详细内容（前10条）

1. ⭐ GSE280744 派氏淋巴集结中肠上皮-免疫动力学对肠道免疫的影响

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、immunity、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
• 📝 描述：Contributor : M. Zeeshan ChaudhrySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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2. ⭐ GSE336633 毛里求斯食蟹猴组织中MHC表达的空间转录组学

• ✍️ 作者：未知作者
• 🏷️ 关键词：MHC、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Julie A Karl ; Anthony J Veltri ; Roger W Wiseman ; William K Gardner ; Max C Ertl ; Miranda R Stauss ; Heather A Simmons ; David H O’ConnorSeries Type : OtherOrganism : Macaca fascicularisA spatial transcriptomics method was developed with the 10X Genomics Visium HD platform and a custom probe panel to study expression of Major Histocompatibility Complex (MHC) genes in tissues from Mauritian-origin cynomolgus macaques. Previous scRNA sequencing studies with these macaque demonstrated a wide range of allele-specific MHC transcript levels in multiple peripheral blood mononuclear cell subsets. The restricted genetic diversity of the Mauritian macaque population made it possible to design a manageable number of custom MHC probes for this pilot study . Tissues examined included kidney, liver, lung and heart that of particular interest for transplant research. The Visium Human Transcriptome Kit v2 performed well with at least 40 different kidney cell types identified based on cell clustering with gene expression definitions in a human kidney cell atlas. In addition, higher overall transcript levels were observed for several major MHC class I alleles compared to minor alleles that tend to be expressed at low levels in peripheral blood mononuclear cells.
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3. ⭐ GSE312015 单细胞空间转录组学揭示小鼠肾上腺皮质中性别依赖性基因表达和细胞间信号传导

