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Zhang, T.

Publications and source records attributed to Zhang, T..

At least 253 records · Page 14Linked to original sources

RIPK1 is essential for Herpes Simplex Virus-triggered ZBP1-dependent necroptosis in human cells

Necroptosis initiated by the host sensor Z-NA Binding Protein-1 (ZBP1) is essential for host defense against a growing number of viruses, including Herpes Simplex Virus-1 (HSV-1). Studies with HSV-1 and other necroptogenic stimuli in murine settings have suggested that ZBP1 triggers necroptosis by directly complexing with the kinase RIPK3. Whether this is also the case in human cells, or whether additional co-factors are needed for ZBP1-mediated necroptosis, is unclear. Here, we show that ZBP1-induced necroptosis in human cells requires RIPK1. We have found that RIPK1 is essential for forming a stable and functional ZBP1-RIPK3 complex in human cells, but is dispensable for the formation of the equivalent murine complex. The RIP Homology Interaction Motif (RHIM) in RIPK3 is responsible for this difference between the two species, because replacing the RHIM in human RIPK3 with the RHIM from murine RIPK3 is sufficient to overcome the requirement for RIPK1 in human cells. These observations describe a critical mechanistic difference between mice and humans in how ZBP1 engages in necroptosis, with important implications for treating human diseases.

cell biology↗

Molecular insights into substrate translocation in an elevator-type metal transporter

The Zrt/Irt-like protein (ZIP) metal transporters are key players in maintaining the homeostasis of a panel of essential microelements. The prototypical ZIP from Bordetella bronchiseptica (BbZIP) is an elevator transporter, but how the metal substrate moves along the transport pathway and how the transporter changes conformation to allow alternating access remain to be elucidated. Here, we combined structural, biochemical, and computational approaches to investigate the process of metal substrate translocation along with the global structural rearrangement. Our study revealed an upward hinge motion of the transport domain in a high-resolution crystal structure of a cross-linked variant, elucidated the mechanisms of metal release from the transport site into the cytoplasm and activity regulation by a cytoplasmic metal-binding loop, and unraveled an unusual elevator mode in enhanced sampling simulations that distinguishes BbZIP from other elevator transporters. This work provides important insights into the metal transport mechanism of the ZIP family.

biochemistry↗

Automatic diagnostics of electroencephalography pathology based on multi-domain feature fusion

Electroencephalography (EEG) serves as a practical auxiliary tool deployed to diagnose diverse brain-related disorders owing to its exceptional temporal resolution, non-invasive characteristics, and cost-effectiveness. In recent years, with the advancement of machine learning, automated EEG pathology diagnostics methods have flourished. However, most existing methods usually neglect the crucial spatial correlations in multi-channel EEG signals and the potential complementary information among different domain features, both of which are keys to improving discrimination performance. In addition, latent redundant and irrelevant features may cause overfitting, increased model complexity, and other issues. In response, we propose a novel feature-based framework designed to improve the diagnostic accuracy of multi-channel EEG pathology. This framework first applies a multi-resolution decomposition technique and a statistical feature extractor to construct a salient time-frequency feature space. Then, spatial distribution information is channel-wise extracted from this space to fuse with time-frequency features, thereby leveraging their complementarity to the fullest extent. Furthermore, to eliminate the redundancy and irrelevancy, a two-step dimension reduction strategy, including a lightweight multi-view time-frequency feature aggregation and a non-parametric statistical significance analysis, is devised to pick out the features with stronger discriminative ability. Comprehensive examinations of the Temple University Hospital Abnormal EEG Corpus V. 2.0.0 demonstrate that our proposal outperforms state-of-the-art methods, highlighting its significant potential in clinically automated EEG abnormality detection.

bioengineering↗

Genome-wide CRISPRi-seq identified ferredoxin-NADP reductase FprB as a synergistic target for gallium therapy in Pseudomonas aeruginosa

