详细内容（前10条）

1. GSE328165 基于mRNA的流感疫苗扩大了人类B细胞反应的范围

• ✍️ 作者：未知作者
• 🏷️ 关键词：vaccine、B cell
• 📝 描述：Contributors : Hanover C Matz ; Tae-Geun Yu ; Kritika Dixit ; Caroline Kikawa ; Julian Q Zhou ; Garazi P Alzua ; Lowrey Peyton ; Anders Madsen ; Fangjie Han ; Ariana G Farrell ; Robert Hoelzl ; Aaron J Schmitz ; Stephen C Horvath ; Hunter K Keplinger ; Benjamin S Strnad ; Mark J Hoegger ; William D Middleton ; Michael K Klebert ; Nina H Lin ; Raffael Nachbagauer ; Florian Krammer ; Robert Paris ; Jesse D Bloom ; Jackson S Turner ; Rachel M Presti ; Jiwon Lee ; Ali H EllebedySeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensEliciting durable antibody responses against rapidly evolving pathogens such as the influenza virus remains a formidable challenge. Conventional influenza virus vaccines are poorly immunogenic and induce antibody responses of limited breadth. Germinal center (GC) reactions in draining lymph nodes are key sites for antibody diversification and affinity maturation following vaccination. Whether an mRNA-based influenza virus vaccine can induce a superior GC response in humans compared to conventional vaccines remains unclear. We assessed B cell responses in an observational study of cohorts of healthy young adults receiving a licensed, split-virion or an investigative mRNA-based quadrivalent seasonal influenza virus vaccine over two consecutive seasons. mRNA-based vaccines consistently elicited higher antibody titers and frequencies of memory B cells. In the draining lymph nodes, mRNA vaccination stimulated sustained GC reactions that persisted for at least 26 weeks post vaccination in five of thirteen participants across the two seasons. To understand how sustained GC activity shapes the secreted serum IgG repertoire, we performed proteomic analysis of serum IgG repertoire. mRNA vaccination increased the number of vaccine-elicited serum IgG clonotypes and promoted intraclonal expansion within pre-existing clonotypes. B cell lineage analyses further indicated that expanded serum clonotypes map to GC B cell-associated subbranches, consistent with ongoing GC-driven evolution underlying intraclonal expansion. This repertoire remodeling was accompanied by increased binding breadth against antigenically divergent influenza viruses. These findings reveal a key role for persistent GC responses in broadening the repertoire of vaccine-induced antibodies.
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2. GSE306718 巨噬细胞 CD163 通过骨桥蛋白促进心肌梗死后心脏修复并维持左心室功能

