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Biology subjects

Tan, X.

Publications and source records attributed to Tan, X..

At least 37 records · Page 2Linked to original sources

Live high-content imaging with automated analysis reveals mitochondrial changes during vascular calcification

Mitochondrial dysfunction is implicated in a wide range of disorders, including cancer, neurodegeneration, and cardiovascular diseases. Conventional assays typically assess mitochondrial function by measuring bulk respiration rates across thousands of cells. While informative, these approaches cannot resolve the behavior of individual mitochondria, may overlook rare mitochondrial events, and often lack sensitivity to subtle changes. Fluorescence microscopy provides single-organelle resolution but is usually low throughput; for example, imaging 1000 cells can require from 20 minutes to an entire day depending on imaging mode. Additionally, analysis of fluorescence images frequently relies on manually selected thresholds, introducing potential bias and variability due to differences in signal-to-background ratios across cells. Here, we present a High-throughput Mitochondrial Imaging Platform (H-MIP) combined with a deep learning segmentation model, enabling rapid imaging and automated characterization of mitochondrial morphology in millions of mitochondria from tens of thousands of cells. We demonstrate the utility of H-MIP by assessing mitochondrial morphology following treatment with Mdivi-1, an inhibitor of mitochondrial division. Furthermore, we employ an in vitro disease model (vascular calcification) to show that mitochondria become elongated in vascular smooth muscle cells undergoing pathological calcification. Overall, H-MIP provides a scalable and robust tool for investigating mitochondrial structure, with the potential to accelerate therapeutic discovery targeting mitochondrial health. HighlightsO_LIH-MIP enables high-throughput imaging of mitochondrial morphology and automated single-mitochondrion analysis at scale. C_LIO_LIH-MIP links mitochondrial morphology to an established disease model, with exciting implications for drug discovery. C_LI

cell biology↗

Spatial pharmaco-multiomics reveals drug distribution, metabolic niches, and spatially constrained resistance in medulloblastoma

Single-cell and spatial transcriptomic studies have provided insights into the developmental origins and intratumoural heterogeneity of SHH medulloblastoma (SHH-MB) and suggested how targeted drugs such as CDK4/6 inhibitors remodel tumour ecosystems, yet the interplay between local drug exposure, metabolism, cell state, and drug resistance remains poorly understood. Here we developed a same-section spatial pharmaco-multiomics framework that integrates MALDI-MSI-based spatial metabolomics with Visium whole-transcriptome profiling and high-resolution Xenium imaging to map palbociclib distribution, metabolite landscapes, and transcriptional programs within the same histological contexts of an SHH-MB PDOX model and primary human tumours. Palbociclib-rich tumour bulk exhibited broad suppression of E2F-driven proliferation and a shift toward neuronal differentiation, corroborating and extending prior findings. In contrast, drug-poor tumour-brain interfaces and perivascular regions retained E2F-high proliferative states and were enriched for mesenchymal-like stromal cells and ECM-remodelling genes, indicating anatomically constrained reservoirs of tolerance. Spatial metabolomics linked these interface niches to ganglioside (GM2) and sphingomyelin enrichment, while differentiated, drug-exposed regions displayed phosphatidylcholine, phosphatidic-acid signatures consistent with neuronal maturation. Integrated pathway analysis further revealed a "mitochondrial tuning" program, with upregulation of histidine, folate/one-carbon, CoA, and lipoate metabolism with redox and oxidative-phosphorylation support. These signatures were specific to therapy-exposed border cells. Rare palbociclib-positive, E2F-high resistant spots additionally exhibited mitotic checkpoint and DNA-repair signatures, implying a drug-induced resistance axis independent of scarcity. Together, our study provides a generalisable same-section spatial pharmaco-multiomics pipeline and a spatially resolved model of CDK4/6 response, nominating interface-focused metabolic and cell-intrinsic vulnerabilities for combination therapy.

