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Yu, F.

Publications and source records attributed to Yu, F..

At least 19 recordsLinked to original sources

Scaling genetic discovery through automated post-GWAS interpretation

Genome-wide association studies (GWAS) have made association discovery systematic and cumulative, yet evidence for interpreting associated loci remains selective, heterogeneous and difficult to accumulate across studies. Here we present Post-GWAS Intelligence (PGI), which couples context-dependent post-GWAS analysis to a common representation of analysis-derived evidence. Its multi-agent engine, VariantAgent, executes workflows, records tool-derived results in standardized variant-centred units and generates trait-level interpretations linked to their analytical basis and evidential status. Complementary benchmarks showed that VariantAgent outperformed tested general-purpose and biomedical agents, with its largest advantage when success required both a correct answer and a valid analytical trace. Across 34 published GWAS, VariantAgent achieved a mean per-study recovery of 82.1% for directly comparable findings. The largest gains lay downstream of association mapping, where uniform analysis extended published interpretations and identified regulatory relationships at established risk loci not previously reported in the source studies. Analysis of 1,041 GWAS yielded 530,949 evidence units and corresponding reports, which PGI organized into a cross-trait catalogue. Catalogue interrogation resolved an apparent cross-trait overlap into distinct signals and trait-specific biological hypotheses. This work demonstrates how PGI can extend genetic discovery beyond association mapping by enabling biological evidence to accumulate across studies.

genetics↗

Structural basis for phosphorylation-induced inactivation of the rice ammonium transporter AMT1;1

Ammonium (NH4+) uptake and transport in plants are mediated by ammonium transporters (AMTs), which are tightly regulated by phosphorylation to prevent excess ammonium influx and toxic accumulation. However, the mechanism of phosphorylation-mediated inactivation is unique and remains unclear. Here, we report cryo-EM structures of the rice (Oryza sativa) ammonium transporter OsAMT1;1 in its wild-type and phosphomimetic variant T452D states. OsAMT1;1 forms a stable homotrimer, with conserved motifs affirming a shared transport mechanism within the AMT/MEP/Rh superfamily. Our structural analysis reveals that T452D phosphomimetic stabilizes an intracellular salt-bridge network and maintains the channel in a closed state, in which the ICL5 loop positions the hydrophobic plug residue Leu360 near the cytoplasmic exit to occlude the channel exit and abolish complementation capacity. Our findings elucidate phosphorylation-induced inactivation mechanism for the plant AMT1 subfamily, providing a structural paradigm for the post-translational regulation of nutrient uptake.

biophysics↗

A sensitive bioassay for detecting Plasmodiophora brassicae in canola field soils

We describe a biodegradable-cup bioassay for detecting viable Plasmodiophora brassicae in soil samples. Soil samples either artificially inoculated with P. brassicae resting spores or collected from canola fields were aliquoted into biodegradable cups containing 20 g of soil per cup. Two cups representing the same soil sample or inoculum concentration were placed in each pot filled with Sunshine Mix. Six seeds of the canola cultivar Westar were sown into each cup and thinned to four seedlings per cup ten days after planting. After four weeks, roots were examined for the presence of clubroot galls. Across three independent inoculated-soil experiments, galls were observed in samples containing as few as 1 resting spore g-1 soil. In contrast, under a qPCR assay evaluated in parallel, consistent amplification across three technical replicates was obtained only at 100 resting spores g-1 soil or greater. In field samples, the bioassay produced galls from 11 qPCR-positive samples and seven of ten qPCR-negative samples. Although the bioassay is not intended for rapid diagnosis or direct quantification, it provides a practical tool for annual clubroot surveys and for studies requiring recovery, propagation, or characterization of viable P. brassicae from soil samples collected across diverse geographic regions.

microbiology↗

A Quartet of Native Orai Channel Isoforms Orchestrates Graded NFAT Activation and Transcription