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、cardiac
• 📝 描述：Contributors : Binbin Liu ; Jingyu Chen ; Cuilian DaiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Cardiac macrophages have been implicated in myocardial repair following myocardial infarction (MI), yet their therapeutic potential in ischemic cardiomyopathy (ICM) remains limited by an incomplete understanding of their molecular regulation. CD163 is highly expressed in these macrophages, yet its functional role in regulating post-MI cardiac repair remains unknown.Methods: A cross-sectional clinical study was conducted to assess the association between circulating soluble CD163 concentration and heart failure due to ICM. To investigate the functional contribution of CD163 in ICM, Wild-type (WT) and Cd163/ mice were subjected to permanent ligation of the left anterior descending coronary artery. Single-cell RNA sequencing was employed to analyze transcriptional changes in cardiac immune cells. Recombinant osteopontin (OPN) and CD163 were administered to assess their therapeutic effect in Cd163/ mice. Results: Circulating soluble CD163 levels were markedly elevated in patients with ICM-induced heart failure compared with individuals without heart failure (median difference 34.5 ng/mL, IQR 13.6–54.6 ng/mL, P = 0.002) and showed a positive correlation with the extent of systolic dysfunction and left ventricular dilation. Cd163/ mice displayed aggravated left ventricular systolic dysfunction, reduced ejection fraction and fractional shortening, impaired myocardial strain, and reduced relative wall thickness post-MI. Recombinant CD163 protein could reverse systolic dysfunction and left ventricular dilation in Cd163/ mice after MI. CD163 was predominantly expressed in CCR2⁻ resident cardiac macrophages, and CD163 deficiency altered transcriptional programs of macrophages without affecting their polarization status, with enrichment in cytokine signaling and extracellular matrix-related pathways. Spp1 (OPN) expression was significantly downregulated in Cd163/ hearts under both sham and MI conditions. Administration of recombinant OPN improved systolic function, reduced ventricular dilation, decreased fibrotic scar size, and restored the elastin-to-collagen ratio in Cd163/ mice. Conclusions: In cardiac macrophages, CD163 contributes to post-myocardial infarction repair by upregulating OPN expression, which in turn helps maintain systolic function.
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3. GSE236359 UHOMi003-A 细胞系来源的 iALI 上皮细胞的单细胞 RNA 测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Said Assou ; Arnaud Bourdin ; John De VosSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe goal of this study was to identifed specifically iALI epithelial cell clusters by using single-cell RNA-sequencing (10x Genomics Chromium). We enriched the epithelial cells based on EpCam cell level, and then used 10X Genomics Chromium technology to capture 10 000 cells. The analyse was then performed using Seurat, to identified each cell cluster. The results reveal all bronchial epithelial cell population on iALI model. This include ciliated cells, basal cells, neuroendocrine cells and secretory cells.
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4. GSE275130 介导亚基 Med4 增强乳腺癌的转移休眠（组蛋白 ChIP-seq_shMed4）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、histone
• 📝 描述：Contributors : Seong-Yeon Bae ; Filippo GiancottiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusBreast cancer metastatic relapse after a latency period, known as metastatic dormancy, involves dormant tumor cells within pre-metastatic niches. Through rigorous genetic screening in mice, we identified the mediator complex subunit 4 gene, Med4, as a novel tumor-cell intrinsic gatekeeper in metastatic reactivation. Med4 downregulation effectively awakened dormant breast cancer cells, prompting reactivation and macroscopic metastatic outgrowth in the lungs. Med4 depletion results in profound changes in nuclear size and three-dimensional (3D) chromatin architecture from compacted to relaxed states in contrast to the known canonical function of the Mediator complex. These changes rewire the expression of extracellular matrix (ECM) proteins, integrins, and signaling components resulting in integrin-mediated mechano-transduction and activation of YAP and MRTF. In parallel, assembly of stress fibers pulls on the nuclear membrane, and thereby contributes to mediating and reinforcing the overall chromatin modifications that occur subsequent to Med4 depletion. MED4 gene deletions were observed in patients with metastatic breast cancer, and reduced MED4 expression correlates with worse prognosis. Our findings unveil a unique function of MED4 and identify an innovative mechanism by which MED4 regulates the epigenetic control of integrin signaling, pivotal in the metastatic reactivation of breast cancer. Additionally, we propose MED4 and related gene signatures as novel biomarkers for stratifying patients prone to recurrence, thus identifying subsets of patients who will benefit from targeting effectors activated by MED4 loss.
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5. GSE290458 IFN-γ诱导GBP1驱动人类皮肤肉芽肿中巨噬细胞异常活化

