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Items 1309 to 1320 of 13914 total
- Reference(Feb 2024) iScience 27 3
PCID2 dysregulates transcription and viral RNA processing to promote HIV-1 latency
SummaryHIV-1 latency results from tightly regulated molecular processes that act at distinct steps of HIV-1 gene expression. Here, we characterize PCI domain-containing 2 (PCID2) protein, a subunit of the transcription and export complex 2 (TREX2) complex, to enforce transcriptional repression and post-transcriptional blocks to HIV-1 gene expression during latency. PCID2 bound the latent HIV-1 LTR (long terminal repeat) and repressed transcription initiation during latency. Depletion of PCID2 remodeled the chromatin landscape at the HIV-1 promoter and resulted in transcriptional activation and latency reversal. Immunoprecipitation coupled to mass spectrometry identified PCID2-interacting proteins to include negative viral RNA (vRNA) splicing regulators, and PCID2 depletion resulted in over-splicing of intron-containing vRNA in cell lines and primary cells obtained from PWH. MCM3AP and DSS1, two other RNA-binding TREX2 complex subunits, also inhibit transcription initiation and vRNA alternative splicing during latency. Thus, PCID2 is a novel HIV-1 latency-promoting factor, which in context of the TREX2 sub-complex PCID2-DSS1-MCM3AP blocks transcription and dysregulates vRNA processing. Graphical abstract Highlights•PCID2 is bound to the latent HIV-1 LTR as a transcriptional repressor•PCID2 enforces latency by acting on transcription initiation•PCID2 establishes blocks to alternative splicing during HIV-1 latency•PCID2 misregulates alternative splicing in cells obtained from people with HIV-1 Virology; Cell biologyCatalog #: Product Name: 19052 EasySep™ Human CD4+ T Cell Enrichment Kit Catalog #: 19052 Product Name: EasySep™ Human CD4+ T Cell Enrichment Kit Safety Data SheetCatalog #: Product Name: 100-1336 Human Recombinant IFN alpha 1 Catalog #: 100-1336 Product Name: Human Recombinant IFN alpha 1 Reference(Feb 2024) Nature Communications 15Regulatory T cells use heparanase to access IL-2 bound to extracellular matrix in inflamed tissue
Although FOXP3+ regulatory T cells (Treg) depend on IL-2 produced by other cells for their survival and function, the levels of IL-2 in inflamed tissue are low, making it unclear how Treg access this critical resource. Here, we show that Treg use heparanase (HPSE) to access IL-2 sequestered by heparan sulfate (HS) within the extracellular matrix (ECM) of inflamed central nervous system tissue. HPSE expression distinguishes human and murine Treg from conventional T cells and is regulated by the availability of IL-2. HPSE-/- Treg have impaired stability and function in vivo, including in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. Conversely, endowing monoclonal antibody-directed chimeric antigen receptor (mAbCAR) Treg with HPSE enhances their ability to access HS-sequestered IL-2 and their ability to suppress neuroinflammation in vivo. Together, these data identify a role for HPSE and the ECM in immune tolerance, providing new avenues for improving Treg-based therapy of autoimmunity. Regulatory T cell (Treg) maintenance and function require IL-2, yet this cytokine is only present in low levels in vivo. In this study, the authors demonstrate that that Treg use heparanase to access IL-2 bound to heparan sulfate proteoglycans in the extracellular matrix of inflamed brain tissue in mice.Catalog #: Product Name: 18782 EasySepâ„¢ Mouse CD25 Regulatory T Cell Positive Selection Kit 19852 EasySepâ„¢ Mouse CD4+ T Cell Isolation Kit Catalog #: 18782 Product Name: EasySepâ„¢ Mouse CD25 Regulatory T Cell Positive Selection Kit Catalog #: 19852 Product Name: EasySepâ„¢ Mouse CD4+ T Cell Isolation Kit Safety Data SheetCatalog #: Product Name: 100-1335 Human Recombinant Visfatin Catalog #: 100-1335 Product Name: Human Recombinant Visfatin Reference(Feb 2024) Immunity, Inflammation and Disease 12 2Galectinâ€9 alleviates acute graftâ€versusâ€host disease after haploâ€hematopoietic stem cell transplantation by regulating regulatory T cell/effector T cell imbalance
AbstractBackgroundAcute graftâ€versusâ€host disease (aGVHD) arises from the imbalance of host T cells. Galectinâ€9 negatively regulates CD4 effector T cell (Th1 and Th17) function by binding to Timâ€3. However, the relationship between Galectinâ€9/Timâ€3 and CD4+ T subsets in patients with aGVHD after Haploâ€HSCT (haploidentical peripheral blood hematopoietic stem cell transplantation) has not been fully elucidated. Here, we investigated the role of Galectinâ€9 and CD4+T subsets in aGVHD after haploâ€HSCT.MethodsFortyâ€two patients underwent Haploâ€HSCT (26 without aGVHD and 16 with aGVHD), and 20 healthy controls were included. The concentrations of Galectinâ€9, interferonâ€gamma (IFNâ€Î³), interleukin (IL)â€4, transforming growth factor (TGF)â€Î², and ILâ€17 in the serum