详细内容（前10条）

1. ⭐ GSE293878 CAR T 细胞驱动的肿瘤相关巨噬细胞中 iNOS 的诱导促进 B 细胞淋巴瘤的 CAR T 细胞耐药性

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、lymphoma、T cell、B cell、resistance
• 📝 描述：Contributors : Maro Davila ; Sae Bom Lee ; Jianmin WangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusChimeric antigen receptor (CAR) T cell therapies have revolutionized B cell malignancy treatment, but subsets of patients with large B cell lymphoma (LBCL) experience primary resistance or relapse after CAR T cell treatment. To uncover tumor microenvironment (TME)-induced resistance mechanisms, we examined patients’ intratumoral immune infiltrates and observed that the elevated levels of immunoregulatory macrophages in pre-infusion tumor biopsies are correlated with poor clinical responses. CAR T cell-produced interferon-gamma (IFN-γ) promotes the expression of inducible nitric oxide synthase (iNOS, NOS2) in immunoregulatory macrophages, impairing CAR T cell functionality. Mechanistically, iNOS-expressing macrophages upregulated the p53 pathway, mediating apoptosis and cell cycle arrest in CAR T cells, while downregulating the MYC pathway involved in ribosome biogenesis and protein synthesis. Furthermore, CAR T cell metabolism is compromised by the depletion of glycolytic intermediates and rewiring of the TCA cycle. Pharmacological inhibition of iNOS enhances the CAR T cell treatment efficacy in B cell tumor-bearing mice. Notably, elevated levels of iNOS+CD14+ monocytes were observed in the leukapheresis material of patients with non-durable response to CAR T cell therapy. These findings suggest that mitigating iNOS in tumor-associated macrophages (TAMs) by blocking IFN-g secretion from CAR T cells will improve outcomes for LBCL patients.
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2. ⭐ GSE293917 CTLA-4 阻断增强淋巴结生发中心反应，从而驱动胶质瘤特异性 IgG 产生和胶质瘤清除 [scRNA/BCR-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、regex:lymph(o|atic)?、glioma、scRNA
• 📝 描述：Contributors : Yumin Kim ; Jeongwoo LA ; Heung Kyu LeeSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Mus musculusThe orchestration of humoral immunity mediated by B cells in lymph nodes (LNs) is essential for generating adaptive immune response. Despite this crucial role in host defense, B cell responses in cancer have been primarily examined in the tumor microenvironment, while their role in LNs remains largely unexplored. We show that B cell responses in LNs induced by αCTLA-4 regulate glioblastoma (GBM) progression. αCTLA-4 promotes germinal center (GC) formation in deep cervical LNs by enhancing B cell–CD4 T cell interactions, leading to expansion of antigen-specific GC B cells and class switching. This generates tumor-specific IgG, which binds glioma cells and triggers antibody-mediated phagocytosis. Mice lacking antibody-secreting cells fail to benefit from CTLA-4 blockade, underscoring the importance of humoral immunity in tumor control. Our study highlights the role of B cells in tumor-draining LNs and uncovers a novel B cell–dependent mechanism underlying αCTLA-4 efficacy in GBM.
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3. ⭐ GSE293916 CTLA-4 阻断增强淋巴结生发中心反应，从而驱动胶质瘤特异性 IgG 产生和胶质瘤清除 [bulk RNA-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、regex:lymph(o|atic)?、glioma、RNA-seq
• 📝 描述：Contributors : Yumin Kim ; Jeongwoo La ; In Kang ; Byeong Hoon Kang ; Heung Kyu LeeSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe orchestration of humoral immunity mediated by B cells in lymph nodes (LNs) is essential for generating adaptive immune response. Despite this crucial role in host defense, B cell responses in cancer have been primarily examined in the tumor microenvironment, while their role in LNs remains largely unexplored. We show that B cell responses in LNs induced by αCTLA-4 regulate glioblastoma (GBM) progression. αCTLA-4 promotes germinal center (GC) formation in deep cervical LNs by enhancing B cell–CD4 T cell interactions, leading to expansion of antigen-specific GC B cells and class switching. This generates tumor-specific IgG, which binds glioma cells and triggers antibody-mediated phagocytosis. Mice lacking antibody-secreting cells fail to benefit from CTLA-4 blockade, underscoring the importance of humoral immunity in tumor control. Our study highlights the role of B cells in tumor-draining LNs and uncovers a novel B cell–dependent mechanism underlying αCTLA-4 efficacy in GBM.
