Theranostics最新文献

{"title":"Recent advances in ferrocene-based nanomedicines for enhanced chemodynamic therapy.","authors":"Gui-Long Wu, Senyou Tan, Xiaofeng Tan, Guodong Chen, Qinglai Yang","doi":"10.7150/thno.101697","DOIUrl":"10.7150/thno.101697","url":null,"abstract":"<p><p>Malignant tumors have been a serious threat to human health with their increasing incidence. Difficulties with conventional treatments are toxicity, drug resistance, and recurrence. For this reason, non-invasive treatment modalities such as photothermal therapy (PTT), photodynamic therapy (PDT), chemodynamic therapy (CDT), and others have received much attention. Among them, Ferrocene (Fc)-based nanomedicines for enhanced Chemodynamic Therapy (ECDT) is a new therapeutic strategy based on the Fenton reaction. Based on ferrocene's good biocompatibility, potentiation in medicinal chemistry, and good stability of divalent iron ions, scientists are increasingly using it as a Fenton's iron donor for tumor therapy. Such ferrocene-based ECDT nanoplatforms have shown remarkable promise for clinical applications and have significantly increased the efficacy of CDT treatment. Ferrocene-based nanomedicines exhibit exceptional consistency owing to their low toxicity, high stability, enhanced bioavailability, and a multitude of advantages over conventional approaches to cancer treatment. As a consequence, a number of tactics have been investigated in recent years to raise the effectiveness of ferrocene-based ECDT. In this review, we detail the different forms and strategies used to enhance Ferrocene-based ECDT efficiency.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 2","pages":"384-407"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibiting autophagy selectively prunes dysfunctional tumor vessels and optimizes the tumor immune microenvironment.","authors":"Wanting Hou, Chaoxin Xiao, Ruihan Zhou, Xiaohong Yao, Qin Chen, Tongtong Xu, Fujun Cao, Yulin Wang, Xiaoying Li, Ouying Yan, Xiaolin Ai, Cheng Yi, Dan Cao, Chengjian Zhao","doi":"10.7150/thno.98285","DOIUrl":"10.7150/thno.98285","url":null,"abstract":"<p><p>Dysfunctional tumor vasculature, hypoxia, and an immunosuppressive microenvironment are significant barriers to effective cancer therapy. Autophagy, which is critical for maintaining cellular homeostasis and apoptosis resistance, is primarily triggered by hypoxia and nutrient deprivation, conditions prevalent in dysfunctional tumor vessels due to poor circulation. However, the role of autophagy in dysfunctional tumor endothelial cells and its impact on treatment and the tumor microenvironment (TME) remain poorly understood. <b>Methods:</b> We used multiplex immunofluorescence and transgene-based imaging to characterize autophagy in endothelial cells from clinical tumor samples, zebrafish xenograft tumors, and murine models. Using a zebrafish xenograft vasculature platform, we analyzed the effects of autophagy inhibitors on the structure and function of the tumor vasculature. In mice, we investigated autophagy inhibition via endothelial-specific autophagy gene knockout (<i>Atg7</i> ^iECKO) and the autophagy inhibitor SBI-0206965 and evaluated the synergistic effects of combining SBI-0206965 with low-dose chemotherapy (5-fluorouracil, 5-FU) or PD-1 antibody. Human umbilical vein endothelial cells (HUVECs) were cultured <i>in vitro</i> under hypoxic, glucose-deprived, and serum-free conditions to simulate dysfunctional tumor endothelial cells and to explore the mechanisms by which autophagy inhibition optimizes tumor vasculature. <b>Results:</b> Elevated autophagy was observed in tumor endothelial cells within the dysfunctional vasculature. Autophagy inhibition, through either genetic knockout or pharmacological inhibition, selectively prunes dysfunctional vessels and improves vascular function. It also stimulates the formation of a perivascular immune niche, thereby optimizing the tumor immune microenvironment (TiME). Furthermore, combining the autophagy inhibitor SBI-0206965 with low-dose 5-FU or PD-1 antibody potentiated the anti-tumor effects. Mechanistic studies have indicated that autophagy acts as a protective response to the hypoxic and nutrient-deprived TME, while its inhibition, mediated by p53 activation, promotes tumor endothelial cell apoptosis in dysfunctional tumor vessels, further optimizing the structure and function of the tumor vasculature. <b>Conclusions:</b> Targeting endothelial cell autophagy is a promising strategy for remodeling the dysfunctional tumor vasculature, optimizing the TiME, and boosting the efficacy of chemotherapy and immunotherapy.