cancer biology↗

IGHV3-53 antibody abundance drives divergent SARS-CoV-2 immune imprinting

The mechanisms driving divergent SARS-CoV-2 immune imprinting in populations with distinct SARS-CoV-2 exposure histories remain unclear. However, conventional wild-type mouse models fail to recapitulate severe imprinting, even after potent ancestral-strain mRNA immunization, hindering imprinting-related mechanistic investigation and vaccine evaluation. Here, we surprisingly found that V(D)J-humanized mice could faithfully recapitulate human severe imprinting phenotypes. Comprehensive antibody repertoire analysis and deep mutational scanning-based epitope mapping of 583 monoclonal antibodies from these models revealed that the pre-existing IGHV3-53/66 antibody abundance determine imprinting severity through antibody-mediated masking of Omicron-specific epitopes. Both passive IGHV3-53/66 antibody transfer and IGHV3-53 knock-in were sufficient to induce severe imprinting in wild-type mice. Together, these findings demonstrate that the V(D)J germline repertoire--even a single germline-encoded antibody response--can profoundly shape humoral imprinting severity. Accordingly, we established an IGHV3-53 knock-in mouse model that accurately recapitulates the human antibody landscape, providing a valuable tool for guiding future COVID-19 vaccine updates.

immunology↗

EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression

Membrane trafficking governs the transport of molecules to both intracellular and extracellular locations, thereby maintaining cell homeostasis. During cancer progression, alterations in membrane trafficking are frequently observed. However, the mechanisms underlying the dysregulation of membrane trafficking in cancer progression remain largely unresolved. Recent evidence has demonstrated that epithelial-to-mesenchymal transition (EMT) in lung adenocarcinoma (LUAD) employs a membrane trafficking program to coordinate cancer cell invasion and immunosuppression in the tumor microenvironment (TME). To further dissect the pro-tumorigenic membrane trafficking program, here we conducted a CRISPR interference (CRISPRi) in vivo screen for membrane trafficking regulators in a syngeneic mouse model with a complete immune system. This screen identified REEP2, an endoplasmic reticulum (ER) shaping protein, as a novel regulator of the EMT-dependent membrane trafficking program, which is associated with a poor prognosis in LUAD patients and is required for LUAD metastasis in a syngeneic orthotopic LUAD mouse model. Mechanistically, the EMT activator ZEB1 upregulates REEP2 expression through miR-183- and miR-193a-mediated regulation that promotes the transportation of secretory cargoes from the ER exit site (ERES) to the Golgi, thereby augmenting the secretion of pro-tumorigenic factors. The REEP2-driven secretion promotes cancer cell proliferation, migration, and the infiltration of myeloid-derived suppressor cells (MDSCs) in the TME. These findings identify REEP2 as a critical mediator of the EMT-driven pro-metastatic membrane trafficking program, revealing a specific vulnerability in mesenchymal LUAD.

cancer biology↗

LRP8 is a Receptor for Yellow Fever Virus

Yellow fever virus (YFV), an arbovirus causing substantial human morbidity and mortality, was the first human virus discovered over a century ago. The live-attenuated 17D vaccine is among the most successful vaccines in medicine. Despite the importance of YFV, its receptor has remained unknown. Here, we performed a barcoded, genome-wide human ORF library screen and identified LRP8 (also named APOER2) as a receptor for YFV. We show that LRP8 expression specifically boosts YFV infection in cell lines by promoting entry. AAV-mediated expression of human LRP8 in mouse liver aggravates infection and pathology. LRP8 knockdown abolishes YFV infection in brain cells, primary human hepatocytes, and notably in mosquitoes. Biochemically, LRP8 directly interacts with YFV particles via the viral envelope protein. This function of LRP8 is conserved across species, particularly in mosquitoes and primates. A soluble LRP8 decoy protein can block YFV infection in vitro and in mice, providing a potential therapeutic or prophylactic strategy. Our findings provide groundwork for understanding YFV entry, tropism, and pathogenesis, and may enable development of novel therapeutics to treat YFV infection.

microbiology↗

A Population-scale Single-cell Spatial Transcriptomic Atlas of the Human Cortex

The genetic and spatial determinants of cell type diversity in human cerebral cortices remain poorly defined. Here, we present a population-level single-cell spatial transcriptomic atlas of human cortices from 71 donors across the lifespan. We identified 906 layer-specific genes showing conserved and divergent laminar expression patterns between humans and other species. Spatial analysis revealed neuronal vulnerability and glial activation during aging, together with a decline in the proportion of superficial SST neurons and their interactions with other cells. Disease-associated genes exhibited high cell-type and layer-specific expression, implicating the pathogenic role of spatially specific gene expression. Spatial cis-eQTL analysis identified regulatory variants linked to genes related to diseases like Tourette syndrome. Cross-species comparison demonstrated glial expansion in the human cortex, accompanied by enhanced neuron-glia communication via the neuregulin signaling. Together, we provide a comprehensive single-cell atlas of the human cortex that is essential for understanding aging, evolution, and disease pathogenesis.

