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- Reference(Jun 2025) Journal for Immunotherapy of Cancer 13 6
Serotonin receptor 5-HT2A as a potential target for HCC immunotherapy
AbstractBackgroundWhile recent clinical trials of combination immunotherapies for hepatocellular carcinoma (HCC) have shown promising clinical efficacy and survival improvements breakthroughs, there is still much room for further improvement. A key limiting factor for HCC immunotherapy is the intrinsic immunosuppression within the liver microenvironment, resulting in suboptimal priming of tumor-specific CD8 cytotoxic T cells and thus immune evasion by the tumor. Hence, identifying new key molecular pathways suppressing T-cell responses within the liver is critical for the rational design of more effective combination immunotherapies for HCC.MethodsWe identified the 5-HT2A serotonin receptor as a potential target for HCC immunotherapy in a chemical screening approach and validated that targeting 5-HT2A signaling could be a viable approach for HCC immunotherapy via in vitro and in vivo studies.ResultsDisruption of 5-HT2A signaling using either a selective antagonist small molecule, ketanserin, or by knockout of its coding gene Htr2a augments the cytotoxic effector phenotype of mouse CD8 T cells activated in vitro with immunosuppressive liver non-parenchymal cells. Ketanserin treatment of in vitro activated human CD8 T cells also increased expression of the cytotoxic effector molecules granzyme B and perforin. Abrogation of 5-HT2A signaling was associated with increased expression of cytotoxicity-related genes such as granzyme B and reduced expression of transcription factors downstream of MAP kinase signaling. In vivo, systemic ketanserin treatment significantly prolonged survival of HCC tumor-bearing mice and was non-inferior to α-programmed death ligand 1 (PD-L1)+α-vascular endothelial growth factor A (VEGFA) combination antibody treatment. Combining ketanserin with αPD-L1+αVEGFA antibodies also significantly prolonged survival relative to control-treated mice while preserving the occurrence of complete tumor regression observed with αPD-L1+αVEGFA treatment alone.ConclusionsTogether, our data describe a role for 5-HT2A as a negative regulator of the cytotoxic effector phenotype in CD8 T cells and highlight the therapeutic potential of targeting 5-HT2A for HCC immunotherapy.Catalog #: Product Name: 18958 EasySep™ Mouse CD90.1 Positive Selection Kit Catalog #: 18958 Product Name: EasySep™ Mouse CD90.1 Positive Selection Kit Reference(Jun 2025) PLOS Biology 23 6Multinucleated giant cells are hallmarks of ovarian aging with unique immune and degradation-associated molecular signatures
The ovary is one of the first organs to exhibit signs of aging, characterized by reduced tissue function, chronic inflammation, and fibrosis. Multinucleated giant cells (MNGCs), formed by macrophage fusion, typically occur in chronic immune pathologies, including infectious and non-infectious granulomas and the foreign body response, but are also observed in the aging ovary. The function and consequence of ovarian MNGCs remain unknown as their biological activity is highly context-dependent, and their large size has limited their isolation and analysis through technologies such as single-cell RNA sequencing. In this study, we define ovarian MNGCs through a deep analysis of their presence across age and species using advanced imaging technologies as well as their unique transcriptome using laser capture microdissection. MNGCs form complex interconnected networks that increase with age in both mouse and nonhuman primate ovaries. MNGCs are characterized by high Gpnmb expression, a putative marker of ovarian and non-ovarian MNGCs. Pathway analysis highlighted functions in apoptotic cell clearance, lipid metabolism, proteolysis, immune processes, and increased oxidative phosphorylation and antioxidant activity. Thus, MNGCs have signatures related to degradative processes, immune function, and high metabolic activity. These processes were enriched in MNGCs compared to primary ovarian macrophages, suggesting discrete functionality. MNGCs express CD4 and