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Małgorzata Blatkiewicz ; Szymon Hryhorowicz ; Marta Szyszka ; Joanna Suszyńska-Zajczyk ; Andrzej Pławski ; Anna Olechnowicz ; Andrea Porzionato ; Ludwik K. Malendowicz ; Marcin RucinskiSeries Type : OtherOrganism : Mus musculusSexual dimorphism profoundly influences adrenal physiology and disease susceptibility, yet its molecular and spatial basis remains poorly understood. The female-predominant X-zone, a transient cortical structure recognized for nearly a century, has lacked comprehensive molecular characterization. Here we use high-resolution Visium HD spatial transcriptomics with Cellpose-based cell segmentation to generate ~203,000 near-single-cell-resolution transcriptomic profiles from sexually mature mouse adrenal glands (four male, four female). We identify ten distinct cell populations with sex differences spatially restricted to inner cortical zones. The X-zone exhibits pronounced sexual dimorphism, with Akr1c18 (20α-hydroxysteroid dehydrogenase) as the definitive marker (log₂FC = −16.28, female-enriched), establishing the X-zone as a specialized progesterone-catabolizing endocrine compartment. Female adrenal glands exhibit greater intercellular communication complexity (435 vs 369 interactions) and higher aggregate signalling strength, with SPP1-integrin pathways enriched in the female X-zone microenvironment. Spatial trajectory inference reveals a dominant centripetal transcriptional gradient from the CT capsule toward the middle zona fasciculata conserved across both sexes, and a secondary centrifugal axis emanating from the JMZ/X region that is prominent in females and reflects the transcriptionally active X-zone. This spatial atlas establishes spatial restriction as a fundamental organizing principle of endocrine sexual dimorphism and provides a foundational resource for investigating sex-specific adrenal physiology, with implications for precision medicine approaches to adrenal disorders.
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4. ⭐ GSE330482 调节性 T 细胞抑制 CD4 T 细胞对 PD-L1 阻断后出现的 MHC-I 缺陷型转移性胰腺癌的控制 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、MHC、ATAC-seq
• 📝 描述：Contributor : Ingunn StromnesSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusWe investigate mechanisms of immunotherapy resistance in pancreatic cancer. PD-L1 blockade selected for metastatic tumor variants with defective IFN-g–inducible MHC-I due to epigenetic Tap1 silencing. Restoration of MHC-I limited primary tumor growth but failed to prevent metastasis. In contrast, regulatory T cell (TREG) depletion abrogated metastasis by unleashing conventional CD4 T cells. Metastasis was also mitigated by transfer of tumor-reactive CD4 T cells or by CTLA-4 blockade. Tumor-specific CD4 T cells adopt a TCF1⁺SLAMF6⁺ progenitor state in lymph nodes and further differentiate in malignant sites. CTLA4 blockade abrogated metastasis, drove intratumoral accumulation CD4 T cells with stemness and tissue residency features, producing a gene signature correlating with improved patient outcomes. MHC-I restoration with anti-CTLA4 prolonged animal survival. TREG and CD4 T cells co-localized in human tumors and abundance correlated with tumor MHC-I and overall survival. Together, these findings identify actionable mechanisms of immune evasion and metastasis in immunotherapy-resistant cancer.
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5. ⭐ GSE330011 调节性 T 细胞抑制 CD4 T 细胞对 PD-L1 阻断后出现的 MHC-I 缺陷型转移性胰腺癌的控制 [scRNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、MHC、scRNA
• 📝 描述：Contributor : Ingunn M StromnesSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusWe investigate mechanisms of immunotherapy resistance in pancreatic cancer. PD-L1 blockade selects for metastatic tumor variants with defective IFNγ-inducible MHC-I due to epigenetic silencing of Tap1. Restoring MHC-I limits primary tumor growth but fails to prevent metastasis. In contrast, regulatory T cell (TREG) depletion suppresses metastasis by unleashing CD4 T helper cells. Adoptive transfer of tumor-specific CD4 T cells impairs metastatic progression. Tumor-specific CD4 T cells in lymph nodes preferentially adopt a TCF1⁺SLAMF6⁺ precursor state. Intratumoral TREG targeting with anti–CTLA-4 abrogates metastasis, drives accumulation of stem-like, tissue-resident helper CD4 T cells, producing a gene signature associated with improved patient outcomes. Combined CTLA-4 blockade and MHC-I restoration eliminates metastasis and prolongs animal survival. In human tumors, TREG and CD4 helper T cells co-localize and correlate with both tumor MHC-I expression and overall survival. Together, these findings identify actionable mechanisms of immune evasion and metastasis in immunotherapy-resistant cancer.
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6. ⭐ GSE264503 通过 RNA-seq 分析临床食管鳞状细胞癌肿瘤、匹配的正常组织和淋巴结转移组织的基因表达谱

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、regex:lymph(o|atic)?、RNA-seq
• 📝 描述：Contributors : Shu-Jun Li ; Zhuo-Ran Liang ; Xiao-Mei YuSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTranscriptomic analysis of clinical tissue samples is important in the precision medicine research. Therefore, we used RNA sequencing to systematically analyze the differentially expressed genes of 17 ESCC tumor tissues and paired normal tissue and lymph node metastatic tissue.
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7. ⭐ GSE330483 调节性 T 细胞抑制 CD4 T 细胞对 PD-L1 阻断后出现的 MHC-I 缺陷型转移性胰腺癌的控制