With the rise of antibiotic-resistant bacteria, non-antibiotic therapies like gallium are increasingly gaining attention. Gallium ions exhibit potent activity against multidrug-resistant bacteria and intravenous gallium nitrite is under phase 2 clinical trials to treat chronic Pseudomonas aeruginosa infections in cystic fibrosis patients. However, its clinical efficacy is constrained by the achievable peak concentration in human tissue. To address this limitation, we applied a genome-wide CRISPR interference approach (CRISPRi-seq), to identify potential synergistic targets with gallium. Through the systemic screening, we classified the essential genes by response time and growth reduction, pinpointing the most vulnerable therapeutic targets in this species. In addition, we identified a highly conserved gene fprB, encoding a ferredoxin-NADP+ reductase, the downregulation of which dramatically sensitized the cells to gallium. Using a null mutant, we confirmed the loss of fprB lowers the minimum inhibitory concentration of gallium from 320 {micro}M to 10 {micro}M and shifted galliums mode of action from bacteriostatic to bactericidal. Further investigation revealed that FprB plays a critical role in modulating oxidative stress induced by gallium, via control of the iron homeostasis and reactive oxygen species accumulation. Deleting fprB also enhanced galliums efficacy against biofilms formation and improved outcomes in murine lung infection model of P. aeruginosa, suggesting FprB as a promising drug target in combination with gallium. Overall, our data showed CRISPRi-seq as a powerful tool for systematic genetic analysis of P. aeruginosa, advancing identification of novel therapeutic targets.

microbiology↗

Investigating the role of axonal localization of sex peptide receptor in post-mating responses of female Drosophila melanogaster

This study elucidates the molecular mechanisms underlying the axonal localization of the sex peptide receptor, a pivotal G-protein coupled receptor in the Drosophila melanogaster post-mating response cascade. Utilizing transgenic expression, neuronal labeling, and bioinformatics analyses, we demonstrate that the N-terminal domain of SPR is indispensable for its axonal targeting in both Drosophila larval ventral nerve cord neurons and mouse hippocampal neurons. Deletion of the N-terminal domain abolished axonal localization, highlighting its critical role in this process. Intriguingly, the C-terminal domain of SPR appears to play a subordinate role in axonal targeting. Bioinformatical analysis revealed a striking homology between the N-terminus of SPR and the Broad-complex, Tramtrack, and Bric-a-brac/poxvirus and zinc finger family of proteins. The BTB domain, a conserved protein-protein interaction domain within this family, is implicated in diverse cellular processes and axonal targeting. Further investigation into the role of the BTB domain-like region in SPR could provide valuable insights into the molecular underpinnings of axonal targeting and post-mating responses in Drosophila. This research contributes to our understanding of the intricate mechanisms governing GPCR localization and function in the context of reproductive biology and neuronal signaling.

neuroscience↗

Low-cost and highly efficient generation of near-complete bacterial pathogen genomes by TELL-Seq