colocalize with T-cells, which were enriched in regions of MNGCs, indicative of a close interaction between these immune cell types. These findings implicate MNGCs in modulation of the ovarian immune landscape during aging given their high penetrance and unique molecular signature that supports degradative and immune functions. Ovarian multinucleated giant cells are a unique macrophage population that arise within the aging mammalian ovary. This study characterizes their transcriptome in mice, uncovering a potential role in degradation of cellular debris and immune signaling, suggesting a potential contribution to ovarian inflammation during aging.Catalog #: Product Name: 20144 EasySepâ„¢ Buffer 100-0659 EasySepâ„¢ Mouse F4/80 Positive Selection Kit Catalog #: 20144 Product Name: EasySepâ„¢ Buffer Catalog #: 100-0659 Product Name: EasySepâ„¢ Mouse F4/80 Positive Selection Kit Reference(Jun 2025) Molecular Medicine 31Effect of anti-CD4 mAb induced by inhibiting B cell disorder on immune reconstruction of HIV-infected immunological non-responders
BackgroundIn persons living with HIV, antiretroviral therapy (ART) reduces HIV RNA in their plasma and increases CD4 + T lymphocytes, thus restoring their immune function and reducing mortality rates.MethodsThe heavy and light chains of B cell receptor (BCR) were amplified, sequenced, analyzed, and determined to be anti-CD4 mAb. The cytotoxicity of NK cells mediated by the anti-CD4 mAb was assessed using CCK-8, flow cytometry, ELISA, and western blotting. Detecting the viability/regulation of CD4 cells involved inhibiting the attachment of autoantibodies against CD4 to crucial receptors and detecting the inhibition of key molecules in B cells to produce anti-CD4 mAb in patients with immune non-responders (INR). Furthermore, through Phage Random Peptide Library Screening, we discovered that the AAPMFHSSVQLP-CD4 peptide has an affinity for the anti-CD4 mAb.ResultsAdministering anti-CD4 mAb enhanced NK cytotoxicity. The simultaneous administration of anti-CD4 mAb alongside GST-CD4 alleviated the harmful impacts of anti-CD4 mAb on the CD3 + population in humanized mice, and HIV virus (p24). Individuals diagnosed with INR displayed abnormal B cell activity, particularly with elevated BAFFR expression and increased levels of anti-CD4 mAb. Nevertheless, suppression of BAFFR hindered B cell function and decreased the production of anti-CD4 mAb. In HIV-infected individuals, the dysregulation of B-cells led to the production of anti-CD4 mAb, which in turn facilitated NK cell cytotoxicity and the CD4 + T effect by upregulating the expression of BAFFR.ConclusionThe dysregulation of B-cells in person living with HIV increased the production of anti-CD4 mAb, which in turn promoted NK cell cytotoxicity and the CD4 + T effect.Supplementary InformationThe online version contains supplementary material available at 10.1186/s10020-025-01286-3. Highlights1) B-cell dysregulation increased anti-CD4 mAb levels.2) B cells are abnormally active in patients with INR.3) Knockdown of BAFFR obviously reduced the secretion of anti-CD4 mAb.Supplementary InformationThe online version contains supplementary material available at 10.1186/s10020-025-01286-3.Catalog #: Product Name: 19054 EasySep™ Human B Cell Enrichment Kit Catalog #: 19054 Product Name: EasySep™ Human B Cell Enrichment Kit Reference(Jun 2025) Nature Communications 16Circulating cell-free DNA methylation patterns indicate cellular sources of allograft injury after liver transplant
Post-transplant complications reduce allograft and recipient survival. Current approaches for detecting allograft injury non-invasively are limited and do not differentiate between cellular mechanisms. Here, we monitor cellular damages after liver transplants from cell-free DNA (cfDNA) fragments released from dying cells into the circulation. We analyzed 130 blood samples collected from 44 patients at different time points after transplant. Sequence-based methylation of cfDNA fragments were mapped to an atlas of cell-type-specific DNA methylation patterns derived from 476 methylomes of purified cells. For liver cell types, DNA methylation patterns and multi-omic