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、MHC
• 📝 描述：Series Type : Expression profiling by high throughput sequencing ; Methylation 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. ⭐ GSE330323 调节性 T 细胞抑制 CD4 T 细胞对 PD-L1 阻断后出现的 MHC-I 缺陷型转移性胰腺癌的控制 [EM-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、T cell、MHC
• 📝 描述：Contributors : Audrey Hilk ; Ingunn StromnesSeries Type : Methylation profiling by high throughput sequencingOrganism : Mus musculusWe investigate mechanisms of immunotherapy resistance in pancreatic cancer. PD-L1 blockade selected for metastatic tumor variants with defective IFN-g–inducible MHC-I due to epigenetic Tap1 silencing. Restoration of MHC-I limited primary tumor growth but failed to prevent metastasis. In contrast, regulatory T cell (TREG) depletion abrogated metastasis by unleashing conventional CD4 T cells. Metastasis was also mitigated by transfer of tumor-reactive CD4 T cells or by CTLA-4 blockade. Tumor-specific CD4 T cells adopt a TCF1⁺SLAMF6⁺ progenitor state in lymph nodes and further differentiate in malignant sites. CTLA4 blockade abrogated metastasis, drove intratumoral accumulation CD4 T cells with stemness and tissue residency features, producing a gene signature correlating with improved patient outcomes. MHC-I restoration with anti-CTLA4 prolonged animal survival. TREG and CD4 T cells co-localized in human tumors and abundance correlated with tumor MHC-I and overall survival. Together, these findings identify actionable mechanisms of immune evasion and metastasis in immunotherapy-resistant cancer.
• 🔗 查看原文

9. ⭐ GSE300463 TET3 通过对 I 型干扰素信号的负调控促进肿瘤免疫逃逸 [ChIP-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、ChIP-seq
• 📝 描述：Contributors : Lu Liu ; Li Tan ; Yujiang ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe Ten-eleven translocation (TET) family genes, which encode 5-methylcytosine (5mC) dioxygenases, have been described as tumor suppressors or oncogenes in various cancers. However, the functional role of TET3 in cancer immunity and the underlying molecular mechanisms remain incompletely understood. Here, we reported that TET3 restrains the innate immune response in MCF7 and B16F10 cells. Mechanistically, TET3 does not influence the generation of endogenous dsRNA but represses the expression of major dsRNA sensor genes (i.e., MDA5 and RIG-I) as well as the activation of JAK-STAT1 pathway. Importantly, depletion of Tet3 in B16F10 melanoma cells significantly curbed the synergistic tumor growth, accompanied with increased proportion of tumor-infiltrating CD4+ T cells, CD8+ T cells and dendritic cells. Analysis of the TCGA data also revealed elevated expression of TET3 in most types of cancer. Notably, elevated TET3 expression levels were inversely associated with overall survival rate and exhibited a negative correlation with tumor-infiltrating cytotoxic CD8+ T cells. Taken together, our findings identify TET3 as a negative regulator of type I interferon signaling, suggesting that TET3 may be a new target of anti-tumor immunity and immunotherapy.
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10. ⭐ GSE300460 TET3 通过对 I 型干扰素信号的负调控促进肿瘤免疫逃逸 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、RNA-seq
• 📝 描述：Contributors : Lu Liu ; Li Tan ; Yujiang ShiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusThe Ten-eleven translocation (TET) family genes, which encode 5-methylcytosine (5mC) dioxygenases, have been described as tumor suppressors or oncogenes in various cancers. However, the functional role of TET3 in cancer immunity and the underlying molecular mechanisms remain incompletely understood. Here, we reported that TET3 restrains the innate immune response in MCF7 and B16F10 cells. Mechanistically, TET3 does not influence the generation of endogenous dsRNA but represses the expression of major dsRNA sensor genes (i.e., MDA5 and RIG-I) as well as the activation of JAK-STAT1 pathway. Importantly, depletion of Tet3 in B16F10 melanoma cells significantly curbed the synergistic tumor growth, accompanied with increased proportion of tumor-infiltrating CD4+ T cells, CD8+ T cells and dendritic cells. Analysis of the TCGA data also revealed elevated expression of TET3 in most types of cancer. Notably, elevated TET3 expression levels were inversely associated with overall survival rate and exhibited a negative correlation with tumor-infiltrating cytotoxic CD8+ T cells. Taken together, our findings identify TET3 as a negative regulator of type I interferon signaling, suggesting that TET3 may be a new target of anti-tumor immunity and immunotherapy.
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1. RNA测序揭示了预测结核病进展的早期免疫特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、sequencing
• 📝 描述：RNA sequencing and single-cell RNA sequencing revealed airway immune signatures that distinguish protective responses from progression to active tuberculosis… The post RNA sequencing reveals early immune signatures that predict tuberculosis progression appeared first on RNA-Seq Blog.
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2. ScQCenrich——单细胞RNA测序的多指标质量控制

