科研日报 2026-06-06

Page content

📅 Daily Report - 2026-06-06

今日筛选出 31 条内容,来自 2 个来源

Powered by 科研普拉斯 & Claude

🤖 今日AI智能总结

🧬 数据前沿

今日焦点

  • mRNA疫苗反应性机制解析:揭示了IFN信号通路在单核细胞中的基线水平及注射部位的抗体介导免疫激活如何影响mRNA疫苗的反应性(涉及人与小鼠模型)。
  • 肿瘤免疫治疗新靶点:发现CD39+肿瘤相关NK细胞对NKG2A阻断疗法在肺癌中产生响应,并揭示了KRAS G12C突变在肺癌中与PD-1联合治疗的增效作用。

主要方向

  • 肿瘤微环境与免疫调控:研究了肿瘤相关巨噬细胞的吞噬作用对血管生成和染色质重塑的影响,以及CD39+ NK细胞在肺癌中的响应机制。
  • 肠道损伤与修复机制:探索了生酮饮食通过JAK2/STAT3/RORγt/IL-17A信号通路及肠道菌群缓解辐射诱导肠损伤的机制。
  • 自身免疫疾病与代谢调控:研究了STK25 m6A修饰调控CD4+ T细胞糖酵解及免疫失衡在系统性红斑狼疮中的作用。

技术亮点

  • 多组学技术整合应用:结合ATAC-seq、10x Xenium/Multiome、NanoString nCounter、RNA-seq等技术,多维度解析基因组结合、转录组表达及细胞相互作用。
  • 疾病模型与类器官研究:利用小鼠模型和类器官系统,结合空间转录组学,研究疾病进展和治疗响应。

🧪 博客更新

今日焦点: 科学家首次成功靶向KRAS突变,新型药物显著延长胰腺癌患者生存期;同时,研究揭示了脑肿瘤(IDH突变胶质瘤)通过基因与细胞状态改变,演变为更具侵袭性、耐药性的肿瘤机制。

主要方向

  • 攻克“不可成药”的胰腺癌KRAS突变靶点。
  • 揭示侵袭性脑肿瘤(IDH突变胶质瘤)耐药机制。

技术亮点

  • 整合DNA与单细胞RNA测序技术,解析肿瘤进化过程。
  • 开发针对KRAS突变的新型药物(daraxonrasib)。

📚 分类浏览

🧬 数据前沿 (29条)

详细内容(前10条)

1.GSE333173 生酮饮食通过肠道微生物群介导的JAK2/STAT3/RORγt/IL-17A信号通路减轻急性放射引起的肠道损伤

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:pathway、gut、regex:gut(-?microbiome)?、regex:intestin(e|al)
  • 📝 描述:Contributors : Jingjing Yang ; Zhi Ling ; Ming Zhou ; Mingyang Tao ; Jingxian Mao ; Yefei Zhu ; Xuebing YanSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis study demonstrates that ketogenic diet (KD), a high-fat and low-carbohydrate dietary regimen, exerts protective effects against RIII through dual mechanisms involving microbial regulation and inflammatory pathway inhibition.
  • 🔗 查看原文

2.GSE333952 单核细胞中的基线干扰素信号传导和注射部位抗体介导的先天激活影响 mRNA 疫苗的反应原性 [ATAC-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:vaccine、antibody、ATAC-seq
  • 📝 描述:Contributors : Natacha Madelon ; Gustavo A Ruiz Buendía ; Arnaud M DidierlaurentSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensThe local and systemic symptoms that follow vaccination -collectively referred to as reactogenicity- are common, yet the mechanisms underlying individual variability remain poorly understood. Through longitudinal immune profiling of vaccinated individuals and mechanistic studies in mice, we identified key immunological determinants of reactogenicity induced by mRNA vaccines. Systemic adverse events were associated with stronger interferon and pro-inflammatory responses following the second dose of COVID-19 vaccine, which were also correlated with the magnitude of the antigen-specific adaptive responses. This heightened inflammation occurred within 24 hours of vaccination and originated primarily from the injection site and was characterized by enhanced recruitment and activation of myeloid cells, particularly monocytes. Two mechanisms contributed to this response: (1) early interferon production by muscle T cells generated after the first dose and (2) FcγR-dependent chemokine induction by antigen-specific antibodies. Consistently, serum antibody levels prior to vaccination correlated positively with reactogenicity. In addition to this local amplification mechanism, variability in reactogenicity was influenced by the baseline immune state, as individuals with a pre-existing interferon-stimulated gene signature in monocytes, detectable at both transcriptomic and epigenetic levels, were more prone to systemic symptoms. Our findings reveal molecular and cellular mechanisms driving vaccine reactogenicity, providing a framework for the design of less reactogenic vaccines.
  • 🔗 查看原文