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage
• 📝 描述：Contributors : Mario Fabri ; David E SaninSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensGranuloma annulare (GA) and cutaneous sarcoidosis (cSAR), non-communicable skin conditions, possess an overlapping immunopathology, in which the aberrant activation of macrophages by IFN-γ constitutes a central driver of disease. Nevertheless, our understanding of the molecular events occurring in pathologically activated GA and cSAR macrophages remains limited. Here, we analyzed published single-cell RNA sequencing data of GA and cSAR and performed in-vitro experiments with primary human cells, allowing us to show that oxidative phosphorylation (OXPHOS) is a dominant metabolic pathway in IFN-γ-activated macrophages. Furthermore, we identify an IFN-γ-induced, OXPHOS-sensitive response network in human GA and cSAR macrophages. Within this network, GBP1 plays a central role in controlling IFN-γ-mediated macrophage activation. Meanwhile, inhibition of OXPHOS and GBP1 both promoted resolution of granulomas and prevented granuloma induction in a human in-vitro granuloma model. Taken together, our study suggests that OXPHOS and GBP1 represent therapeutic strategies for treating cutaneous granulomatous diseases.
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6. GSE255473 介导亚基 Med4 增强乳腺癌的转移休眠（ATAC-seq_shMed1）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Seongyeon S Bae ; Filippo GiancottiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusBreast cancer metastatic relapse after a latency period, known as metastatic dormancy, involves dormant tumor cells within pre-metastatic niches. Through rigorous genetic screening in mice, we identified the mediator complex subunit 4 gene, Med4, as a novel tumor-cell intrinsic gatekeeper in metastatic reactivation. Med4 downregulation effectively awakened dormant breast cancer cells, prompting reactivation and macroscopic metastatic outgrowth in the lungs. Med4 depletion results in profound changes in nuclear size and three-dimensional (3D) chromatin architecture from compacted to relaxed states in contrast to the known canonical function of the Mediator complex. These changes rewire the expression of extracellular matrix (ECM) proteins, integrins, and signaling components resulting in integrin-mediated mechano-transduction and activation of YAP and MRTF. In parallel, assembly of stress fibers pulls on the nuclear membrane, and thereby contributes to mediating and reinforcing the overall chromatin modifications that occur subsequent to Med4 depletion. MED4 gene deletions were observed in patients with metastatic breast cancer, and reduced MED4 expression correlates with worse prognosis. Our findings unveil a unique function of MED4 and identify an innovative mechanism by which MED4 regulates the epigenetic control of integrin signaling, pivotal in the metastatic reactivation of breast cancer. Additionally, we propose MED4 and related gene signatures as novel biomarkers for stratifying patients prone to recurrence, thus identifying subsets of patients who will benefit from targeting effectors activated by MED4 loss.
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7. GSE255278 介导亚基 Med4 增强乳腺癌的转移休眠

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributor : Seongyeon S BaeSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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8. GSE255277 介导亚基 Med4 增强乳腺癌的转移休眠 (ATAC-seq_shMed4)