The Ca{superscript 2} release-activated Ca{superscript 2} (CRAC) channel mediates store-operated calcium entry (SOCE), a ubiquitous pathway essential for many cell types, including immune cells. Three Orai (Orai1/2/3) proteins constitute the plasma membrane pore-forming units of CRAC channels that are activated by the endoplasmic reticulum (ER) Ca2+-sensing STIM1/2 proteins when ER Ca2+ stores are depleted. Orai1/2/3 are differentially expressed across primary cells with discernible differences in their structures and biophysical properties. Further, Orai1 has two alternatively translated isoforms: long mammalian-specific Orai1 and the 63-residue shorter Orai1{beta}, which is evolutionarily older and conserved across vertebrates. Whether Orai1/1{beta}/2/3 produce unique cytosolic Ca{superscript 2} signatures that bias transcriptional responses through effectors like NFAT is unclear. Here, we used HEK293 cells engineered to express one native Orai isoform and show that all Orai isoforms couple to NFAT1/4 induction. The magnitude of NFAT1/4 induction for each Orai isoform matches that of SOCE, with the following profile: Orai1{beta}>Orai1>>Orai2>Orai3. Near-native re-expression of either Orai1 or Orai1{beta} in primary murine Orai1-/- CD4 T cells restored SOCE, NFAT activation, cytokine production and promoted near identical transcriptional responses enriched for immune activation pathways. An analysis of genetic and clinical data of human individuals showed that homozygous null mutations selectively abolishing Orai1 are not associated with disease resembling CRAC channelopathy. Primary T cells from individuals homozygous or heterozygous for an Orai1 null mutation showed enhanced, rather than impaired, SOCE and NFAT induction. Our data indicate that NFAT activation and transcriptional outputs are primarily driven by the graded strength of SOCE mediated by each isoform of the Orai quartet.

cell biology↗

Unearthing a fungal giant: Dianjunaceae fam. nov., a novel Paleocene lineage of Xylariales harbouring Dianjunus rex gen. et sp. nov.

During mycological surveys in Yunnan Province, China, specimens of a fungus producing massive, upright stromata up to 50 cm high and individually 2.2 Kg in weight were sampled. Through an integrative taxonomic approach combining detailed morphology, multilocus phylogeny (ITS, LSU, RPB2, TUB2), and phylogenomic analyses, this fungus is proposed as the new species Dianjunus rex gen. et sp. nov., the type of the new family Dianjunaceae (Xylariales). Phylogenetic analyses robustly place Dianjunaceae as a distinct sister clade to Graphostromataceae. Divergence time estimation dates the origin of this family to the early Paleocene ([~]65 Mya), coinciding with the post-K-Pg extinction period, when an estimated 75% of all plant and animal species went extinct, and a significant ecological reorganization of life on earth happened. The stromata of D. rex represent the largest fructifications documented within the Ascomycota, significantly expanding the known morphological range of the Xylariales. The study provides a comprehensive description, including a nodulisporium-like anamorph with periconiella-like branching patterns, and discusses the taxons phylogenetic placement, and distinctive morphology. This discovery highlights the unexplored fungal diversity in East Asian forests.

microbiology↗

Extracellular salicylic acid activates immune signaling through cell-surface receptors

Salicylic acid (SA) is a central immune hormone that accumulates in both intracellular and extracellular compartments during pathogen infection. While intracellular SA signaling is well established, whether extracellular SA (eSA) directly activates immune responses remains unknown. Here we show that eSA functions as an extracellular signal potentially perceived by the plasma membrane-localized lectin receptor kinases LecRK-I.8 and LecRK-VI.2 in Arabidopsis. The extracellular domains of both receptors bind SA with micromolar affinity, SA rapidly induces LecRK-I.8 phosphorylation, and the kinase activities of LecRK-I.8 and LecRK-VI.2 are required for downstream signaling. Moreover, mutagenesis of a computationally predicted binding pocket in LecRK-VI.2 abolishes SA binding and immune function, providing evidence for receptor-mediated perception. Genetic analyses further demonstrate that LecRK receptors are required for SA-induced resistance, transcriptional reprogramming, and phosphoproteomic responses. Together, these findings expand current models of SA signaling by revealing a potential receptor-mediated cell-surface perception mechanism for a classical immune hormone.

plant biology↗

Real-time artificial intelligence prediction of peptide characteristics and MSFragger search improves multiplexed quantification of non-canonical HLA presented peptides in clear cell renal cell carcinoma.