Recent evidences suggest that de novo genome assembly can provide additional insights into genomic variation landscape beyond short-read NGS analyses. Despite the advent of longread sequencing technologies, generating high-quality bacterial genome assemblies remains expensive and requires high-quality and large quantities of DNA. TELL-Seq, an emerging linked-read technology, has been reported as a low-cost alternative for producing nearcomplete genome assembly in certain bacterial species. However, a systematic assessment of its performance and characteristics in de novo bacterial genome assembly has not yet been conducted. To address this, we benchmarked TELL-Seq using a set of clinical and standard bacterial pathogens with a wide range of genome size (2.0 6.4 Mbp), GC-content (32% - 68%), genome complexity (mappability from 0.15 to 0.60) and Gram types. Our findings indicate that, with 1/6 cost and 1/15,000 of DNA compared to PacBio HiFi, TELL-Seq could generate as high quality near-complete bacterial genome assemblies. The optimal depth for assembly is around 200x, as increased depth improves contiguity and completeness, though quality plateaus at 250x. In general, genome complexity was significantly correlated with assembly quality, but GC-content was not. Nevertheless, genomes with extreme GC-content may require higher depths for accurate assembly. Our study suggests that TELL-Seq could be a scalable method for large-scale bacterial genomic surveys. The data generated from this study could serve as a benchmark dataset for further algorithm development. Impact StatementAn increasing body of literature have shown that de novo genome assembles could provide additional insights into genomic variation beyond standard short-read technologies. Its particularly useful in clinical and epidemiological studies of bacteria, due to high variable nature of their genomes. Although great advances have been made in long-read sequencing technology, its still expensive with high requirement over sample DNAs quality and quantity, limiting its adoption in large-scale studies or surveys. Linked-read technology is an inexpensive alternative which used single molecule barcoding to mark origin of reads for better scaffolding of contigs assembled from normal short reads. TELL-Seq, as one of these promising technologies, was reported to be able to inexpensively and efficiently generate near-complete bacterial de novo genomic assemblies with low DNA inputs. Theres not yet a systematic benchmarking of this technology in bacterial pathogens. In this study, a set of clinically important bacterial pathogens with a wide spectrum of GC-content, genome size, genome complexity, and Gram Type were used to investigate the performance of TELL-Seq technology in de novo genome assembly. We found that, with about 1/6 of cost and 1/15000 of DNA quantity, it could generate comparable de novo assemblies compared to standard reference genomes or PacBio HiFi assemblies, while beating conventional short-read assemblies. We found several key factors, such as genome complexity, and sequencing depth, which would impact the quality of the assembly. Our study suggests that a sequencing depth of 200x is sufficient to achieve satisfactory results. Our study has revealed characteristics of this technology in bacterial genome assembly and paved the way for its large-scale application in clinical or epidemiological surveys. Data SummaryO_LIRaw sequencing data for all isolates have been deposited to SRA, accessible through these NCBI BioProject PRJNA1133244. C_LIO_LIA full list of SRA BioSample accession numbers are available in Tab S5. C_LIO_LIAssemblies and analyses companion this paper is available at: https://github.com/x-lab/tellseq_bacteria C_LI

bioinformatics↗

Targeting Interferon-Driven Inflammatory Memory Prevents Epigenetic Evolution of Cancer Immunotherapy Resistance

Acquired resistance is a growing obstacle to durable responses after cancer immune checkpoint blockade (ICB). The mechanisms by which heterogeneous tumors evolve under immunotherapy pressure and strategies targeting key populations to prevent relapse are poorly understood. We show that chronic interferon (IFN) enables a subpopulation of cancer cells to acquire inflammatory memory and express memory ISGs, a subset of IFN-stimulated genes enriched for immune evasion properties, leading to subclonal epigenetic evolution of ICB-resistant states. Inflammatory memory is epigenetically encoded through chronic virus mimicry - feedforward MDA5 signaling likely activated by endogenous retroelements. While JAK inhibitors can improve ICB response, combining them with TBK1 inhibitors collapses this feedforward mechanism, erasing inflammatory memory and preventing differentiation into resistance states. Across human cancers, small subpopulations of memory ISG-expressing cells are prevalent and coupled to T cell exhaustion, suggesting inflammatory memory may be a common mechanism of acquired resistance targetable by JAK plus TBK1 inhibition.

immunology↗

A Self-Assembling Immune-Featured Osteosarcoma Patient/PDX Derived Organoid Model and Biobank for Personalized Immune Therapy

