaccharide (LPS) challenge of m.5019A>G mice results in elevated type I IFN signalling and exacerbated sickness behaviour. These findings reveal that a pathogenic mtDNA mutation promotes an imbalanced innate immune response, which has potential implications for the progression of pathology in mtDNA disease patients.

PMID:41266309 | DOI:10.1038/s41467-025-65023-4

Microb Genom. 2025 Nov;11(11). doi: 10.1099/mgen.0.001561.

ABSTRACT

Salmonella enterica serovar Paratyphi A is a significant but under-characterised cause of enteric fever in South Asia. In Pakistan, where the typhoid conjugate vaccine has been introduced to combat S. Typhi, S. Paratyphi A remains a prominent cause of bacteraemia, raising concerns about shifts in disease burden and antimicrobial resistance (AMR). Here, we provide a comprehensive genomic and phylogenetic analysis of 354 S. Paratyphi A isolates collected from three provinces in Pakistan between 2017 and early 2022. Whole-genome sequencing revealed the dominance of genotypes 2.3.3 and 2.4.5, indicating a largely stable population structure over time, and the presence of widespread fluoroquinolone-associated gyrA mutations. Although multidrug resistance was not detected, we identified one isolate harbouring an acrB-R717Q mutation associated with azithromycin resistance. Plasmid and replicon analysis revealed low prevalence of extrachromosomal elements, including cryptic plasmids with unknown function. Phylogenetic placement of these isolates in a global context demonstrated close relatedness to contemporary South Asian organisms. Our findings establish a genomic baseline for S. Paratyphi A in Pakistan, essential for future surveillance, AMR monitoring, and evaluating the potential impact of forthcoming paratyphoid vaccines.

PMID:41217957 | DOI:10.1099/mgen.0.001561

Nat Commun. 2025 Nov 3;16(1):9484. doi: 10.1038/s41467-025-65417-4.

ABSTRACT

α/β-hydrolase domain-containing protein 11 (ABHD11) is a mitochondrial hydrolase that maintains the catalytic function of α-ketoglutarate dehydrogenase (α-KGDH), and its expression in CD4 + T-cells has been linked to remission status in rheumatoid arthritis (RA). However, the importance of ABHD11 in regulating T-cell metabolism and function is yet to be explored. Here, we show that pharmacological inhibition of ABHD11 dampens cytokine production by human and mouse T-cells. Mechanistically, the anti-inflammatory effects of ABHD11 inhibition are attributed to increased 24,25-epoxycholesterol (24,25-EC) biosynthesis and subsequent liver X receptor (LXR) activation, which arise from a compromised TCA cycle. The impaired cytokine profile established by ABHD11 inhibition is extended to two patient cohorts of autoimmunity. Importantly, using murine models of accelerated type 1 diabetes (T1D), we show that targeting ABHD11 suppresses cytokine production in antigen-specific T-cells and delays the onset of diabetes in vivo in female mice. Collectively, our work provides pre-clinical evidence that ABHD11 is an encouraging drug target in T-cell-mediated inflammation.

PMID:41184294 | DOI:10.1038/s41467-025-65417-4

Nat Immunol. 2025 Oct 28. doi: 10.1038/s41590-025-02301-9. Online ahead of print.

ABSTRACT

The long-term impact of systemic hypoxia resulting from acute respiratory distress syndrome (ARDS) on the function of short-lived innate immune cells is unclear. We show that patients 3-6 months after recovering from ARDS have persistently impaired circulating neutrophil effector functions and an increased susceptibility to secondary infections. These defects are linked to a widespread loss of the activating histone mark H3K4me3 in genes that are crucial for neutrophil activities. By studying healthy volunteers exposed to altitude-induced hypoxemia, we demonstrate that oxygen deprivation alone causes this long-term neutrophil reprogramming. Mechanistically, mouse models of systemic hypoxia reveal that persistent loss of H3K4me3 originates in proNeu and preNeu progenitors within the bone marrow and is linked to N-terminal histone 3 clipping, which removes the lysine residue for methylation. Thus, we present new evidence that systemic hypoxia initiates a sustained maladaptive reprogramming of neutrophil immunity by triggering histone 3 clipping and H3K4me3 loss in neutrophil progenitors.

PMID:41152617 | DOI:10.1038/s41590-025-02301-9