Non-canonical HLA-presented peptides are promising therapeutic targets, but their low abundance makes them difficult to reproducibly identify and quantify, particularly in multiplexed immunopeptidomics workflows. Here we present MIRA-MS (Model-Informed Real-time Acquisition for Mass Spectrometry), a real-time acquisition strategy that combines fragment ion-indexed database searching with artificial intelligence-based prediction of peptide fragmentation and retention time to guide quantitative scan acquisition. In a clear cell renal cell carcinoma model, MIRA-MS increased the number of quantified non-canonical immunopeptides by 97-107% relative to standard acquisition methods while also improving recovery of canonical peptides by 45-89%. These results establish real-time AI-guided acquisition as a powerful approach for deeper and more reproducible immunopeptidome profiling.

cancer biology↗

A Moonlighting Function of Kinetochore Complex Proteins in Golgi Assembly of Neural Stem Cells

Kinetochores play an essential role in mitosis, and human kinetochore variants are associated with microcephaly. However, their functions in quiescent/interphase cells are unknown. Here, we demonstrate that Drosophila kinetochore proteins promote the reactivation of quiescent NSCs and their regeneration upon injury by organizing Golgi-dependent acentrosomal microtubules. Drosophila kinetochore proteins localize to the Golgi vicinity in quiescent NSCs and are required for proper localization of Golgi proteins, including the Golgi-resident small GTPase Arf1 known to regulate quiescent NSC reactivation and regeneration. Moreover, Drosophila kinetochore proteins physically associate with Arf1 and function upstream of it during reactivation. Remarkably, human kinetochore protein SPC25 localizes to Golgi in interphase NSCs and HEK293T cells. Furthermore, human kinetochores have a conserved function in promoting Golgi organization and, in turn, microtubule dynamics, in interphase cells. Together, our findings reveal a conserved moonlighting role for kinetochores in Golgi assembly in quiescent Drosophila NSCs and human interphase cells.

neuroscience↗

CAD rewires nucleotide metabolism to drive oxidative stress in myocardial ischemia/reperfusion injury

Myocardial ischemia/reperfusion (I/R) injury is a major determinant of infarct size and clinical outcome, yet effective therapies remain limited. Although metabolic remodeling is central to I/R pathology, the contribution of nucleotide biosynthesis remains unclear. Here, we identify CAD, the multifunctional rate-limiting enzyme of de novo pyrimidine biosynthesis, as a previously unrecognized regulator of myocardial reperfusion injury. CAD activation exacerbated cardiomyocyte death during simulated I/R, whereas CAD knockdown or pharmacological inhibition was protective in vitro. Mechanistically, CAD enhanced dihydroorotate dehydrogenase (DHODH)-dependent electron transfer, increased the CoQH2/CoQ ratio, and promoted complex I reverse electron transport (RET), thereby amplifying mitochondrial ROS. In parallel, CAD suppressed de novo purine synthesis, causing purine insufficiency, DIS3L-dependent RNA decay, and cytosolic ROS. Importantly, cardiomyocyte-specific CAD deletion protected against cardiac I/R injury in vivo. Together, these findings establish CAD as a metabolic hub linking nucleotide flux to dual-compartment ROS signaling and identify nucleotide metabolism as a therapeutic vulnerability in myocardial I/R injury. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=187 HEIGHT=200 SRC="FIGDIR/small/725578v1_ufig1.gif" ALT="Figure 1"> View larger version (87K): org.highwire.dtl.DTLVardef@14c4fedorg.highwire.dtl.DTLVardef@1138ed2org.highwire.dtl.DTLVardef@1057d8borg.highwire.dtl.DTLVardef@17546bd_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Survivin inhibition induces PD-L1 expression through cGAS stabilization and attenuates antitumor immunity