neuroscience↗

Integrating 12 Spatial and Single Cell Technologies to Characterise Tumour Neighbourhoods and Cellular Interactions in three Skin Cancer Types

Cutaneous squamous cell carcinoma (cSCC), basal cell carcinoma (BCC), and melanoma - the three major skin cancers - collectively comprise over 70% of all cancer cases. Despite their prevalence, much understanding of cellular interactions in the skin cancer microenvironment is needed, both in the outer skin layer where the cancer originates and at the deeper junctional and dermal layers into which it progresses. To address this gap, we integrated 12 complementary spatial and single-cell technologies to generate orthogonally-validated cell signatures, spatial maps, and interactomes for cSCC, BCC, and melanoma. Through comprehensive comparisons and integrating these spatial methods, we provided practical benchmarking guidelines for experimental design and analysis. By identifying keratinocyte cancer cells and melanomas, we found distinct signatures of these cells compared to non-cancer keratinocytes and melanocytes. Spatial integration of transcriptomics, proteomics and glycomics uncovered cancer niches enriched for cancer initiating cells (melanocytes or keratinocytes) and fibroblast and T-cell (MKFT) clusters, with altered tyrosine and pyrimidine metabolism. Ligand-receptor analysis across >700 cell-type combinations and >1.5 million interactions highlighted key roles for CD44, integrins, and collagens, with CD44-FGF2 emerging as a potential therapeutic target. Consistently, melanoma showed strong MFT interactions, validated by Opal Polaris, RNAScope, Proximal Ligation Assay and two additional single-cell spatial platforms (making a total of 14 technologies). For population-scale generalisation, genetic associations from >500,000 individuals were mapped onto spatial skin tissues, identifying SNPs enriched in domains containing melanocytes and T cells and their ligand-receptor pairs, shedding light on functional mechanisms linking genetic heritability to cells within cancer tissue. We built an interactive multiomics resource for exploring spatially-resolved molecular signatures and cellular crosstalk in skin cancer, available at https://skincanceratlas.com.

cancer biology↗

Electric fields trigger ceramide-dependent budding of exosome vesicles into multivesicular endosomes and boost the generation of exosomes

Exosomes hold immense therapeutic and diagnostic potential, yet their clinical translation remains constrained by low yields. Physiological electric fields (EFs), naturally occurring during wound healing and embryo development, have unexplored roles in exosome biogenesis. Here, we demonstrate that physiological-strength EFs (Direct Current, 50-200 mV/mm) dramatically enhance cellular exosome secretion, achieving a nearly 100-fold increase in a strength-dependent manner. Mechanistically, EFs augmented intraluminal vesicle formation within multivesicular bodies. We proposed a novel EF-driven membrane electroassembly and vesiculogenesis hypothesis and tested it using giant plasma membrane vesicles. We reconstructed EF-induced membrane remodeling and observed EFs driving inward budding of nanoscale exosome-like vesicles. Notably, alternating current EFs (50-400 Hz) exhibited significantly diminished efficacy compared to direct current EFs, highlighting membrane electropolarization-dependent modulation. Pharmacological inhibition of the lipid raft and ceramide almost abolishes EF-induced exosome secretion. Inhibition of the PI3K partially attenuated EF-triggered exosome release. Our findings not only unveil EFs as a potent physiological regulator of exosome secretion but also establish a novel, high-yield production strategy leveraging bioelectric cues. Significant statementWe reported that the bodys natural bioelectricity, the faint electric currents in healing wounds and embryo development, can trigger cells to release 100 times more "natural nanoscale vesicle couriers" called exosomes. This pure physical method is far more efficient than current available technologies, paving the way for breakthroughs in cancer early detection, stem cell therapies, and precision medicine. We found that gentle electric fields can "blow" the cell membrane to release exosomes like "soap bubbles". This explains how bioelectricity controls cell communication during development and wound healing. In short, harnessing the bodys hidden "electric language" unlocks a fast and natural way to mass-produce exosomes.