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：RNA sequencing quality improves with scQCenrich, which combines multiple biological and technical metrics to preserve valuable cells while reducing unnecessary filtering… The post ScQCenrich – multi-metric quality control for single-cell RNA sequencing appeared first on RNA-Seq Blog.
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3. FDA批准的药物或许最终能帮助免疫疗法战胜罕见的肝癌

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、regex:immuno(logy|therapy|suppression)
• 📝 描述：Researchers found that a rare liver cancer evades immunotherapy by luring immune T cells away from the tumor and trapping them in nearby fibrous tissue. An FDA-approved drug called AMD3100 freed those T cells to attack the cancer, significantly improving the effectiveness of immunotherapy in tumor samples.
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4. 高级产品经理 | RNA-seq

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNA-seq
• 📝 描述：Plasmidsaurus is expanding its RNA sequencing services beyond gene expression to support applications including cell line quality control, cellular phenotyping, and differentiation state assessment… The post Senior Product Manager | RNA-seq appeared first on RNA-Seq Blog.
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5. 这种常见的维生素缺乏症会造成类似正常衰老的症状。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Vitamin B12 is needed in microscopic amounts, but a shortage can have major effects on health and energy. The vitamin was first linked to a lifesaving liver treatment for pernicious anemia nearly 100 years ago. Today, researchers are finding that B12 may also help keep cellular powerhouses called mitochondria functioning properly. This could explain why some people experience fatigue and brain fog even before traditional signs of deficiency show up.
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• GSE325774 WDR82 通过抑制 ERK 驱动的趋化因子表达和中性粒细胞浸润来抑制乳腺癌进展
• GSE316441 人类胆管癌表观遗传调控因子和代谢重编程的转录组分析
• GSE316440 人类胆管癌[肝脏]表观遗传调控因子和代谢重编程的转录组分析
• GSE315405 系统生物学方法揭示了福尔马林灭活疫苗诱导小鼠抗伯氏考克斯体保护性免疫的细胞和分子机制
• GSE314257 人类胆管癌表观遗传调控因子和代谢重编程的转录组分析 [HuCCT-1]
• GSE294339 BMAL1 和 YAP 协同劫持增强子并促进衰老表皮的炎症 [RNA-seq Col14]
• GSE294336 BMAL1 和 YAP 协同劫持增强子并促进衰老表皮的炎症 [RNA-seq Aged_adult]
• GSE293809 乳腺癌乳头溢液、囊内液和肿瘤组织表面的细胞外囊泡 miRNA 谱