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 1","pages":"258-276"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting ion channels: innovative approaches to combat cancer drug resistance.","authors":"Qian Shi, Zijing Yang, Huan Yang, Lihui Xu, Jing Xia, Jie Gu, Mengting Chen, Yan Wang, Xiaohong Zhao, Zehua Liao, Yiping Mou, Xidong Gu, Tian Xie, Xinbing Sui","doi":"10.7150/thno.103384","DOIUrl":"10.7150/thno.103384","url":null,"abstract":"<p><p>Ion channels, as functional molecules that regulate the flow of ions across cell membranes, have emerged as a promising target in cancer therapy due to their pivotal roles in cell proliferation, metastasis, apoptosis, drug resistance, and so on. Recently, increasing evidence suggests that dysregulation of ion channels is a common characteristic of cancer cells, contributing to their survival and the resistance to conventional therapies. For example, the aberrant expression of sodium (Na⁺) and potassium ion (K⁺) channels is significantly correlated with the sensitivity of chemotherapy drugs. The endogenous calcium (Ca²⁺) channels contribute to the acquired resistance of osimertinib in epidermal growth factor receptor (EGFR) mutant non-small cell lung cancer cell lines. Ferrous ions (Fe²⁺) enhance the sensitivity of breast cancer cells to doxorubicin treatment. Preclinical models have also demonstrated the effect of specific ion channel blockers or modulators on anticancer drug resistance. This review describes the current understanding about the interaction between ion channels and the therapeutic efficacy of anticancer drugs. Then, the therapeutic potential of ion channel blockers or modulators in enhancing the sensitivity or overcoming the resistance of cancer cells to anticancer therapies is discussed. Targeting ion channels will hopefully offer a novel and promising strategy for overcoming cancer drug resistance.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 2","pages":"521-545"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leveraging plant-derived nanovesicles for advanced nucleic acid-based gene therapy.","authors":"Meihong Chai, Bowen Gao, Shihua Wang, Liping Zhang, Xing Pei, Baosen Yue, Xueyan Zhen, Mingzhen Zhang","doi":"10.7150/thno.104507","DOIUrl":"10.7150/thno.104507","url":null,"abstract":"<p><p>Gene therapy has evolved into a pivotal approach for treating genetic disorders, extending beyond traditional methods of directly repairing or replacing defective genes. Recent advancements in nucleic acid-based therapies-including mRNA, miRNA, siRNA, and DNA treatments have expanded the scope of gene therapy to include strategies that modulate protein expression and deliver functional genetic material without altering the genetic sequence itself. This review focuses on the innovative use of plant-derived nanovesicles (PDNVs) as a promising delivery system for these nucleic acids. PDNVs not only enhance the stability and bioavailability of therapeutic nucleic acids but also improve their specificity and efficacy in targeted gene therapy applications. They have shown potential in the treatment of various diseases, including cancer and inflammatory conditions. By examining the unique properties of PDNVs and their role in overcoming the limitations of conventional delivery methods, this review highlights the transformative potential of PDNV-based nucleic acid therapies in advancing the field of gene therapy.