and culture supernatant were measured using enzymeâ€linked immunosorbent assay or cytometric bead array. The expression levels of Galectinâ€9, PI3K, pâ€PI3K, and pâ€mTOR protein were detected by western blot analysis. Flow cytometry was used to analyze the proportions of CD4+ T cell subsets. Bioinformatics analysis was performed.ResultsIn patients with aGVHD, regulatory T (Treg) cells and Galectinâ€9 decreased, and the Th1, Th17, and Treg cells were significantly imbalanced. Moreover, Treg and Galectinâ€9 were rapidly reconstituted in the early stage of patients without aGVHD after Haploâ€HSCT, but Th17 cells were reconstituted slowly. Furthermore, Timâ€3 upregulation on Th17 and Th1 cells was associated with excessive activation of the PI3K/AKT pathway in patients with aGVHD. Specifically, in vitro treatment with Galectinâ€9 reduced IFNâ€Î³ and ILâ€17 production while augmenting TGFâ€Î² secretion. Bioinformatics analysis suggested the potential involvement of the PI3K/AKT/mTOR pathway in aGVHD. Mechanistically, exogenous Galectinâ€9 was found to mitigate aGVHD by restoring the Treg/Teffs (effector T cells) balance and suppressing PI3K.ConclusionGalectinâ€9 may ameliorate aGVHD after haploâ€HSCT by modulating Treg/Teffs balance and regulating the PI3K/AKT/mTOR pathway. Targeting Galectinâ€9 may hold potential value for the treatment of aGVHD. In patients with acute graftâ€versusâ€host disease (aGVHD), the expression of Timâ€3 is significantly increased. Galectinâ€9 binding to Timâ€3 may inhibit the activation of the PI3K/AKT pathway and enhance the function of Treg cells. On the other hand, transforming growth factor (TGF)â€Î² promotes the differentiation of Treg cells through autocrine secretion, while TGFâ€Î² induces the expression of Galectinâ€9 in a paracrine manner. The increased Treg cells can inhibit the activation of Th1 and Th17 cells by secreting TGFâ€Î², thus alleviating aGVHD and inducing immune toleranceCatalog #: Product Name: 18000 EasySepâ„¢ Magnet Catalog #: 18000 Product Name: EasySepâ„¢ Magnet Safety Data SheetCatalog #: Product Name: 100-1334 Human Recombinant MIP-4 Catalog #: 100-1334 Product Name: Human Recombinant MIP-4 Reference(Feb 2024) Inflammation and Regeneration 44 3Novel artificial nerve transplantation of human iPSC-derived neurite bundles enhanced nerve regeneration after peripheral nerve injury
BackgroundSevere peripheral nerve damage always requires surgical treatment. Autologous nerve transplantation is a standard treatment, but it is not sufficient due to length limitations and extended surgical time. Even with the available artificial nerves, there is still large room for improvement in their therapeutic effects. Novel treatments for peripheral nerve injury are greatly expected.MethodsUsing a specialized microfluidic device, we generated artificial neurite bundles from human iPSC-derived motor and sensory nerve organoids. We developed a new technology to isolate cell-free neurite bundles from spheroids. Transplantation therapy was carried out for large nerve defects in rat sciatic nerve with novel artificial nerve conduit filled with lineally assembled sets of human neurite bundles. Quantitative comparisons were performed over time to search for the artificial nerve with the therapeutic effect, evaluating the recovery of motor and sensory functions and histological regeneration. In addition, a multidimensional unbiased gene expression profiling was carried out by using next-generation sequencing.ResultAfter transplantation, the neurite bundle-derived artificial nerves exerted significant therapeutic effects, both functionally and histologically. Remarkably, therapeutic efficacy was achieved without immunosuppression, even in xenotransplantation. Transplanted neurite bundles fully dissolved after several weeks, with no tumor formation or cell proliferation, confirming their biosafety. Posttransplant gene expression analysis highlighted the immune system’s role in recovery.ConclusionThe combination of newly developed microfluidic devices and iPSC technology enables the preparation of artificial nerves from organoid-derived neurite bundles in advance for future treatment of peripheral nerve injury patients. A promising, safe, and effective peripheral nerve treatment is now ready for clinical application.Supplementary InformationThe online version contains supplementary material available at 10.1186/s41232-024-00319-4.Catalog #: Product Name: 17899 EasySep™ Dead Cell Removal (Annexin V) Kit Catalog #: 17899 Product Name: EasySep™ Dead Cell Removal (Annexin V) Kit Safety Data SheetCatalog #: Product Name: 100-1333 Human Recombinant Fetuin B Catalog #: 100-1333 Product Name: Human Recombinant Fetuin B Reference(Feb 2024) Nature Communications 15Heat shock protein gp96 drives natural killer cell maturation and anti-tumor immunity by counteracting Trim28 to stabilize Eomes