Osteosarcoma (OS) exhibit intra- and inter-heterogeneity, complicating the exploration of effective therapeutic strategies. Traditional in vitro and in vivo models are limited in inheriting biological and genomic heterogeneities of OS patients, even in inheriting the features on tumor microenvironment. The prolonged generation time of current models makes the drug development of OS slow and is not suitable to clinically rapid timing. Here, we introduce methods for generating and biobanking patient/PDX-derived osteosarcoma organoids (OS PD(X)Os) that recapitulate the histological, biological and genomic features of their paired OS patients. OS PD(X)Os can be generated quickly with high reliability in vitro or transplanted to immunodeficient mice. We further demonstrate an immune-featured OS PD(X)O (named iOS) model and its method for testing personalized chemotherapy response, personalized immune therapeutic strategy and target drug development, such as a novel PRMT5MTA inhibitor ARPN2169 on MTAP-deleted OS. Our studies show that iOS models maintain many typical features of OS and could be rapidly employed to investigate patient-specific therapeutic strategies. Additionally, our biobank establishes a rich resource for basic, translational and even clinical OS researches.

cancer biology↗

Metabolic Segregation and Characteristic Genes of the Key Functional Populations in Anaerobic Digestion Consortia

Enrichment experiment integrated with genome-centric meta-omics analysis revealed that metabolic specificity, rather than metabolic flexibility, governs the anaerobic digestion (AD) ecosystem. This study provides new insights into interspecies electron transfer in the AD process, highlighting a segregation in the metabolism of H2 and formate. Our findings indicate that H2 serves as the primary electron sink for recycling redox cofactors, NAD and oxidized ferredoxin (Fdox), during primary fermentation. In contrast, formate predominates in the co- occurring secondary fermentation, particularly under conditions of elevated H2 concentrations. Notably, no evidence of biochemical interconversion between H2 and formate was identified in the primary fermenting bacteria or in syntrophs enriched in this study. This segregation of H2 and formate metabolism likely benefit the anaerobic oxidation of butyrate and propionate with a higher tolerance to H2 accumulation. Furthermore, this study underscores the functional partitioning among microbial populations within key niches of the AD bioprocess: primary fermentation, secondary fermentation (syntrophic acetogenesis), hydrogenotrophic methanogenesis, and acetoclastic methanogenesis. Through genome-centric analysis of the AD microbiome, we identified several key functional gene clusters, highlighting the potential for improving genome-centric genotype-phenotype correlations, which is particularly valuable for strict anaerobes that remain challenging to isolate and characterize in pure culture.

genomics↗

Human Vascularized Macrophage-Islet Organoids to Model Immune-Mediated Pancreatic β cell Pyroptosis upon Viral Infection

There is a paucity of human models to study immune-mediated host damage. Here, we utilized the GeoMx spatial multi-omics platform to analyze immune cell changes in COVID-19 pancreatic autopsy samples, revealing an accumulation of proinflammatory macrophages. Single cell RNA-seq analysis of human islets exposed to SARS-CoV-2 or Coxsackievirus B4 (CVB4) viruses identified activation of proinflammatory macrophages and {beta} cell pyroptosis. To distinguish viral versus proinflammatory macrophage-mediated {beta} cell pyroptosis, we developed human pluripotent stem cell (hPSC)-derived vascularized macrophage-islet (VMI) organoids. VMI organoids exhibited enhanced marker expression and function in both {beta} cells and endothelial cells compared to separately cultured cells. Notably, proinflammatory macrophages within VMI organoids induced {beta} cell pyroptosis. Mechanistic investigations highlighted TNFSF12-TNFRSF12A involvement in proinflammatory macrophage-mediated {beta} cell pyroptosis. This study established hPSC- derived VMI organoids as a valuable tool for studying immune cell-mediated host damage and uncovered mechanism of {beta} cell damage during viral exposure.

developmental biology↗

A biodegradable and restorative peripheral neural interface for the interrogation of neuropathic injuries