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 1","pages":"324-339"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11667239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk.","authors":"Xin Wang, Xu-Jie Zhou, Xue Qiao, Mario Falchi, Jing Liu, Hong Zhang","doi":"10.7150/thno.104631","DOIUrl":"10.7150/thno.104631","url":null,"abstract":"<p><p>The interplay between multiple organs, known as inter-organ crosstalk, represents a complex and essential research domain in understanding the mechanisms and therapies for kidney diseases. The kidneys not only interact pathologically with many other organs but also communicate with other systems through various signaling pathways. It is of paramount importance to comprehend these mechanisms for the development of more efficient therapeutic strategies. Despite extensive research in IgA nephropathy (IgAN), the most common kidney disease, the elaboration mechanism of IgAN remains challenging. Numerous studies suggest that alterations in the intestinal microbiome and its metabolites are pivotal in the progression of IgAN, opening new avenues for understanding its mechanisms. Interestingly, certain presumed probiotics, such as <i>Akkermansia muciniphila</i>, have been implicated in the onset of IgAN, making the exploration of gut microbiota in the context of IgAN pathogenesis even more intriguing. In this review, we summarize the status of gut microbiology studies of IgAN and explore the possible mechanisms and intervention prospects. Future research and treatment directions may increasingly emphasize systemic, multi-organ combined interventions to decelerate the advancement of kidney disease and enhance the overall prognosis of patients.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 2","pages":"656-681"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RPS23RG1 inhibits SORT1-mediated lysosomal degradation of MDGA2 to protect against autism.","authors":"Yuanhui Huo, Dongdong Zhao, Xiang Zhu, Naizhen Zheng, Dingting Yang, Jian Meng, Yiqing Chen, Yun-Wu Zhang","doi":"10.7150/thno.100451","DOIUrl":"https://doi.org/10.7150/thno.100451","url":null,"abstract":"<p><p><b>Rationale:</b> Mutations in the synaptic protein MAM domain containing glycosylphosphatidylinositol anchor 2 (MDGA2) have been associated with autism spectrum disorder (ASD). Therefore, elucidating the regulatory mechanisms of MDGA2 can help develop effective treatments for ASD. <b>Methods:</b> Liquid chromatography-tandem mass spectrometry was carried out to identify proteins interacting with the extracellular domain of RPS23RG1 and with MDGA2, followed by co-immunoprecipitation assays to confirm protein-protein interactions. RPS23RG1 and SORT1 levels were downregulated by siRNAs to study their effects on MDGA2 degradation, with additional applications of immunoblotting and immunostaining assays. Lysosome isolation was performed to determine the lysosomal degradation of MDGA2 further. <i>Rps23rg1</i> knockout mice and <i>Mdga2</i> ^+/- mice were subjected to various behavioral tests to study their ASD-like phenotypes. AAVs expressing MDGA2 were delivered in <i>Rps23rg1</i> knockout mice, and RPS23RG1-derived peptide was delivered in <i>Mdga2</i> ^+/- mice to study their rescuing effects. <b>Results:</b> We found that both RPS23RG1 and SORT1 interacted with MDGA2. MDGA2 was primarily degraded through the SORT1-mediated lysosomal degradation pathway. RPS23RG1 competed with SORT1 for MDGA2 binding to inhibit MDGA2 degradation. Furthermore, we showed that <i>Rps23rg1</i> knockout mice exhibited decreased MDGA2 levels and ASD-like behaviors, whereas restoration of MDGA2 levels attenuated social defects in <i>Rps23rg1</i> KO mice. Moreover, we identified a crucial region of RPS23RG1 for MDGA2 interaction and found that a peptide derived from this region not only bound MDGA2 and promoted MDGA2 levels, but also rescued social defects in <i>Mdga2</i> ^+/- mice. <b>Conclusion:</b> Our findings highlight a crucial role of RPS23RG1 in antagonizing SORT1-mediated lysosomal degradation of MDGA2 and suggest a potential for targeting the RPS23RG1-MDGA2 axis to treat ASD with MDGA2 deficiency.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 4","pages":"1338-1352"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer-targeted pro-theranostic bi-metallic organo-coordination nanoparticles.","authors":"Hengbo Huang, Lei Fang, Janaka Wansapura, Julie L Prior, Brad Manion, Baogang Xu, Cody Hongsermeier, Nisha Gamadia, Nicole Blasi, Rui Tang, Christopher Egbulefu, Monica Shokeen, James D Quirk, Samuel Achilefu","doi":"10.7150/thno.99863","DOIUrl":"10.7150/thno.99863","url":null,"abstract":"<p><p><b>Rationale:</b> Cancer remains a leading cause of mortality, with aggressive, treatment-resistant tumors posing significant challenges. Current