BackgroundSurvivin is a mitotic regulator frequently overexpressed in human cancers and an attractive therapeutic target. However, how Survivin inhibition influences tumor immune regulation remains incompletely understood. This study aimed to investigate whether Survivin inhibition modulates antitumor immunity and to elucidate the underlying mechanisms. MethodsProgrammed death-ligand 1 (PD-L1) expression was evaluated in multiple tumor cell lines following pharmacological or genetic inhibition of Survivin. Mechanistic studies included RNA sequencing, immunoblotting, flow cytometry, cGAS knockdown, and NF-{kappa}B inhibition. Immune profiling was performed using CD8 T-cell cytotoxicity assays, mass cytometry, flow cytometry, immunofluorescence and single-cell RNA sequencing. Clinical relevance was assessed using patient tumor specimens and public immunotherapy cohorts. ResultsSurvivin inhibition, either by YM155 treatment or genetic depletion, increased PD-L1 expression at both mRNA and protein levels in tumor cells. Mechanistically, Survivin inhibition stabilized cyclic GMP - AMP synthase (cGAS) by reducing its ubiquitination and activated NF-{kappa}B signaling, thereby promoting transcriptional upregulation of PD-L1. Functionally, the induced PD-L1 enhanced PD-1 engagement and suppressed CD8 T-cell cytotoxicity, promoting immune evasion. In immunocompetent ovarian cancer models, pharmacological inhibition of Survivin increased PD-L1 expression in tumor and immune compartments and attenuated cytotoxic immune activity. PD-L1 blockade restored antitumor immunity and significantly enhanced the therapeutic efficacy of Survivin inhibition. In addition, analyses of patient samples and public single-cell datasets revealed an inverse association between Survivin and PD-L1 expression, and high Survivin expression was associated with reduced benefit from PD-1/PD-L1 blockade. ConclusionsThese findings identify a Survivin-cGAS-PD-L1 axis linking mitotic stress to immune suppression and provide a mechanistic rationale for combining Survivin-targeted therapy with immune checkpoint blockade.

cancer biology↗

Membrane progesterone receptor signaling reverses hyperglycemia and insulin resistance in obese mice

Progesterone (P4) plays key roles in reproductive and metabolic function and signals through two receptor classes: classical nuclear receptors that regulate gene transcription and membrane progesterone receptors (mPR) that mediate rapid, non-genomic signaling. Whether mPR signaling influences systemic glucose homeostasis remains unclear. Here, we investigated whether mPR activation regulates glucose homeostasis and insulin sensitivity. Using the selective mPR agonist OD02-0, we show that mPR activation enhances glucose uptake in skeletal muscle and hepatocytes, associated with AMP-activated protein kinase (AMPK) activation. In HepG2 cells, mPR activation induces metabolic reprogramming characterized by reduced mitochondrial respiration and increased glycolytic flux. Pharmacological inhibition of AMPK suppresses this effect, indicating that these responses require AMPK activity. In diet-induced obese mice, chronic mPR activation reduces fasting glucose and insulin levels, improves glucose tolerance, and restores glucose-stimulated insulin secretion without detectable toxicity. Integrated proteomic and phosphoproteomic analyses in mouse liver reveal modulation of AMPK signaling and inhibition of mTORC1. Transcriptomic changes were limited, supporting a predominantly non-genomic mode of action. Together, these findings identify mPR signaling as a regulator of glucose homeostasis that engages central energy-sensing pathways to improve metabolic control in obesity.

physiology↗

Single-cell atlas of pig-to-monkey kidney xenotransplantation reveals macrophage chimerism and an IFN-ε orchestrated graft protective immune niche

The clinical translation of xenotransplantation is constrained by an incomplete understanding of the cellular circuitry governing graft rejection versus adaptation under current immunosuppressive regimens. Here, we present a high-resolution single-cell atlas of pig-to-monkey kidney xenotransplantation in a preclinical model, capturing the early immune dynamics preceding graft loss. Our analysis reveals a landscape dominated by innate immunity, characterized by species-specific distribution of macrophages. We identify recipient-derived macrophage subsets (ACKR1+, FN1+, MARCO+, IDO1+) enriched for multiple immune checkpoint molecules, alongside donor-resident subpopulations (APOE+, CCL2+, IL-1A+) exhibiting pro-inflammatory pathogenic signatures, and leverage their transcriptional profiles to computationally predict candidate therapies (belatacept, abatacept, pexidartinib). Further analysis demonstrates that despite divergent differentiation trajectories, both recipient-derived and donor-resident macrophages converge toward hybrid M1/M2 states at their terminal stages. Notably, we uncover a graft-protective circuit orchestrated by epithelial-derived interferon-epsilon (IFN-{varepsilon}), which specifically engages multiple subsets including IDO1+ macrophages to establish a localized immune-tolerant niche. This study establishes the xenograft epithelium as an active participant in immune modulation via the IFN-{varepsilon} axis and reveals macrophage functional chimerism as a key actionable feature of cross-species immune responses.

genomics↗

Experimental Data Driven AI Framework for Flexible Protein Conformational Reconstruction