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4. ⭐ GSE315742 CTLA-4阻断可增强淋巴结生发中心反应，从而促进胶质瘤特异性IgG的产生和胶质瘤的清除

• ✍️ 作者：未知作者
• 🏷️ 关键词：lymph、regex:lymph(o|atic)?、glioma
• 📝 描述：Contributors : Yumin Kim ; Heung Kyu LeeSeries Type : OtherOrganism : Mus musculusHumoral immunity, which is mediated by B cells that mature in germinal centers (GCs) in lymph nodes (LNs), is essential for adaptive immune responses. However, the involvement of B cell responses in anti-tumor and immunotherapy responses remains largely unexplored. Here, we show that activation of B cells in GCs of tumor-draining deep cervical LNs (dcLNs) is necessary for the efficacy of CTLA-4 immune checkpoint blockade in glioma in vivo. We demonstrate that anti-CTLA-4 therapy enhances follicular helper T cell (Tfh) expansion in dcLNs, leading to GC B cell formation, class switching to IgG, and the generation of glioma-specific antibodies. Glioma-bearing mice lacking antibody-secreting cells did not benefit from CTLA-4 blockade. Furthermore, using our new in vivo reporter system, we show that distally-secreted glioma-specific IgG infiltrates the tumor microenvironment and triggers glioma cell phagocytosis. Our study uncovers a previously unknown B cell–dependent mechanism underlying anti-CTLA-4 mediated control of glioma, which could be harnessed to treat other tumor types.
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5. ⭐ GSE313849 RNA 核酸外切酶 REXO4 解析 m6A 标记的 R 环并抑制抗肿瘤免疫 [REXO4-dTAG HeLa 细胞中的 RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、RNAseq
• 📝 描述：Contributors : Jieyou Zhang ; Kaiwen Bao ; Qi Chen ; Lei ShiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensTo determine if REXO4 depletion directly induces R-loop accumulation independent of transcription, we generated a HeLa cell line expressing endogenous REXO4 tagged with an N-terminal HA-FKBP12/F36V degron (REXO4-dTAG) via microhomology-mediated end joining (MMEJ)-based CRISPR/Cas9. Acute REXO4 degradation, achieved by a 4-hr treatment with dTAG-13 (dTAG), was then analyzed by RNA-seq to assess transcriptomic changes
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6. ⭐ GSE289625 RNA 核酸外切酶 REXO4 可解析 m6A 标记的 R 环并抑制抗肿瘤免疫 [RNAseq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity、RNAseq
• 📝 描述：Contributors : Jieyou Zhang ; Kaiwen Bao ; Chunyong Zhang ; Lei ShiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiens ; Mus musculusTranscription blockage frequently occurs in tumor cells, and aberrant R-loop forming during this process drives genome instability. However, the regulation of R-loop homeostasis and its dysregulation in tumorigenesis are still under investigation. Here, we report that the RNA exonuclease REXO4 preserves genome stability by reducing excessive R-loops. Mechanistically, REXO4 resolves R-loops by 3’-5’ exonucleolytic cleavage of the RNA strand on RNA-DNA hybrids, where an accessible end is created by RNA endonuclease and N6-methyladenosine (m6A) modification on RNA moieties promotes REXO4 localization and R-loop removal. REXO4 ablation-induced DNA damage stimulates interferon response and tumor immune infiltration to suppress squamous cell carcinoma (SCC) growth and metastasis. Importantly, targeting the exonuclease activity of REXO4 via the inhibitor we developed synergizes with PD-1 blockade to inhibit SCC progression by recruiting and activating CD8+ T cells. Thus, our study provides mechanistic insight into how m6A couples with exonuclease in R-loop clearance and genome maintenance, and uncovers a druggable epi-transcriptional machinery that blocks innate immune response and enables SCC immune evasion.