combination therapies and imaging approaches often fail due to disparate pharmacokinetics and difficulties correlating drug delivery with therapeutic response. <b>Methods:</b> In this study, we developed radionuclide-activatable theranostic nanoparticles (NPs) comprising folate receptor-targeted bimetallic organo-nanoparticles (Gd-Ti-FA-TA NPs). Polyvalent tannic acid was used to coordinate titanium (Ti), a reactive oxygen species (ROS)-generating catalyst, gadolinium (Gd), a magnetic resonance imaging (MRI) contrast agent, and cypate, a near-infrared fluorescent dye. <b>Results:</b> The NPs exhibited higher magnetic field-dependent relaxivities (<i>r</i> ₁ = 20.8 mM⁻¹s⁻¹, <i>r</i> ₂ = 72.1 mM⁻¹s⁻¹) than Gd-DTPA (<i>r</i> ₁ = 4.8 mM⁻¹s⁻¹, <i>r</i> ₂ = 4.9 mM⁻¹s⁻¹) on a 3 T MRI scanner. Tannic acid coordination reduced the Ti band gap from 3.3 eV in TiO₂ NPs to 2.0 eV, tripling ROS generation under UV light exposure. In breast cancer models (4T1 and PyMT-Bo1), Cerenkov radiating radiopharmaceuticals activated Gd-Ti-FA-TA NPs <i>in vitro</i> and <i>in vivo</i>, generating cytotoxic ROS to inhibit tumor cell viability and prevent tumor progression. <i>In vivo</i>, the NPs selectively accumulated in 4T1 tumors and enhanced both T₁ and T₂ MRI contrast, highlighting a strategy to locally activate cytotoxic ROS generation with radiopharmaceuticals for cancer treatment, utilizing cross-modality PET/MRI and optical imaging for shallow and deep tissue visualization. <b>Conclusion:</b> The integrated nanoplatform allows direct imaging of drug delivery, providing guidance for the optimal timeline to activate therapeutic effects of pro-theranostic NPs via external triggers such as radionuclide-stimulated dynamic treatment.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 4","pages":"1205-1220"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143012091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A specific and adaptable approach to track CD206⁺ macrophages by molecular MRI and fluorescence imaging.","authors":"Cuihua Wang, Negin Jalali Motlagh, Gregory R Wojtkiewicz, Hongzhi Yang, Hyung-Hwan Kim, John W Chen","doi":"10.7150/thno.96488","DOIUrl":"https://doi.org/10.7150/thno.96488","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Rationale:&lt;/b&gt; The mannose receptor (CD206, expressed by the gene &lt;i&gt;Mrc1&lt;/i&gt;) is a surface marker overexpressed by anti-inflammatory and pro-tumoral macrophages. As such, CD206&lt;sup&gt;+&lt;/sup&gt; macrophages play key roles in the immune response to different pathophysiological conditions and represent a promising diagnostic and therapeutic target. However, methods to specifically target these cells remain challenging. In this study, we describe a multi-mannose approach to develop CD206-targeting fluorescent and MRI agents that specifically and sensitively detect and monitor CD206&lt;sup&gt;+&lt;/sup&gt; macrophage immune response in different disease conditions. &lt;b&gt;Methods:&lt;/b&gt; We designed and synthesized fluorescent agents MR1-cy5 and MR2-cy5, and MRI agents Mann2-DTPA-Gd and MannGdFish. Cellular assays using pro-inflammatory and anti-inflammatory macrophages differentiated from RAW 264.7 cells were performed, and signals were detected by fluorescence microscopy and inductively coupled plasma mass spectrometry (ICP-MS) to validate specificity &lt;i&gt;in vitro&lt;/i&gt;. &lt;i&gt;In vivo&lt;/i&gt; specificity and efficacy of the agents were evaluated by MRI in a subcutaneous wound healing model and experimental glioma with &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;+/+&lt;/sup&gt; without and with D-mannose treatment, &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;+/-&lt;/sup&gt;, and &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;-/-&lt;/sup&gt; mice, and in stroke. One-way ANOVA and two-way ANOVA tests were used for data analysis. P &lt; 0.05 was considered statistically different. &lt;b&gt;Results:&lt;/b&gt; Both &lt;i&gt;in vitro&lt;/i&gt; fluorescence imaging with MR2-cy5, ICP-MS with Mann2-DTPA-Gd, and &lt;i&gt;in vivo&lt;/i&gt; MRI in &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;-/-&lt;/sup&gt; mice confirmed the specificity of our approach. Mann2-DTPA-Gd MRI can track the changes of