Deep learning has revolutionized structural biology by prediction with near experimental accuracy static protein folds from amino acid sequence alone. However, proteins function as dynamic ensembles of protein conformation states, and current sequence-only models often fail to capture the specific conformational states and heterogeneity dictated by cellular environments or ligand binding. While recent generative models can sample broad conformational landscapes, they remain unconstrained by physical reality, often hallucinating plausible but experimentally invalid states. Here, we present AlphaSAXS, an end-to-end framework that constrains artificial intelligence (AI) inference using Small Angle X-ray Scattering (SAXS) experimental solution scattering data. By integrating real-space pair distance distributions (P(r)) directly into the AlphaFold architecture, AlphaSAXS effectively steers the structural hypothesis toward the experimentally observed structures. We demonstrate that AlphaSAXS resolves documented failure modes of sequence-only models in Apo-Holo transitions, successfully distinguishing between states with identical sequences but distinct scattering profiles. Furthermore, we introduce a hybrid inference protocol that couples deep learning with biophysical hydration modeling, enabling the reconstruction of solution state protein ensembles compatible with experimental data. This work establishes a paradigm for experimentally guided AI, bridging the gap between probabilistic sampling and biophysical measurement.

biophysics↗

Vps35 p.D620N causes Lrrk2 kinase hyperactivity, chronic microglial activation and inflammation

Pathogenic variants in leucine-rich repeat kinase 2 (LRRK2), RAB32, and vacuolar protein sorting 35 (VPS35) cause dominantly inherited, late-onset Parkinson's disease (PD). Mutations in all three genes constitutively activate LRRK2 kinase activity, enhancing innate immune defense against pathogens; however, chronic activation is linked to dopaminergic neuronal degeneration. LRRK2 and RAB32 are highly expressed in all myeloid cells including brain microglia, whereas VPS35, a core component of the retromer, is ubiquitously expressed. Nevertheless, the VPS35 p.D620N substitution induces the greatest constitutive increase in endogenous LRRK2 kinase activity, and its consequences for immune function remain unclear. We therefore examined the transcriptomic and functional effects of wild type (WT) and Vps35 p.D620N knock-in mice (VKI) from microglia, isolated from brains of naive animals at six-month of age, and initially analyzed by single-cell RNA sequencing (scRNAseq). Despite the absence of overt behavioral differences, differential gene expression revealed genotype-dependent changes in antimicrobial humoral immunity, lysosomal stress sensing, and phagocytosis. S100 family genes and lipocalin 2 were markedly upregulated, a finding subsequently validated by gene expression and immunohistochemistry. Downregulation was also observed in pathways governing microglial regulation of synaptic transmission, neuronal development and homeostatic immune signaling. Peripherally-administered lipopolysaccharide (LPS) stimulated microglial activation and phagocytic markers in WT brain, and further increased morphological activation and synaptic engulfment in VKI animals. Compared to WT, Vps35 p.D620N drives a chronic pro-inflammatory microglial state characterized by elevated innate immune signaling, lysosomal stress and enhanced phagocytic activity. Hence, heightened microglial sensitivity, further exacerbated by a peripheral immune challenge, offers a parsimonious, if multicellular, explanation for the multifactorial etiology of PD, and may help to account for its penetrance and variable expressivity. Together, these findings provide mechanistic insight into how retromer dysfunction and LRRK2 kinase hyperactivity intersect with microglial biology to influence PD pathogenesis, potentially promoting synaptic remodeling and neurodegenerative vulnerability.

neuroscience↗

L-Lactate reprograms tumor-associated macrophages to drive pancreatic cancer progression via BCL3 lactylation

Metabolic reprogramming fuels pancreatic ductal adenocarcinoma (PDAC) malignancy, creating a nutrient-deprived and waste-rich microenvironment. How this extreme metabolic pressure dictates the phenotypic remodeling of infiltrating immune cells remains largely unclear. Metabolomic profiling of PDAC reveals that robust tumor glycolysis proceeds without a commensurate accumulation of extracellular lactate. Integrated single-cell profiling and tissue multiplex immunofluorescence demonstrate that tumor-associated macrophages (TAMs) act as the primary consumers of tumor-secreted lactate. The uptake of L-lactate directs macrophages toward a pro-tumorigenic state through site-specific L-lactylation of the transcriptional co-regulator BCL3 at lysine 21 (K21). Functioning as a molecular switch, K21 lactylation triggers BCL3 nuclear translocation and enhances its interaction with the NF-{kappa}B p50 subunit. The ensuing BCL3-p50 complex competitively displaces the pro-inflammatory p65 subunit, rewiring the transcriptional output to suppress inflammation and enforce tumor-supporting networks. In vivo, macrophage-specific expression of a lactylation-deficient BCL3 mutant (K21R) abolishes lactate-driven phenotypic shifts and restricts tumor growth. Clinically, a BCL3-lactylated macrophage signature spatially correlates with CD8+ T cell exclusion and predicts poor patient survival, providing a strong rationale for targeting the BCL3-lactylation axis to reverse TAM-driven PDAC progression. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/710237v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@173159eorg.highwire.dtl.DTLVardef@9065f3org.highwire.dtl.DTLVardef@153e0aorg.highwire.dtl.DTLVardef@9c2678_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Expanding Glycopeptide Identification with Match-Between-Glycans in FragPipe