cell biology↗

Perivascular matrix densification dysregulates angiogenesis and activates pro-inflammatory endothelial cells

Fibrosis is central to numerous fatal conditions including solid cancers, pulmonary fibrosis, cirrhosis and post-infarct cardiac fibrosis amongst many others, thereby collectively contributing to 45% of all deaths in developed nations. The potential for fibrosis across most organ systems may stem from its connections to wound healing and the ubiquitous presence of vascular endothelium. Endothelial cells (ECs) and angiogenesis, cells and associated biological program central to wound healing, have been heavily implicated in many organ-specific fibroses, but the relationship between angiogenesis and fibrogenesis remains debated and little has been established in terms of how the EC phenotype governs tissue healing vs. fibrosis. Here, we examine a murine lung injury model enabling EC lineage tracing and observe the invasion of aberrant ECs from the bronchial microvasculature following lung injury along with concurrent densification of matrix fibers surrounding these vessels. To investigate the underlying mechanisms governing their appearance, we established a microphysiological system (MPS) of arteriole/venule-scale microvessels embedded within a tunable stromal mimetic matrix and find that heightened extracellular matrix fiber density activates ECs, drives endothelial to mesenchymal transition, and promotes aberrant tip EC (ATEC) invasion into the matrix. ATECs remain adherent to fibrotic matrix and possess a pro-inflammatory phenotype that secretes TGF-{beta}2. Notably, our studies establish that the formation of ATECs is gated by destabilization of endothelial adherens junction upon EC adhesion to fibrous matrix, and associated regulation of TGF-{beta} signaling that is mediated by a novel VE-cadherin - TGF-{beta}R2 axis. The current lack of effective anti-fibrotic therapies suggests potential critical involvement of other cell types such as ECs, and our findings suggest new contributions of ECs to fibrotic progression that may better inform future targets for novel anti-fibrotic therapeutics.

bioengineering↗

Triad-LMF: A Hierarchical Low-Rank Multimodal Fusion Framework for Robust Cancer Subtype Classification Using Multi-Omics Data

Cancer heterogeneity poses a major challenge for accurate molecular subtype classification. Conventional methods often fail to exploit complementary information across multiple omics modalities, leading to overfitting on high-dimensional data and limited representation of subtype heterogeneity. To address this, we propose Triad-LMF, a multiomics integration framework based on low-rank multimodal fusion to improve classification accuracy. Triad-LMF harmonizes heterogeneous omics data and integrates information through a two-stage hierarchical fusion strategy. Local Pairwise Fusion and Global Triadic Fusion are combined via the Two-Feature and Three-Way LMF modules, enabling a gradual transition from local modality interactions to global feature integration. Experimental results show that Triad-LMF consistently outperforms existing methods. UMAP visualization confirms enhanced subtype separability, and SHAP-based analysis highlights biologically meaningful features. Across independent datasets, Triad-LMF demonstrates strong generalization, offering a robust and interpretable framework for multiomics-driven cancer subtype classification.

bioinformatics↗

Engineering novel AAV capsids by global de-targeting and subsequent muscle-specific tropism in mice and NHPs

Recombinant adeno-associated viral (rAAV) vectors are a potent tool, but their clinical application is restricted by insufficient target tissue transduction and liver toxicity. We employed a novel two-step engineering strategy to create novel rAAV capsids with global tissue de-targeting, then produced strong tissue-specific expression by adding a peptide sequence. We created a novel capsid, AAV.Zero1, with globally de-targeted transduction by loop swapping domains from AAV9 into AAV2. Making an R585A substitution (AAV.Zero2) re-targeted tissues but deleting residues 585-587 (AAV.Zero3) abrogated transduction. Inserting a myogenic peptide into AAV.Zero3 produced a novel capsid (AAV.eM) with strong muscle-specific transgene expression while maintaining minimal off-target expression, including in liver, which was conserved in two mouse strains and non-human primates. AAV.eM showed similar expression as the leading myotropic vector MyoAAV.4A but had a more favorable safety profile. Importantly, AAV.eM was able to functionally rescue a mouse model of Duchenne Muscular Dystrophy following systemic delivery of a micro-dystrophin gene. Thus, AAV.eM is an improved myotropic rAAV capsid that de-targets other tissues, especially the liver, and proof-of-concept for a platform to create capsids with specific properties that translate across species by addition of peptides onto low transduction backbones.