Monitoring the early-stage healing of severe traumatic nerve injuries is essential to gather physiological and pathological information for timely interventions and optimal clinical outcomes. While implantable peripheral nerve interfaces provide direct access to nerve fibers for precise interrogation and modulation, conventional non-degradable designs pose limited utilization in nerve injury rehabilitation. Here, we introduce a biodegradable and restorative neural interface for wireless real-time tracking and recovery of long-gap nerve injuries. Leveraging machine learning techniques, this electronic platform deciphers nerve recovery status and identifies traumatic neuroma formation at the early phase, enabling timely intervention and significantly improved therapeutic outcomes. The biodegradable nature of the device eliminates the need for retrieval procedures, reducing infection risks and secondary tissue damage. This research sheds light on bioresorbable multifunctional peripheral nerve interfaces for probing neuropathic injuries, offering vital information for early diagnosis and therapeutic intervention.

bioengineering↗

PerturbAtlas: A Comprehensive Atlas of Public Genetic Perturbation Bulk RNA-seq Datasets

Manipulating gene expression is crucial for understanding gene function, with high-throughput sequencing techniques such as RNA-seq elucidating the downstream mechanisms involved. However, the lack of a standardized metadata format for small-scale perturbation expression datasets in public repositories hinders their reuse. To address this issue, we developed PerturbAtlas, an add-value resource that re-analyzes publicly archived RNA-seq libraries to provide quantitative data on gene expression, transcript profiles, and alternative splicing events following genetic perturbation. PerturbAtlas assists users in identifying trends at the gene and isoform levels in perturbation assays by re-analyzing a curated set of 122,801 RNA-seq libraries across 13 species. This resource is freely available at https://perturbatlas.kratoss.site as both raw data tables and an interactive browser, allowing searches by species, tissue, or genomic features. The results provide detailed information on alterations following perturbations, accessible through both forward and reverse approaches, thereby enabling the exploration of perturbation consequences and the identification of potential causal perturbations. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=199 SRC="FIGDIR/small/605482v1_ufig1.gif" ALT="Figure 1"> View larger version (76K): org.highwire.dtl.DTLVardef@150012org.highwire.dtl.DTLVardef@b7ac25org.highwire.dtl.DTLVardef@86c4feorg.highwire.dtl.DTLVardef@1ef3341_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗

Investigating the antimicrobial and immunomodulatory effects of honeybee venom peptide apamin in the Drosophila genetic platform.

Apamin, an 18-amino acid peptide neurotoxin, constitutes a significant portion of honeybee venom. Although traditionally recognized for its neurotoxic effects, our research demonstrates that apamin exhibits potent antimicrobial properties when genetically expressed in Drosophila. The antimicrobial efficacy of apamin is independent of its disulfide bonds and is enhanced when the peptide is membrane-tethered. This expression selectively targets and inhibits specific harmful bacterial species, such as Pseudomonas aeruginosa, Enterococcus faecalis, and Escherichia coli, while promoting beneficial bacteria like Lactobacillus plantarum thereby improving the gut microbiome. The antimicrobial activity of apamin is localized to the gut and is associated with increased proliferation of intestinal stem cells, acidification of the midgut pH, and activation of enteroendocrine cell calcium signaling. Furthermore, apamins antimicrobial function is dependent on specific peptidoglycan recognition proteins, with PGRP-LA and PGRP-SCs being essential. Apamin expression alone is sufficient to restore the integrity of the gut barrier compromised by stressed conditions. Ultimately, apamin supplementation enhances honeybee gut health, particularly in the presence of ingested bacteria. The expression of other honeybee antimicrobial peptides also significantly reduces bacterial infection in flies. Overall, our study provides a comprehensive understanding of the molecular function and regulation of honeybee venom peptides and antimicrobial peptides, utilizing the Drosophila model system to unravel their mechanisms of action and therapeutic potential.