CD206&lt;sup&gt;+&lt;/sup&gt; macrophages at different stages of wound healing, correlating well with flow cytometry data using another anti-inflammatory macrophage marker (arginase-1). The specificity and efficacy of Mann2-DPTA-Gd were further validated in experimental glioma, in which Mann2-DTPA-Gd imaging detected CD206&lt;sup&gt;+&lt;/sup&gt; tumor-associated macrophages (TAMs), demonstrated significantly decreased signals in &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;+/-&lt;/sup&gt; mice and &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;-/-&lt;/sup&gt; mice, and tracked treatment changes in D-mannose-treated &lt;i&gt;Mrc1&lt;/i&gt; &lt;sup&gt;+/+&lt;/sup&gt; mice. Furthermore, Mann2-DTPA-Gd can report microglia/macrophages and correlate with histology in stroke. The more Gd-stable agent MannGdFish demonstrated similar efficacy as Mann2-DTPA-Gd &lt;i&gt;in vivo&lt;/i&gt; with favorable biodistribution and pharmacokinetics. &lt;b&gt;Conclusion:&lt;/b&gt; We have developed a fluorescent agent (MR2-cy5) and MRI agents (Mann2-DTPA-Gd and MannGdFish) with two mannose moieties that are highly specific to CD206 and can track CD206&lt;sup&gt;+&lt;/sup&gt; macrophages in disease models of wound healing, tumor, and neurological disease. Importantly, MannGdFish, with its high specificity, stability, favorable biodistribution, and pharmacokinetics, is a promising translational candidate to noninvasively monitor CD206&lt;sup","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 3","pages":"1094-1109"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Ex vivo</i> enhancement of CD8+ T cell activity using functionalized hydrogel encapsulating tonsil-derived lymphatic endothelial cells.","authors":"Heesun Hong, Chan Hum Park, Ji Seung Lee, Kyunghee Kim, Sudarshini Nath, Moon Sik Oh, Sol Kim, Chul Hee Lee, Ki Hyun Kim, Woo Hee Choi, Kyu Young Choi, Hae Sang Park, Ok Joo Lee, In-Sun Hong, Soon Hee Kim","doi":"10.7150/thno.100079","DOIUrl":"https://doi.org/10.7150/thno.100079","url":null,"abstract":"<p><p><b>Rationale:</b> This study investigates a method for programming immune cells using a biomaterial-based system, providing an alternative to traditional <i>ex vivo</i> cell manipulation techniques. It addresses the limitations of engineered adoptive T cell therapies, such as T cell exhaustion, by introducing a gelatin-hyaluronic acid (GH-GMA) hydrogel system. <b>Methods:</b> We characterized tonsil mesenchymal stem cells (TMSCs), lymphatic endothelial cells (T-LECs), stimulated T-CD8⁺ T cells (STCs), and GH-GMA biomaterials. The 10% 5:1 GH-GMA hydrogel, loaded with anti-CD28, cytokines interleukin-2 (IL-2) and vascular endothelial growth factor C (VEGF-C), forms a functional hydrogel capable of releasing these immune-stimulating factors. T-LEC spheroids, derived from tonsil mesenchymal stem cells (TMSCs), were encapsulated within the hydrogel to act as antigen-presenting cells for T cells. <b>Results:</b> Co-encapsulation of STCs and T-LEC spheroids in the functional hydrogel resulted in significant expansion and enrichment of STCs during cultivation. Moreover, when cancer cells were co-encapsulated with STCs and T-LECs, there was increased migration of STCs towards the cancer cells and elevated expression of PD-L1 on the cancer cells. <b>Conclusions:</b> These findings suggest that the GH-GMA hydrogel, combined with anti-CD28, IL-2, VEGF-C, and T-LEC spheroids, enhances T cell activity, presenting a promising platform for cancer immunotherapies and modulation of the suppressive tumor microenvironment.</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 3","pages":"850-874"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Piezo1 specific deletion in macrophage protects the progression of liver fibrosis in mice: Erratum.","authors":"Shangfei Luo, Xiaoduo Zhao, Jintao Jiang, Bo Deng, Silin Liu, Honglin Xu, Qiaorui Tan, Yu'an Chen, Ziyan Zhang, Xianmei Pan, Rentao Wan, Xiaoting Chen, Youfen Yao, Jing Li","doi":"10.7150/thno.107640","DOIUrl":"https://doi.org/10.7150/thno.107640","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.7150/thno.86103.].</p>","PeriodicalId":22932,"journal":{"name":"Theranostics","volume":"15 3","pages":"1156-1157"},"PeriodicalIF":12.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}