bioengineering↗

Angel Wing: a class of alternative splicing regulators in animals

Alternative splicing (AS) regulates the diversity and level of the proteome. The specificity in AS is in turn regulated by RNA binding proteins, but our understanding of how they act is far from complete. Here we identify the Angel wing (Anw) protein as a novel AS regulator. Loss of Anw in Drosophila disrupts splicing in muscle genes and subsequently muscle function. Based on a mini-gene assay in which Anw and its RNA targets are co-expressed in cultured cells, we demonstrated orthologous splicing regulation of the minigene transcripts, interaction between Anw and its RNA targets, and a remarkable functional conservation among Anw homologs. Anw forms nuclear foci, and genetic ablation of Anw domains suggests that maintaining distinctive features of these foci is important for its function. The evolution of Anw is dynamic with gene gains and losses, but preserves a cross-phyla "ultra conserved element" as an alternative exon that potentially regulates its own level by non-sense mediated mRNA decay. As the human anw homolog is a candidate gene for myasthenia gravis, our work suggests a mechanism for cellular dysfunction in this disease.

genetics↗

Modular Engineering of Escherichia coli for Enhanced Nickel Uptake, Survival, Biomineralization, and Hydrogen-Supported Bioremediation

Nickel contamination poses increasing environmental and industrial challenges, demanding effective and sustainable remediation strategies. Here, we present a modular synthetic biology approach to engineer Escherichia coli for efficient nickel enrichment, resilience in toxic environments, intracellular biomineralization, and hydrogen-based co-culture stability. Our system comprises four functional modules: (1) a nickel enrichment module, in which the fusion protein NixA-F1v outperformed existing uptake systems, and a mutant repressor RcnRC35L enhanced retention by suppressing nickel efflux; (2) a survival module where heterologous expression of Helicobacter pylori Hpn conferred tolerance to high nickel concentrations, and YejM increased phage resistance; (3) a nickel microparticle module enabling intracellular bioconversion of nickel into detectable microparticles even without engineered uptake proteins; and (4) a hydrogen supply module supporting co-culture stability through E. coli-cyanobacteria adhesion for sustained hydrogen production. These modules were experimentally validated through comparative uptake assays, survival profiling, and microscopy-based particle detection. Our findings demonstrate a customizable and integrative microbial platform for metal bioremediation and biosensing, with potential applications in environmental engineering and industrial waste treatment.

synthetic biology↗

A humanized 16A antibody conjugated with DNA topoisomerase I inhibitors, targeting a GSTA glycosite-signature epitope.

BackgroundWe previously reported the 16A antibody, which binds to the abnormally glycosylated tandem repeat region of the MUC1 glycoprotein, and developed 16A-MMAE as an antibody-drug conjugate. However, its antitumor efficacy as an antibody-drug conjugate with DNA topoisomerase Iinhibitors remains unknown. MethodsWe humanized the 16A antibody and conjugated it to DXd and MF6, two DNA topoisomerase I inhibitors. The antitumor efficacy of the conjugates was evaluated in vitro and in vivo. ResultsThe humanized 16A-DXd conjugate showed potent antitumoral efficacy, with an IC50 in the nM range against CFPAC1 cells. In vivo, h16A-DXd and h16A-MF6 inhibited tumor growth in asubcutaneous mouse tumor transplantation model using CT26-COSMC KO-hMUC1 cells, administered at a dose of 10 mg/kg. ConclusionsThe high antitumor efficacy of h16A-conjugated DNA topoisomerase I inhibitors supports further clinical development. The relatively low toxicity of h16A-DXd and h16A-MF6 may enable a higher therapeutic window, since MUC1-positive cells internalize the antibody-drug conjugate more efficiently.

pharmacology and toxicology↗

Structural variants contribute to the gut microbiome, blood metabolic traits and their causal relationships