data integration show distinct enrichment in open chromatin and functionally important regulatory regions. We find that multi-tissue cellular damages post-transplant recover in patients without allograft injury during the first post-operative week. However, sustained elevation of hepatocyte and biliary epithelial cfDNA within the first month indicates early-onset allograft injury. Further, cfDNA composition differentiates amongst causes of allograft injury indicating the potential for non-invasive monitoring and intervention. Current approaches to detect allograft damages non-invasively are limited and do not differentiate between cellular mechanisms. Here, the authors show that the composition of cell-free DNA in blood samples can reveal cellular causes of allograft injury after liver transplant.Catalog #: Product Name: 18000 EasySepâ„¢ Magnet Catalog #: 18000 Product Name: EasySepâ„¢ Magnet Reference(May 2025) Nature Methods 22 6Single-cell ultra-high-throughput multiplexed chromatin and RNA profiling reveals gene regulatory dynamics
Enhancers and transcription factors (TFs) are crucial in regulating cellular processes. Current multiomic technologies to study these elements in gene regulatory mechanisms lack multiplexing capability and scalability. Here we present single-cell ultra-high-throughput multiplexed sequencing (SUM-seq) for co-assaying chromatin accessibility and gene expression in single nuclei. SUM-seq enables profiling hundreds of samples at the million cell scale and outperforms current high-throughput single-cell methods. We demonstrate the capability of SUM-seq to (1) resolve temporal gene regulation of macrophage M1 and M2 polarization to bridge TF regulatory networks and immune disease genetic variants, (2) define the regulatory landscape of primary T helper cell subsets and (3) dissect the effect of perturbing lineage TFs via arrayed CRISPR screens in spontaneously differentiating human induced pluripotent stem cells. SUM-seq offers a cost-effective, scalable solution for ultra-high-throughput single-cell multiomic sequencing, accelerating the unraveling of complex gene regulatory networks in cell differentiation, responses to perturbations and disease studies. This work presents SUM-seq, an ultra-high-throughput method for co-profiling chromatin accessibility and gene expression in single nuclei across multiplexed samples, advancing the study of gene regulation in diverse biological systems.Catalog #: Product Name: 10981 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium 18000 EasySepâ„¢ Magnet 100-0956 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Catalog #: 10981 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium Catalog #: 18000 Product Name: EasySepâ„¢ Magnet Catalog #: 100-0956 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Reference(May 2025) Frontiers in Pharmacology 16 1Enhanced resistance to Listeria infection in mice surviving sepsis: the role of lipid metabolism and myeloid cell reprogramming
IntroductionImmune resilience is the capacity of the immune system to recover from sepsis-induced organ injury and reestablish host defense. While sepsis survivors are often viewed as immunocompromised, recent studies suggest that some may acquire adaptive immune traits that enhance resistance to secondary infections.MethodsWe employed a murine cecal ligation and puncture (CLP) model to study polymicrobial sepsis and subsequent immune responses. Listeria monocytogenes was used as a model intracellular pathogen to assess immune protection. We analyzed myeloid cell phenotypes using single-cell RNA sequencing and evaluated lipid metabolic changes through quantitative RT-PCR, immunohistochemistry, serum cytokine assays, and plasma lipidomics.ResultsSepsis-surviving mice showed enhanced resistance to Listeria infection. Single-cell RNA sequencing revealed transcriptional reprogramming in splenic CD11b+Ly6Chigh myeloid cells, including downregulation of lipoprotein lipase and lipid efflux genes. CD11b+ myeloid cells exhibited increased lipid droplet accumulation, accompanied by elevated serum interferon-gamma (IFN-γ) levels. Plasma lipidomics identified systemic lipid