immunology↗

Structural characterization of two full length γδTCR/CD3 complexes

The T-cell receptor (TCR)/CD3 complex plays an essential role in the immune response and is a key player in cancer immunotherapies. There are two classes of TCR/CD3 complexes, defined by their TCR chain usage ({beta} or {gamma}{delta}). Recently reported structures have revealed the organization of the {beta} TCR/CD3 complex, but similar studies regarding the {gamma}{delta} TCR/CD3 complex have lagged behind. Here, we report cryoelectron microscopy (cryoEM) structural analysis of two full-length {gamma}{delta} TCRs, G115 (V{gamma}9V{delta}2) and 9C2 (V{gamma}5V{delta}1), in complex with CD3 subunits. Our results show that the overall subunit organization of the {gamma}{delta} TCR-CD3 complexes is similar to {beta} TCRs. However, both {gamma}{delta} TCRs display highly mobile extracellular domains (ECDs), unlike {beta} TCRs, which have TCR ECDs that are rigidly coupled to its transmembrane (TM) domains. We corroborate this finding in cells by demonstrating that a {gamma}{delta} T-cell specific antibody can bind a site that would be inaccessible in the more rigid {beta} TCR/CD3 complex. Furthermore, we observed that a V{gamma}5V{delta}1 complex forms a TCR {gamma}5-chain mediated dimeric species whereby two TCR/CD3 complexes are assembled. Collectively, these data shed light on {gamma}{delta} TCR/CD3 complex formation and may aid the design of {gamma}{delta} TCR-based therapies.

biochemistry↗

Equip Fusobacterium nucleatum genetic tool kits with compatible shuttle vectors and engineered intermediatory E. coli strains for enhanced transformation efficiency

Fusobacterium nucleatum, an oral microbe, is implicated in various human diseases, including oral-related diseases and tumors. However, efficient transformation was only achieved in limited strains of this bacterium. The challenges in conducting molecular level investigations of most strains due to their genetic intractability have hindered the biological studies of F. nucleatum. The restriction-modification (RM) systems is one of the known obstacles for efficient DNA transformation. Here, we used single molecule real time sequencing to elucidate the RM recognition sites and the corresponding methyltransferases (MTases) in two F. nucleatum strains. Based on the identified MTases, we engineered intermediatory E. coli host strains to bypass the RM systems, and showed that the plasmids harbored by these intermediatory strains can be efficiently electro-transformed, reaching 5000 transformants per microgram plasmids, paving the way for the development of efficient genetic modification tools. Furthermore, we successfully demonstrated that the conjugation-based DNA delivery to F. nucleatum can bypass the requirement of MTase methylations. By exploring the native plasmids from F. nucleatum, we identified new backbones for construction of shuttle vectors and established a dual-plasmid system for the first time, offering new avenues for genetic manipulation in this bacterium. Additionally, we evaluate promoters with variable strengths with a luciferase-based reporter system in F. nucleatum, providing valuable insights for future gene editing studies in bacterium and contributing to our understanding of its pathogenesis. All the tools developed in this study was shared via the WeKwikgene (https://wekwikgene.wllsb.edu.cn/). Impact StatementFusobacterium nucleatum, a key opportunistic pathogen implicated in periodontal diseases, rheumatoid arthritis, and tumors, presents significant challenges due to its limited transformation efficiency and lack of gene-editing tools. In this study, we present an advancement -a streamlined and robust pipeline that enhances transformation efficiency by approximately 103-fold in F. nucleatum, reaching 5000 CFU per microgram plasmids. This represents a significant breakthrough, marking the first report to achieve such a remarkable improvement in transformation efficiency in this pathogen. This improvement paves the way for the genome-wide level mutagenesis study in this bacterium.

microbiology↗

TDP-43 mutations-induced defects in miRNA biogenesis and cytotoxicity by differentially obstructing Dicer activity in Drosophila and in vitro