Research on genetic variants affecting the gut microbiome and blood metabolites has mainly focused on single nucleotide variants (SNPs), with structural variants (SVs) remaining largely unexamined. In this study, we utilized an advanced structural variant detection pipeline on whole-genome sequencing data from 2,002 individuals with an average sequencing depth of 42 folds, identifying 138,859 high-confidence SVs, 49.57% of which were previously unreported. We performed genome-wide association studies on 22,519 common SVs with 616 gut microbial features and 121 blood metabolic traits, uncovering 30 significant links between SVs and microbial taxa/pathways and 48 connections between SVs and blood metabolites. Notable results include 19 associations reaching study-wide significance, such as an Asian-specific 6.5k deletion at the TENT2 gene, which is strongly associated with the abundance of Coprobacillus sp. 29_1 ({beta}=0.158, p=2.5x10-9), and a deletion covering HBA1/HBA2/HBM/HBQ118 linked to nine blood metabolic traits, most significantly with mean corpuscular volume (MCV; {beta}=-0.570, p=1.22x10-91). Most SVs showed a greater impact than nearby SNPs in their associations with the microbiome/metabolites. Analysis of rare SVs also identified multiple genes associated with the microbiome/metabolites. Additionally, Mendelian randomization using SVs demonstrated causal relationships, including effects from the microbiome to metabolites, such as Clostridium ramosums impact on serum uric acid and hyperuricemia, and from metabolites to the microbiome, like the influence of mean corpuscular hemoglobin concentration on MF0064: triacylglycerol degradation. This study provides a detailed SV catalog for the Chinese population and highlights the significant role of SVs in the gut microbiome, blood metabolites, and their causal relationships. HighlightsO_LIProvides a catalog of 138,859 high-confidence SVs and 49.57% of which were novel C_LIO_LIIdentify 30 genome-wide significant "SVs--microbial taxa/pathways" and 48 "SVs--blood metabolites" associations, respectively C_LIO_LIAn Asian-specific 6.5k deletion at TENT2 gene associated with the species Coprobacillus sp. 29_1 C_LIO_LIA deletion spanning HBA1/HBA2/HBM/HBQ118 associated with 9 blood metabolic traits C_LIO_LIThe majority of SVs demonstrated a more pronounced impact than neighboring SNPs in the associations with microbiome/metabolites C_LIO_LISVs help to reveal the host-microbe causal relationships such as Clostridium ramosums causal effects on serum uric acid and hyperuricemia C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=155 SRC="FIGDIR/small/643427v2_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@e660d0org.highwire.dtl.DTLVardef@ddfe4dorg.highwire.dtl.DTLVardef@62a704org.highwire.dtl.DTLVardef@c31bb5_HPS_FORMAT_FIGEXP M_FIG Graphic abstract Based on a multi-omics cohort of 2,002 individuals comprising high-depth whole genome and metagenomic sequencing data, blood metabolites, and detailed questionnaires, we identified 138,859 high-confidence SVs, uncovering 36 significant associations between SVs and microbial taxa/pathways, as well as 48 associations between SVs and blood metabolites. Mendelian randomization using SVs demonstrated causal relationships, such as Clostridium ramosums causal effect on serum uric acid and hyperuricemia. This study provides a detailed SV catalog for the Chinese population and highlights the significant role of SVs in the gut microbiome, blood metabolites, and their causal relationships. C_FIG

genomics↗

CD8+ T cells mediate vaccination-induced lymphatic containment of latent Mycobacterium tuberculosis infection following immunosuppression, while B cells are dispensable