The maturation process of natural killer (NK) cells, which is regulated by multiple transcription factors, determines their functionality, but few checkpoints specifically targeting this process have been thoroughly studied. Here we show that NK-specific deficiency of glucose-regulated protein 94 (gp96) leads to decreased maturation of NK cells in mice. These gp96-deficient NK cells exhibit undermined activation, cytotoxicity and IFN-γ production upon stimulation, as well as weakened responses to IL-15 for NK cell maturation, in vitro. In vivo, NK-specific gp96-deficient mice show increased tumor growth. Mechanistically, we identify Eomes as the downstream transcription factor, with gp96 binding to Trim28 to prevent Trim28-mediated ubiquitination and degradation of Eomes. Our study thus suggests the gp96-Trim28-Eomes axis to be an important regulator for NK cell maturation and cancer surveillance in mice. Natural killer (NK) cell maturation and function are regulated by multiple transcription factors (TF), but detailed molecular insights are scarce. Here the authors show that a TF, Eomes, is important for NK cell responses and cancer surveillance, in which Eomes expression is regulated by gp96 and Trim28 via the ubiquitination and degradation pathways.Catalog #: Product Name: 19855 EasySep™ Mouse NK Cell Isolation Kit Catalog #: 19855 Product Name: EasySep™ Mouse NK Cell Isolation Kit Safety Data SheetCatalog #: Product Name: 100-1332 Human Recombinant Apolipoprotein H Catalog #: 100-1332 Product Name: Human Recombinant Apolipoprotein H Reference(Aug 2025) PLOS Pathogens 21 8Inactivation of branched-chain amino acid uptake halts Staphylococcus aureus growth and induces bacterial quiescence within macrophages
Staphylococcus aureus is a notorious human pathogen that thrives in macrophages. It resides in mature phagolysosomes, where a subset of the bacteria eventually begin to proliferate. How S. aureus acquires essential nutrients, such as amino acids, for growth in this niche is poorly understood. Using a long-term primary human macrophage infection model, we show that branched-chain amino acid (BCAA) uptake mediated by the major transporter BrnQ1 is required by S. aureus for intracellular replication in macrophages and we provide mechanistic insight into the role of BCAAs in the success of intracellular S. aureus. Loss of BrnQ1 function renders intracellular S. aureus non-replicative and non-cytotoxic. The defective intracellular growth of S. aureus brnQ1 mutants can be rescued by supplementation with BCAAs or by overexpression of the BCAA transporters BrnQ1 or BcaP. Inactivation of the CodY repressor rescues the ability of S. aureus brnQ1 mutants to proliferate intracellularly independent of endogenous BCAA synthesis but dependent on BcaP expression. Non-replicating brnQ1 mutants in primary human macrophages become metabolically quiescent and display aberrant gene expression marked by failure to respond to intraphagosomal iron starvation. The bacteria remain, however, viable for an inordinate length of time. This dormant, yet viable bacterial state is distinct from classical persisters and small colony variants. Author summaryStaphylococcus aureus is a prominent human pathogen causing acute and chronic disease. It is facultatively intracellular and can reside within many host cell types, including professional phagocytes such as macrophages. The intracellular state contributes to dissemination, recurrence and infection chronicity. Chronic and relapsing infections are often associated with so-called persister phenotypes. Growth arrest and metabolic quiescence, accompanied by antibiotic tolerance, are hallmarks of persistence in bacteria. Antibiotic pressure is a major factor in triggering intracellular persistence. The small colony variant (SCV), an extensively studied form of S. aureus persister, can arise in the absence of antibiotic pressure and exhibits very distinctive phenotypic characteristics.Here, we describe a different growth-arrested state of S. aureus, which conforms to the definition of a non-antibiotic-driven form of intracellular dormancy, triggered by branched-chain amino acid starvation in macrophages. We show that loss of function of the major branched-chain amino acid transporter BrnQ1 renders intracellular S. aureus non-replicative and metabolically quiescent for an inordinate period of time. Upon stochastic exit from infected macrophages, brnQ1 mutants retain full virulence. This dormancy differs from classical persistence or SCVs and uncovers an underestimated role for BCAA uptake in the success of intracellular S. aureus.Catalog #: Product Name: 17858 EasySepâ„¢ Human CD14 Positive Selection Kit II Catalog #: 17858 Product Name: EasySepâ„¢ Human CD14 Positive Selection Kit II Safety Data SheetCatalog #: Product Name: 100-1331 Human Recombinant ASAM Catalog #: 100-1331 Product Name: Human Recombinant ASAM Items 1309 to 1320 of 13914 total
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