3.GSE319755 细胞毒性 CD39+ 肿瘤相关 NK 细胞对肺癌中的 NKG2A 阻断有反应(10 倍 Xenium)

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、cancer、10x
  • 📝 描述:Contributors : Wiebke Rackwitz ; Annalena Brüggemann ; Carina A Pawlow ; Evgeny Chichelnitskiy ; Clara Serger ; Alfred Zippelius ; Lavinia Neubert ; Christine FalkSeries Type : OtherOrganism : Homo sapiensNatural killer (NK) cell–targeting immunotherapies are emerging, yet the differentiation and functional states of tumor-infiltrating NK cells remain poorly understood. Using matched single-nucleus RNA and ATAC sequencing of samples from patients with non–small cell lung cancer (NSCLC), we resolved the transcriptional and epigenetic landscape of intratumoral NK cells. We identified two tumor-associated NK (taNK) cell subsets marked by expression of ITGAE (CD103) and ITGA1 (CD49a) that display features of tissue residency and dysfunction while preserving cytotoxic function. Trajectory and regulon analyses revealed an inflammation-driven transition from early granzyme K (GZMK)+ NK cells toward an ENTPD1+ (CD39+) effector state characterized by interferon-stimulated gene (ISG) programs. Functional profiling established CD39+ taNK cells as the dominant cytotoxic NK cell population with superior killing capacity that was further potentiated by NKG2A blockade. This study offers mechanistic insights into NK cell differentiation in NSCLC and establishes CD39+ taNK cells as a targetable effector population for immunotherapy.
  • 🔗 查看原文

4.GSE304741 细胞毒性 CD39+ 肿瘤相关 NK 细胞对肺癌中 NKG2A 阻断的反应 (10X Multiome)

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor、cancer、10x
  • 📝 描述:Contributors : Clara Serger ; Lucas Rebuffet ; Michael T Sandholzer ; Eric Vivier ; Andrea Romagnani ; Alfred ZippeliusSeries Type : Genome binding/occupancy profiling by high throughput sequencing ; Expression profiling by high throughput sequencingOrganism : Homo sapiensNatural killer (NK) cell–targeting immunotherapies are emerging, yet the differentiation and functional states of tumor-infiltrating NK cells remain poorly understood. Using matched single-nucleus RNA and ATAC sequencing of samples from patients with non–small cell lung cancer (NSCLC), we resolved the transcriptional and epigenetic landscape of intratumoral NK cells. We identified two tumor-associated NK (taNK) cell subsets marked by expression of ITGAE (CD103) and ITGA1 (CD49a) that display features of tissue residency and dysfunction while preserving cytotoxic function. Trajectory and regulon analyses revealed an inflammation-driven transition from early granzyme K (GZMK)+ NK cells toward an ENTPD1+ (CD39+) effector state characterized by interferon-stimulated gene (ISG) programs. Functional profiling established CD39+ taNK cells as the dominant cytotoxic NK cell population with superior killing capacity that was further potentiated by NKG2A blockade. This study offers mechanistic insights into NK cell differentiation in NSCLC and establishes CD39+ taNK cells as a targetable effector population for immunotherapy.
  • 🔗 查看原文