remodeling, with increased phosphatidylserine and decreased phosphatidylinositol and phosphatidylglycerol levels.DiscussionOur findings suggest that sepsis survival induces lipid metabolic reprogramming in myeloid cells, contributing to enhanced immunity against intracellular pathogens. These insights reveal potential therapeutic targets within lipid metabolic pathways to improve host defense in sepsis survivors.Catalog #: Product Name: 19861 EasySep™ Mouse Monocyte Isolation Kit Catalog #: 19861 Product Name: EasySep™ Mouse Monocyte Isolation Kit Reference(Jun 2025) BMJ Oncology 4 1Osteoclast-expanded supercharged NK cells perform superior antitumour effector functions
AbstractObjectiveNatural killer (NK) cells are the largest innate lymphocyte subset with potent antitumour and antiviral functions. However, clinical utilisation of human NK cells is hampered due to a lack of reliable methods to augment their antitumour potential. We demonstrated technology in which human NK cells were cocultured with osteoclasts in the presence of probiotic bacteria. This approach significantly augmented the antitumour cytotoxicity and polyfunctionality of human NK cells, resulting in the generation of supercharged NK (sNK) cells.Methods and analysisWe explored the proteomic, transcriptomic and functional characterisation of sNK cells using cell imaging, flow cytometric analysis, 51-chromium release cytotoxicity assay, ELISA, ELIspot, IsoPLexis single-cell secretome analysis, proteomic analysis, RNA analysis, western blot and enzyme kinetics.ResultsWe found that sNK cells were less susceptible to split anergy and tumour-induced exhaustion. Proteomic analyses revealed that sNK cells significantly increased their cell motility and proliferation. Single-cell transcriptomes uncovered sNK cells undertaking a unique differentiation trajectory and turning on STAT1, JUN, BHLHE40, ELF1, MAX and MYC regulons essential for augmenting antitumour effector functions and proliferation, respectively. Both proteomic and single-cell transcriptomes revealed that an increase in Cathepsin C helped to augment the quantity and function of Granzyme B.ConclusionsThese results support that this unique method produces potent NK cells for clinical utilisation and delineate the molecular mechanisms associated with this process.Catalog #: Product Name: 19055 EasySepâ„¢ Human NK Cell Enrichment Kit 19059 EasySepâ„¢ Human Monocyte Enrichment Kit Catalog #: 19055 Product Name: EasySepâ„¢ Human NK Cell Enrichment Kit Catalog #: 19059 Product Name: EasySepâ„¢ Human Monocyte Enrichment Kit Reference(May 2025) Frontiers in Immunology 16H3K27me3 modulates trained immunity of monocytes in HDM-allergic diseases
BackgroundMonocytes have been confirmed to increase in persistently food-allergic children. A phenomenon of innate immune memory, called trained immunity, has also been observed in monocytes from allergic children. However, the underlying mechanism remains poorly understood.MethodsWe enrolled a cohort of HDM-allergic children alongside age-matched healthy controls and established an HDM-sensitized allergic mouse model. Flow cytometric analyses were conducted to quantify monocyte frequencies in clinical cohorts and experimental animals. We performed integrated transcriptomic profiling via RNA-seq combined with chromatin occupancy analysis using CUT&Tag technology in parallel human and murine samples to elucidate the molecular mechanisms.ResultsIn our study, we demonstrated a reduced H3K27me3 methylation level accompanied by an increased proportion and a proinflammatory transcriptional memory in monocytes from house dust mite (HDM)-allergic human subjects. The same transcriptional and epigenetic phenotype was also confirmed in HDM-sensitized mice. Finally, the administration of GSK-J4, which upregulates H3K27me3 level in murine monocytes, attenuated the inflammatory response in vitro and in vivo.ConclusionsOur study confirms that H3K27me3 methylation modulates the trained immunity in monocytes and regulates HDM-allergic diseases through an inflammatory-dependent mechanism.Catalog #: Product Name: 19861 EasySepâ„¢ Mouse Monocyte Isolation Kit Catalog #: 19861 Product Name: EasySepâ„¢ Mouse Monocyte Isolation Kit Reference(May 2025) STAR Protocols 6 2Protocol for CRISPR-mediated deletion of cis-regulatory element in murine Th17 cells for in vivo assessment of effector function