Mutations in the DNA/RNA-binding protein 43 (TDP-43) can cause amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). As an RNA-binding protein, TDP-43 plays a diverse physiological role in RNA processing and is potentially involved in the pathological progression caused by disease mutations. However, the precise mechanisms linking RNA dysregulation and TDP-43 mutations, which propel disease progression, are not yet fully understood. Here, we demonstrate that TDP-43 and its Drosophila homolog, TBPH, whose mutations crucially perturb Dicer presentation, result in dysregulated miRNA profiles. Genetically modulating the expression or pharmacologically activating Dicer implies unique interactions of TDP-43 A315T and M337V with the Dicer protein, suggesting a specific mechanism of C-terminal disease mutations contributes to the pathological process. Unlike TDP-43 A315T, the M337V mutation causes the assembly of aggregates and reorganizes but functionally preserves the Dicer activity in miRNA processing. Mutations in TDP-43 disrupt miRNA biogenesis by hindering its interaction with Dicer, leading to cytotoxicity and providing mechanistic insight into the pathogenic mutations associated with ALS-FTD.

molecular biology↗

Vimentin promotes collective cell migration through collagen networks via increased matrix remodeling and spheroid fluidity

The intermediate filament (IF) protein vimentin is associated with many diseases with phenotypes of enhanced cellular migration and aggressive invasion through the extracellular matrix (ECM) of tissues, but vimentins role in in-vivo cell migration is still largely unclear. Vimentin is important for proper cellular adhesion and force generation, which are critical to cell migration; yet the vimentin cytoskeleton also hinders the ability of cells to squeeze through small pores in ECM, resisting migration. To identify the role of vimentin in collective cell migration, we generate spheroids of wide-type and vimentin-null mouse embryonic fibroblasts (mEFs) and embed them in a 3D collagen matrix. We find that loss of vimentin significantly impairs the ability of the spheroid to collectively expand through collagen networks and remodel the collagen network. Traction force analysis reveals that vimentin null spheroids exert less contractile force than their wild-type counterparts. In addition, spheroids made of mEFs with only vimentin unit length filaments (ULFs) exhibit similar behavior as vimentin-null spheroids, suggesting filamentous vimentin is required to promote 3D collective cell migration. We find the vimentin-mediated collective cell expansion is dependent on matrix metalloproteinase (MMP) degradation of the collagen matrix. Further, 3D vertex model simulation of spheroid and embedded ECM indicates that wild-type spheroids behave more fluid-like, enabling more active pulling and reconstructing the surrounding collagen network. Altogether, these results signify that VIF plays a critical role in enhancing migratory persistence in 3D matrix environments through MMP transportation and tissue fluidity.

biophysics↗

An organoid co-culture model for probing systemic anti-tumor immunity in lung cancer

Deciphering the interactions between tumor micro- and systemic immune macro-environment is essential for developing more effective cancer diagnosis and treatment strategies. Here, we established a gel-liquid interface (GLI) co-culture of lung cancer organoids (LCOs) and paired peripheral blood mononuclear cells (PBMCs), featuring with enhanced interactions of immune cells and tumor organoids, to mimic the in vivo systemic anti-tumor immunity induced by immune checkpoint inhibitors (ICI). The co-culture model recapitulates the in vivo ICI-induced T cell recruitment and subsequent tumor regression, predicting the clinical results precisely. We demonstrated that circulating tumor-reactive T cells, which are effector memory-like with high expression levels of GNLY, CD44 and CD9, can serve as an indicator of the immunotherapy efficacy. Interestingly, enhanced inflammatory signaling in blood T cells is accompanied with prompted exhaustion and compromised anti-tumor function, when encountering with organoids. Our findings suggest that the GLI co-culture can be used for developing diagnostic strategies for precision immunotherapies as well as understanding the underlying mechanisms. Summary figure O_FIG O_LINKSMALLFIG WIDTH=178 HEIGHT=200 SRC="FIGDIR/small/597327v1_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@a0829dorg.highwire.dtl.DTLVardef@1df3083org.highwire.dtl.DTLVardef@1ea1065org.highwire.dtl.DTLVardef@1da9464_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