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7. GSE329199：单细胞RNA测序揭示波瓦桑病毒感染后中枢神经系统对年龄的依赖性反应

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Marcos R. Matos de Souza ; Erich R. MackowSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusPowassan virus (POWV) causes highly lethal encephalitis in the elderly and long-term cognitive deficits in survivors. Mirroring human severity, POWV LI9 directs age-dependent lethality in B6 mice resulting in spongiform encephalitis, gliosis and inflammatory cytokine/chemokine responses in the CNS. Here we analyzed POWV LI9 infected brains from 10 (young) and 50 week old (aged) B6 mice using 10x Genomics scRNA-seq to define CNS responses that direct age-dependent lethality.
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8. GSE313850 RNA 核酸外切酶 REXO4 解析 m6A 标记的 R 环并抑制抗肿瘤免疫 [CUT&Tag-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity
• 📝 描述：Contributors : Jieyou Zhang ; Kaiwen Bao ; Qi Chen ; Lei ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTo map the genome-wide distribution of R-loops and REXO4, we performed CUT&Tag-seq with antibodies against S9.6 (for R-loops) and REXO4.
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9. GSE313848 RNA 核酸外切酶 REXO4 解析 m6A 标记的 R 环并抑制抗肿瘤免疫 [MRC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity
• 📝 描述：Contributors : Jieyou Zhang ; Kaiwen Bao ; Qi Chen ; Lei ShiSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensTo achieve a more specific mapping of m6A-marked R-loops, we developed an m6A-marked R-loop CUT&Tag sequencing (MRC-seq) approach to map m6A-marked R-loops, which involves the specific isolation of R-loops using an S9.6 antibody-based CUT&Tag approach followed by m6A immunoprecipitation.
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10. GSE313847 RNA 核酸外切酶 REXO4 可解析 m6A 标记的 R 环并抑制抗肿瘤免疫 [END_seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immunity
• 📝 描述：Contributors : Jieyou Zhang ; Kaiwen Bao ; Qi Chen ; Lei ShiSeries Type : OtherOrganism : Homo sapiensTo investigate the features of DNA structures that are protected by REXO4, we performed END-seq, a method that maps DSBs at nucleotide resolution in REXO4-depleted cells.
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1. CBD可能通过镇静大脑免疫系统来延缓阿尔茨海默病的发展。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、Alzheimer
• 📝 描述：CBD may be doing far more than just easing pain or anxiety — new research suggests it could help fight Alzheimer’s disease by calming the brain’s runaway immune response. In experiments using Alzheimer’s mice, scientists found that inhaled CBD reduced key drivers of neuroinflammation, a damaging process increasingly linked to memory loss and brain degeneration.