SummaryStudying the cis-regulatory elements (CREs) of genes in Th17 cells during autoimmune disease progression, such as experimental autoimmune encephalomyelitis (EAE), is often limited by the availability of gene-edited mice. Here, we present a protocol for CRISPR-mediated deletion of a CRE in murine Th17 cells for in vivo assessment of effector function in EAE. We describe steps for dual U6gRNA construction, preparation of retroviruses, viral delivery, and Th17 differentiation. We then detail procedures for in vivo functionality analysis.For complete details on the use and execution of this protocol, please refer to Zhong et al.1,2 Graphical abstract Highlights•Steps for designing and cloning dual U6gRNA cassettes to delete a specific CRE•Instructions for optimized retrovirus production and transduction into CD4+ T cells•Guidance on Th17 differentiation and confirmation of CRE deletion in cultured T cells•Procedures for adoptive transfer of CRISPR-edited Th17 cells to assess in vivo function Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics. Studying the cis-regulatory elements (CREs) of genes in Th17 cells during autoimmune disease progression, such as experimental autoimmune encephalomyelitis (EAE), is often limited by the availability of gene-edited mice. Here, we present a protocol for CRISPR-mediated deletion of a CRE in murine Th17 cells for in vivo assessment of effector function in EAE. We describe steps for dual U6gRNA construction, preparation of retroviruses, viral delivery, and Th17 differentiation. We then detail procedures for in vivo functionality analysis.Catalog #: Product Name: 18000 EasySep™ Magnet Catalog #: 18000 Product Name: EasySep™ Magnet Reference(May 2025) GigaScience 14 3Lifting the curse from high-dimensional data: automated projection pursuit clustering for a variety of biological data modalities
AbstractUnsupervised clustering is a powerful machine-learning technique widely used to analyze high-dimensional biological data. It plays a crucial role in uncovering patterns, structures, and inherent relationships within complex datasets without relying on predefined labels. In the context of biology, high-dimensional data may include transcriptomics, proteomics, and a variety of single-cell omics data. Most existing clustering algorithms operate directly in the high-dimensional space, and their performance may be negatively affected by the phenomenon known as the curse of dimensionality. Here, we show an alternative clustering approach that alleviates the curse by sequentially projecting high-dimensional data into a low-dimensional representation. We validated the effectiveness of our approach, named automated projection pursuit (APP), across various biological data modalities, including flow and mass cytometry data, scRNA-seq, multiplex imaging data, and T-cell receptor repertoire data. APP efficiently recapitulated experimentally validated cell-type definitions and revealed new biologically meaningful patterns.Catalog #: Product Name: 19058 EasySepâ„¢ Human Monocyte Enrichment Kit without CD16 Depletion 19654 EasySepâ„¢ Direct Human PBMC Isolation Kit Catalog #: 19058 Product Name: EasySepâ„¢ Human Monocyte Enrichment Kit without CD16 Depletion Catalog #: 19654 Product Name: EasySepâ„¢ Direct Human PBMC Isolation Kit Reference(May 2025) Journal of Inflammation (London, England) 22LL-37 and citrullinated-LL-37 modulate IL-17A/F-mediated responses and selectively suppress Lipocalin-2 in bronchial epithelial cells