• GSE328185 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [RNA-Seq 上皮]
• GSE326641 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [scRNA-seq]
• GSE326490 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [RNAseq 小鼠局部 NEDD8i]
• GSE326489 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [RNA-Seq SUMO2, NEDD8]
• GSE326488 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [RNA-Seq 小鼠]
• GSE326487 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [RNA-Seq]
• GSE300777 剪接体蛋白指导 RNA 甲基化以调节基因表达并沉默逆转录转座子 [RNA-seq]
• GSE300775 剪接体蛋白指导 RNA 甲基化以调节基因表达并沉默逆转录转座子 [ChIP-seq]
• GSE316466 ALKBH5 在癌症相关成纤维细胞中通过 HSF1–LIF 轴促进胰腺癌转移 [ATAC-seq]
• GSE301266 DNAmBERT：一种基于Transformer的模型，利用DNA序列和甲基化数据进行稳健、无创的癌症诊断
• GSE300464 TET3通过负调控I型干扰素信号通路促进肿瘤免疫逃逸
• GSE298183 METTL3依赖的m6A甲基化在动脉粥样硬化内皮炎症中的作用[eCLIP]
• GSE298180 METTL3 依赖的 m6A 甲基化在动脉粥样硬化内皮炎症中的作用 [RNA]
• GSE336580 γ-生育酚通过PSEN1–SYT7–PI3K/Akt轴减弱COPD相关巨噬细胞炎症
• GSE336537 转录组变化驱动TGF-β诱导的前囊下白内障涉及的多个调控通路
• GSE325528 RNA-seq 分析在微创超声心动图引导的退行性二尖瓣反流小鼠模型中左心房重构
• GSE321667 抗PD-1或抗PD-1纳米胶囊治疗后小鼠肺组织中潜在免疫相关不良事件的评估
• GSE320559 LUCAT1 通过 STAT1 介导的转录调控驱动槟榔碱诱导的头颈癌进展
• GSE308710 茄碱通过ROS/p38 MAPK信号通路诱导肝内胆管癌细胞凋亡和铁死亡
• GSE304220 癌症恶病质诱导棕色脂肪组织衰老重编程和脂肪细胞分泌促恶病质的S100A9
• GSE301978 诱导条件性敲除 Satb1 对胸腺细胞亚群的影响 [RNA-seq]
• GSE301891 RNA-Seq 分析类风湿性关节炎背景下用叶黄素处理的成纤维细胞样滑膜细胞
• GSE276749 哺乳动物 T 细胞中的元结构域基因组关联（CD4/CD8 数据）
• GSE276057 哺乳动物T细胞中的元结构域基因组关联
• GSE266505 转录和黏连蛋白直接基因组定位和结构域边界可塑性
• GSE93797 独特的驱动基因和 Hedgehog 表达定义了形态学基底细胞癌
• GSE336609 KRAS抑制剂是阑尾腺癌的有效疗法
• GSE333732 一年生鳉鱼早期免疫细胞发育先于原肠胚形成
• GSE333518 老年马凡氏综合征小鼠胸主动脉瘤生长停滞
• GSE327545 SARS-CoV-2 核衣壳通过巨噬细胞中的 Toll 样受体信号通路诱导过度炎症和血管渗漏
• GSE326753 类泛素蛋白 NEDD8 和 SUMO2 调控上皮稳态、再生和炎症
• GSE326639 类泛素蛋白 NEDD8 和 SUMO2 控制上皮稳态、再生和炎症 [Xenium]
• GSE300779 剪接体蛋白指导 RNA 甲基化以调节基因表达并沉默逆转录转座子 [RIP-seq]
• GSE300776 剪接体蛋白指导 RNA 甲基化以调节基因表达并沉默逆转录转座子 [smallRNA-seq]
• GSE336584 新着丝粒无法维持 DNA 甲基化边界，导致 CENP-A 漂移、不稳定和染色体分离错误
• GSE336209 肺结核分枝杆菌感染的肺部环境影响局部单核细胞分化
• GSE304436 ALKBH5 在癌症相关成纤维细胞中通过 HSF1–LIF 轴促进胰腺癌转移 [MeRIP-seq]
• GSE304433 ALKBH5 在癌症相关成纤维细胞中通过 HSF1–LIF 轴促进胰腺癌转移 [RIP-seq]
• GSE304431 ALKBH5 在癌症相关成纤维细胞中通过 HSF1–LIF 轴促进胰腺癌转移 [CUT&Tag]
• GSE329556 木糖基转移酶-II缺乏症会重塑先天免疫信号传导并破坏人类巨噬细胞的极化状态
• GSE307588 人类肾脏类器官缺氧损伤的空间分布分析
• GSE289335 TRIM37 与 TRIM28 相互作用，在迁移过程中维持原始生殖细胞的特性 [bulkRNA-seq, scRNA-seq]
• GSE289333 TRIM37 与 TRIM28 相互作用，在迁移过程中维持原始生殖细胞的特性 [ATAC-seq]