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2. Decima 能够以单细胞分辨率预测基因表达。

• ✍️ 作者：未知作者
• 🏷️ 关键词：single-cell
• 📝 描述：RNA sequencing from more than 22 million cells trained a model that predicts cell-type-specific gene expression and noncoding variant…
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• GSE313845 RNA 核酸外切酶 REXO4 可解析 m6A 标记的 R 环并抑制抗肿瘤免疫 [ChIP-Rx]
• GSE304692 肝细胞昼夜节律时钟控制胆固醇代谢并防止代谢功能障碍相关的脂肪性肝炎 (MASH) [RNAseq_palmitate_silencing]
• GSE304691 肝细胞昼夜节律时钟控制胆固醇代谢并防止代谢功能障碍相关的脂肪性肝炎 (MASH) [RNAseq_diurnal]
• GSE291757 利用多重转录组学筛选药物组合，并在单细胞分辨率下定义治疗作用机制
• GSE289626 RNA外切酶REXO4可解析m6A标记的R环并抑制抗肿瘤免疫
• GSE333670 SOX4驱动脂肪基质细胞发生与癌症相关的成纤维细胞样转变，从而促进代谢性疾病的发生。
• GSE326012 ESR1 突变影响 CDK4/6 抑制剂获得性耐药的克隆动态、遗传多样性和细胞状态。[scRNA-Seq]
• GSE324094 ESR1 突变塑造了 CDK4/6 抑制剂获得性耐药的克隆动态、遗传多样性和细胞状态 [ATAC-seq]
• GSE324093 ESR1 突变塑造了 CDK4/6 抑制剂获得性耐药的克隆动态、遗传多样性和细胞状态 [RNA-seq]
• GSE298091 甘蓝型油菜雄性发生过程中的转录和表观遗传重编程 [RNA-seq]
• GSE298089 甘蓝型油菜雄性发生过程中的转录和表观遗传重编程 [ChIP-seq]
• GSE326132 USP18 通过调节 DNA 修复影响卵巢癌细胞的铂类耐药性
• GSE333323 STRIP2 稳定 LCN2 以抑制铁死亡并促进结直肠癌恶性转化
• GSE317738 研究发现，白色脂肪组织中的 Otopetrin 1 可预测癌症恶病质的进展并防止体重减轻。
• GSE305290 Largazole 通过 miR-125b-5p 靶向 Musashi 蛋白表达，并增强三阴性乳腺癌细胞对辐射的敏感性
• GSE333477 拓扑异构酶 1 在超级增强子处的结合动态性调节巨噬细胞中 TLR 反应基因表达程序
• GSE326806 免疫记忆获得过程中的3D染色质动力学
• GSE319144 MARCHF6-ERAD 调控肝脏脂质代谢和 MASLD 的发展
• GSE310550 人类内皮细胞中 miR-29a/c-3p 的性别二态性调控：细胞功能和转录组
• GSE333251 研究发现，靶向 WNK1 可抑制急性髓系白血病进展并增强对维奈托克的敏感性。
• GSE333202 复杂型CVID病程中BAFF和B细胞表型的共存改变
• GSE333156 寄生植物菟丝子在侵染本氏烟草期间的小RNA测序
• GSE331230 合成增强子的慢病毒单细胞MPRA揭示了基于基序亲和力的细胞状态特异性编码
• GSE331072 合成增强子的慢病毒单细胞 MPRA 揭示了基于基序亲和力的细胞状态特异性编码 [sc-lentiMPRA]
• GSE331030 合成增强子的慢病毒单细胞 MPRA 揭示了基于基序亲和力的细胞状态特异性编码 [sc-lentiMPRA 2]
• GSE330812 指尖血干样本中的microRNA生物标志物可预测转移性前列腺癌患者的生存期
• GSE329677 DNA损伤驱动神经元中一种独特的、与阿尔茨海默病相关的衰老状态
• GSE298515 CNP-Cre 小鼠中致癌慢病毒诱导的小鼠少突胶质细胞来源的胶质母细胞瘤。
• GSE298090 甘蓝型油菜雄性发生过程中的转录和表观遗传重编程 [亚硫酸氢盐测序]
• GSE268439 小 RNA 测序揭示了 miRNA 在拟南芥愈伤组织响应干旱和氮素缺乏胁迫中的重要功能
• GSE333674 MAPK 和/或 Wnt 信号激活后 TCF7 敲除细胞和对照细胞的批量 RNA 测序。
• GSE325514 研究发现，去分化黑色素瘤细胞中 IFNγ 反应增强是由于染色质重塑所致，该结果已通过 ATAC-seq 测序得到证实。