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Seongyeon S Bae ; Filippo GiancottiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusBreast cancer metastatic relapse after a latency period, known as metastatic dormancy, involves dormant tumor cells within pre-metastatic niches. Through rigorous genetic screening in mice, we identified the mediator complex subunit 4 gene, Med4, as a novel tumor-cell intrinsic gatekeeper in metastatic reactivation. Med4 downregulation effectively awakened dormant breast cancer cells, prompting reactivation and macroscopic metastatic outgrowth in the lungs. Med4 depletion results in profound changes in nuclear size and three-dimensional (3D) chromatin architecture from compacted to relaxed states in contrast to the known canonical function of the Mediator complex. These changes rewire the expression of extracellular matrix (ECM) proteins, integrins, and signaling components resulting in integrin-mediated mechano-transduction and activation of YAP and MRTF. In parallel, assembly of stress fibers pulls on the nuclear membrane, and thereby contributes to mediating and reinforcing the overall chromatin modifications that occur subsequent to Med4 depletion. MED4 gene deletions were observed in patients with metastatic breast cancer, and reduced MED4 expression correlates with worse prognosis. Our findings unveil a unique function of MED4 and identify an innovative mechanism by which MED4 regulates the epigenetic control of integrin signaling, pivotal in the metastatic reactivation of breast cancer. Additionally, we propose MED4 and related gene signatures as novel biomarkers for stratifying patients prone to recurrence, thus identifying subsets of patients who will benefit from targeting effectors activated by MED4 loss.
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9. GSE255221 介导亚基 Med4 增强乳腺癌的转移休眠（RNA-seq_shMed4）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Seongyeon S Bae ; Filippo GiancottiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBreast cancer metastatic relapse after a latency period, known as metastatic dormancy, involves dormant tumor cells within pre-metastatic niches. Through rigorous genetic screening in mice, we identified the mediator complex subunit 4 gene, Med4, as a novel tumor-cell intrinsic gatekeeper in metastatic reactivation. Med4 downregulation effectively awakened dormant breast cancer cells, prompting reactivation and macroscopic metastatic outgrowth in the lungs. Med4 depletion results in profound changes in nuclear size and three-dimensional (3D) chromatin architecture from compacted to relaxed states in contrast to the known canonical function of the Mediator complex. These changes rewire the expression of extracellular matrix (ECM) proteins, integrins, and signaling components resulting in integrin-mediated mechano-transduction and activation of YAP and MRTF. In parallel, assembly of stress fibers pulls on the nuclear membrane, and thereby contributes to mediating and reinforcing the overall chromatin modifications that occur subsequent to Med4 depletion. MED4 gene deletions were observed in patients with metastatic breast cancer, and reduced MED4 expression correlates with worse prognosis. Our findings unveil a unique function of MED4 and identify an innovative mechanism by which MED4 regulates the epigenetic control of integrin signaling, pivotal in the metastatic reactivation of breast cancer. Additionally, we propose MED4 and related gene signatures as novel biomarkers for stratifying patients prone to recurrence, thus identifying subsets of patients who will benefit from targeting effectors activated by MED4 loss.
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10. GSE255220 介导亚基 Med4 增强乳腺癌的转移休眠（RNA-seq_shMed1）

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Contributors : Seongyeon S Bae ; Filippo GiancottiSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBreast cancer metastatic relapse after a latency period, known as metastatic dormancy, involves dormant tumor cells within pre-metastatic niches. Through rigorous genetic screening in mice, we identified the mediator complex subunit 4 gene, Med4, as a novel tumor-cell intrinsic gatekeeper in metastatic reactivation. Med4 downregulation effectively awakened dormant breast cancer cells, prompting reactivation and macroscopic metastatic outgrowth in the lungs. Med4 depletion results in profound changes in nuclear size and three-dimensional (3D) chromatin architecture from compacted to relaxed states in contrast to the known canonical function of the Mediator complex. These changes rewire the expression of extracellular matrix (ECM) proteins, integrins, and signaling components resulting in integrin-mediated mechano-transduction and activation of YAP and MRTF. In parallel, assembly of stress fibers pulls on the nuclear membrane, and thereby contributes to mediating and reinforcing the overall chromatin modifications that occur subsequent to Med4 depletion. MED4 gene deletions were observed in patients with metastatic breast cancer, and reduced MED4 expression correlates with worse prognosis. Our findings unveil a unique function of MED4 and identify an innovative mechanism by which MED4 regulates the epigenetic control of integrin signaling, pivotal in the metastatic reactivation of breast cancer. Additionally, we propose MED4 and related gene signatures as novel biomarkers for stratifying patients prone to recurrence, thus identifying subsets of patients who will benefit from targeting effectors activated by MED4 loss.
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1. 多吃水果蔬菜与意想不到的肺癌风险有关

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：A surprising new study suggests that eating a very healthy diet—packed with fruits, vegetables, and whole grains—might be linked to a higher risk of lung cancer in younger non-smokers. Researchers found that patients under 50 diagnosed with lung cancer often had better-than-average diets, raising the possibility that pesticide exposure from conventionally grown produce could be a hidden culprit.
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• GSE328037 CD74 缺陷小鼠 BMDM 中转座酶可及染色质的高通量测序检测
• GSE328020 LXR干预对脊髓损伤小鼠损伤区域转录组表达的影响
• GSE327941 探索人源化小鼠模型中胶质母细胞瘤的免疫环境