Glycosylation is one of the most important, but also most complex, post-translational modifications of proteins, playing a pivotal role in various pathological processes. Mass spectrometry-based large-scale glycoproteomics analysis offers a powerful approach to explore the fundamental roles of glycosylation in both physiological and pathological contexts. Traditionally, DDA glycopeptide assignment relies on information-dense MS2 spectra, containing sufficient fragmentation information to identify both the peptide and glycan moieties. Achieving this fragmentation can be difficult, especially for low-abundant glycopeptides and/or large, complex glycans. These glycopeptides are often not assigned using current data analysis software, yet they can be of biological relevance. Here, we introduce a method called match-between-glycans (MBG), which expands glycopeptide identification while maintaining the existing glycoproteome analysis workflow. MBG enables expanding the set of identified glycopeptides to include those without MS2 spectra, or with lower quality MS2 spectra, by looking for MS1 signals displaced from other identified glycopeptides by one or multiple monosaccharide unit(s). MBG can also identify glycans not included in the glycan database, such as those containing adducts or modifications, allowing these glycans to be recovered without a drastic expansion of the search space. Combined with target-decoy FDR control, we show this method is capable of accurately expanding glycopeptide identifications and providing a more complete quantitative profile of glycosylation at each glycosite. MBG is fully integrated into the glycoproteomics workflows in FragPipe, allowing seamless, one-click operation.

bioinformatics↗

Disentangled multimodal evolutionary representations for cross-virus predictive modeling of antigenic change

Antigenic evolution drives immune escape and complicates early assessment of emerging pathogens, especially when genomic surveillance is sparse and functional measurements lag behind real-world spread. Early prediction and generalization to unknown viruses require faithful and information-rich representations of viral evolution, a need that is not fully addressed by existing protein language model-based approaches. Here we introduce DERIVE, a flow-based generative framework that learns a disentangled latent representation of multimodal evolutionary history by integrating sequence homology with physicochemical and structural features. Using only pre-pandemic SARS-CoV-2 sequences, DERIVE prioritizes high-risk mutations, reconstructs strain-level evolutionary trajectories, forecasts immune escape and prevalence trends, and produces mutation-level effect maps. The learned representation transfers robustly across viral families, with strong concordance to functional data for influenza virus, HIV, rabies lyssavirus and chikungunya virus. Together, these results position DERIVE as a generalizable and interpretable framework for anticipating antigenic evolution and supporting early, actionable assessment of future "Disease X" threats.

bioinformatics↗

Immune checkpoint inhibitors amplify type 2 immune mediated repair bypro-regenerative scaffolds

Extracellular matrix (ECM) scaffolds induce type 2 immunity to promote repair. Here, we show that immune cells recruited to ECM-treated murine muscle injuries and clinical soft tissue defects express immune checkpoints. Specifically, TH2 cells and regulatory T cells (Tregs) increase LAG3 expression, while macrophages express PDL2. TCR analysis and a triple-reporter strain for interleukin (IL)-13 and Treg fate-mapping suggest that Tregs in ECM-treated wounds transition into TH2-like exTregs that express LAG3. Immune checkpoint inhibition (ICI) significantly stimulated type 2 immunity in ECM-treated wounds, including increased TH2 cells, Treg transition to TH2-like exTregs, and pro-regenerative macrophages. Moreover, ICI enhanced muscle repair and reduced fibrosis in ECM-treated wounds. Collectively, these findings show Treg/TH2 plasticity in wound healing and introduce a novel ICI application to enhance immune-mediated regeneration.

bioengineering↗