BackgroundLevels of the human cationic antimicrobial host defence peptide LL-37 are enhanced in the lungs during neutrophilic airway inflammation. LL-37 drives Th17 differentiation, and Th17 cells produce IL-17A and IL-17F which form the biologically active heterodimer IL-17A/F. While IL-17 is a critical mediator of neutrophilic airway inflammation, LL-37 exhibits contradictory functions; LL-37 can both promote and mitigate neutrophil recruitment depending on the inflammatory milieu. The impact of LL-37 on IL-17-induced responses in the context of airway inflammation remains largely unknown. Therefore, we examined signaling intermediates and downstream responses mediated by the interplay of IL-17A/F and LL-37 in human bronchial epithelial cells (HBEC). As LL-37 can become citrullinated during airway inflammation, we also examined LL-37-mediated downstream responses compared to that with citrullinated LL-37 (citLL-37) in HBEC.ResultsUsing an aptamer-based proteomics approach, we identified proteins that are altered in response to IL-17A/F in HBEC. Proteins enhanced in response to IL-17A/F were primarily neutrophil chemoattractants, including chemokines and proteins associated with neutrophil migration such as lipocalin-2 (LCN-2). We showed that selective depletion of LCN-2 mitigates neutrophil migration, functionally demonstrating LCN-2 as a critical neutrophil chemoattractant. We further demonstrated that LL-37 and citLL-37 selectively suppress IL-17A/F-induced LCN-2 abundance in HBEC. Mechanistic studies revealed that LL-37 and citLL-37 suppresses IL-17 A/F-mediated enhancement of C/EBPβ, a transcription factor required for LCN-2 production. In contrast, LL-37 and citLL-37 enhance the abundance of ribonuclease Regnase-1, which is a negative regulator of IL-17 and LCN-2 in HBEC. In an animal model of allergen-challenged airway inflammation with elevated IL-17A/F and neutrophil elastase in the lungs, we demonstrated that CRAMP (mouse orthologue of LL-37) negatively correlates with LCN-2.ConclusionsOverall, our findings showed that LL-37 and citLL-37 can selectively suppress the abundance of IL-17A/F-mediated LCN-2, a protein that is critical for neutrophil migration in HBEC. These results suggest that LL-37, and its modified citrullinated form, have the potential to negatively regulate IL-17-mediated neutrophil migration during airway inflammation. To our knowledge, this is the first study to report that the immunomodulatory function of LL-37 enhances the RNA binding protein Regnase-1, suggesting that a post-transcriptional mechanism of action is mediated by the peptide.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12950-025-00446-w.Catalog #: Product Name: 19666 EasySep™ Direct Human Neutrophil Isolation Kit Catalog #: 19666 Product Name: EasySep™ Direct Human Neutrophil Isolation Kit Reference(May 2025) The Journal of Experimental Medicine 222 8A CARMIL2 gain-of-function mutation suffices to trigger most CD28 costimulatory functions in vivo
Zhang et al. demonstrate that the expression of a mutated CARMIL2 protein in CD28-deficient mice induces most of the developmental and functional consequences known to result from CD28 costimulation and in turn triggers potent tumor-specific T cell responses resistant to PD-1 and CTLA-4 blockade. Naive T cell activation requires both TCR and CD28 signals. The CARMIL2 cytosolic protein enables CD28-dependent activation of the NF-κB transcription factor via its ability to link CD28 to the CARD11 adaptor protein. Here, we developed mice expressing a mutation named Carmil2QE and mimicking a mutation found in human T cell malignancies. Naive T cells from Carmil2QE mice contained preformed CARMIL2QE-CARD11 complexes in numbers comparable to those assembling in wild-type T cells after CD28 engagement. Such ready-made CARMIL2QE-CARD11 complexes also formed in CD28-deficient mice where they unexpectedly induced most of the functions that normally result from CD28 engagement in a manner that remains antigen-dependent. In turn, tumor-specific T cells expressing Carmil2QE do not require CD28 engagement and thereby escape to both PD-1 and CTLA-4 inhibition. In conclusion, we uncovered the overarching role played by CARMIL2-CARD11 signals among those triggered by CD28 and exploited them to induce potent solid tumor–specific T cell responses in the absence of CD28 ligands and immune checkpoint inhibitors.Catalog #: Product Name: 19851 EasySep™ Mouse T Cell Isolation Kit Catalog #: 19851 Product Name: EasySep™ Mouse T Cell Isolation Kit Items 1057 to 1068 of 13914 total
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