It is estimated that two billion people are latently infected with Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). Latent Mtb infection (LTBI) can occur in multiple organs, including the lymphatics. The risk of LTBI reactivation increases in immunocompromised conditions, such as coinfection with human immunodeficiency virus (HIV), and during treatment of autoimmune diseases and organ transplantation. The immunological correlates of protection against TB, including against reactivation of LTBI, remain largely elusive. Here, we used a mouse model of latent lymphatic Mtb infection to dissect the immunological mechanisms underlying LTBI containment versus reactivation. We show that immunosuppression-mediated reactivation of lymphatic LTBI and the subsequent spread to non-lymphatic organs can be prevented by vaccination with multiple recombinant BCG (rBCG) strains despite the deficiency of CD4+ T cells. Using spatial transcriptomics, multi-parameter imaging, network analysis and bioinformatic integration of histopathological images, we reveal that immunosuppression is associated with a distinct repositioning of non-CD4 immune cells at the edge of TB lesions within the infection-draining cervical lymph nodes. While B cells increased in numbers, they are dispensable for the containment of LTBI. Lymphatic Mtb infection in different immune cell-deficient mouse strains, antibody-mediated cell depletion and adoptive transfer experiments into highly susceptible mice unequivocally show that vaccination-mediated prevention of LTBI reactivation is critically dependent on CD8+ T cells. These findings have profound implications for our understanding of immunity to TB and the management of LTBI. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=92 SRC="FIGDIR/small/634479v1_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@151fdd6org.highwire.dtl.DTLVardef@1efed47org.highwire.dtl.DTLVardef@c2e7e0org.highwire.dtl.DTLVardef@555c7_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

MAIT cell deficiency exacerbates neuroinflammation in P301S human tau transgenic mice

The role of immune cells in neurodegeneration remains incompletely understood. Our recent study revealed the presence of mucosal-associated invariant T (MAIT) cells in the meninges, where they express antioxidant molecules to maintain meningeal barrier integrity. Accumulation of misfolded tau proteins are a hallmark of neurodegenerative diseases. The role of MAIT cells in tau-related neuroinflammation and neurodegeneration, however, remains unclear. Here we report that the meninges of P301 mutant human tau transgenic mice had increased numbers of MAIT cells, which retained their expression of antioxidant molecules. Mr1-/-P301S mice that lacked MAIT cells exhibited increased tau pathology and hippocampus atrophy compared to control Mr1+/+ P301S mice. Adoptive transfer of MAIT cells reduced tau pathology and hippocampus atrophy in Mr1-/- P301S mice. Meningeal barrier integrity was compromised in Mr/-/-P301S mice, but not in control Mr1+/+ P301S mice. A distinctive microglia subset with proinflammatory gene expression profile (M-inflammatory) was enriched in the hippocampus of Mr1-/- P301S mice. The transcriptomes of the remaining microglia in these mice also shifted towards a proinflammatory state, with increased expression of inflammatory cytokines, chemokines, and genes related with ribosome biogenesis and immune responses to toxic substances. The transfer of MAIT cells restored meningeal barrier integrity and suppressed microglial inflammation in the Mr1-/- P301S mice. Together, our data indicate an important role for MAIT cells in regulating tau-pathology-related neuroinflammation and neurodegeneration.

immunology↗

Gut bacterial sphingolipid production modulates dysregulated skin lipid homeostasis

Sphingolipids are an essential lipid component of the skin barrier with alterations in skin sphingolipid composition associated with multiple skin disorders including psoriasis, atopic dermatitis, and ichthyosis. Contributions to skin sphingolipid abundance are not well characterized, thus the main method of modulating skin lipid levels is the topical application of creams rich with sphingolipids at the skin surface. Evidence that diet and gut microbiome function can alter skin biology proposes an intriguing potential for the modulation of skin lipid homeostasis through gut microbial metabolism, but potential mechanisms of action are not well understood. Sphingolipid synthesis by prominent gut microbes has been shown to affect intestinal, hepatic and immune functions with the potential for sphingolipid-producing bacteria to affect skin biology through altering skin sphingolipid levels. To address this question, we used bioorthogonal chemistry to label lipids from the sphingolipid-producing bacteria Bacteroides thetaiotaomicron and trace these lipids to the skin epidermis. Exposing mice to B. thetaiotaomicron strains mutant in the ability to produce sphingolipids resulted in significantly lower transfer of gut microbiome-derived lipids to the skin, while also altering skin biology and altering expression of skin barrier genes. Measurement of skin ceramide levels, a class of sphingolipids involved in skin barrier function, determined that skin sphingolipid levels were altered in the presence of gut sphingolipid-producing bacteria. Together this work demonstrates that gut bacterial lipids can transfer to the skin and provides a compelling avenue for modulating sphingolipid-dominant compartments of the skin using sphingolipid-producing bacteria of the gut microbiome.

microbiology↗