5.GSE334067 配对突变检测和空间转录组学鉴定出与小鼠结肠炎肿瘤发生相关的细胞群

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:spatial、spatial transcriptomics、transcriptomics
  • 📝 描述:Contributors : Elisa B Moutin ; Giada Giavara ; Filipe C Lourenco ; Nefeli Skoufou-Papoutsaki ; Douglas WintonSeries Type : OtherOrganism : Mus musculusIn the progression from Inflammatory Bowel Disease to associated cancer, the clonal mutational landscape shifts from selection of mutations in inflammatory genes to selection for cancer-driver mutations. How prevalence and expansion of either type of mutant clones could be impacted by the cellular environments in which they arise, and how this affects the neoplastic outcome of colitis, remains unknown. Here, we combine in vivo lineage tracing, in silico modelling, mutational profiling and spatial transcriptomics in a mouse model of colitis-associated tumorigenesis to capture clone fates associated with chronic inflammation. We identify epithelial- and immune-enriched neighbourhoods and propose a model in which establishment of a reparative tissue environment facilitates tumour initiation by promoting the selection and expansion of pro-oncogenic clones, reducing the span of inflammation-resistant neighbourhoods containing non-oncogenic clones.
  • 🔗 查看原文

6. GSE334206 STK25 m6A 修饰调节系统性红斑狼疮中 CD4+ T 细胞糖酵解介导的免疫失衡

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:immune、T cell
  • 📝 描述:Contributors : Ming Li ; Yunfei Li ; Lijun Pang ; Junjie Chen ; Shuangshuang Shang ; Chuanbing HuangSeries Type : OtherOrganism : Homo sapiensSystemic lupus erythematosus (SLE) is a complex autoimmune disease with an incompletely understood pathogenesis. N6-methyladenosine (m6A) has been implicated in immune regulation and disease progression, yet its role in disrupting immune homeostasis in SLE, particularly in CD4+ T-cell differentiation, remains poorly understood. In the present study, m6A-modified RNA immunoprecipitation sequencing (m6A-seq) and RNA sequencing (RNA-seq) of peripheral blood mononuclear cells from patients with SLE identified serine/threonine protein kinase 25 (STK25) as a candidate gene exhibiting abnormal m6A modification, and its expression was subsequently validated using reverse transcription-quantitative (RT-q)PCR. CD4+ T cells isolated from MRL/lupus-prone mice underwent lentiviral-mediated STK25 knockdown, and glycolytic activity was evaluated through measuring glucose uptake and lactate production. Western blotting and RT-qPCR demonstrated that STK25 knockdown reduced the expression of glycolysis-associated genes (glucose transporter 1, hexokinase 2, pyruvate kinase M2 and lactate dehydrogenase A) and the Treg-specific transcription factor Foxp3, while increasing the expression of the Th17- and Th2-associated transcription factors, RORγt and Gata3. Flow cytometry further confirmed enhanced differentiation of Th17 and Th2 cells accompanied by a reduction in Treg cells, indicating disruption of immune homeostasis. Collectively, these findings suggested that aberrant m6A modification contributes to the downregulation of STK25 expression, thereby promoting glycolytic reprogramming and CD4+ T-cell subset imbalance in SLE. STK25 may therefore represent a potential therapeutic target for restoring immune homeostasis in SLE.
  • 🔗 查看原文

7. GSE264036 Pcbp1 由于调节碳水化合物和氨基酸代谢,对幼稚型多能性向启动型多能性转变至关重要 [ChIP-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:metabolism、ChIP-seq
  • 📝 描述:Contributors : Evgeny Bakhmet ; Evgeny Potapenko ; Nadezhda VorobyevaSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusEmbryo implantation coincides with the Naïve-to-Primed pluripotency transition. From fertilization to implantation only a number of cleavages is observed without significant embryo growth. Embryo-uterine connection provides necessary nutrients for further development while metabolism intensification is occurred. We have found that in vitro Naïve-to-Primed pluripotency transition of ESCs with Pcbp1 knockout is worsened – reduction of proliferation and cell death is observed. By using ChIP-seq, RNA-seq and Mass-spectrometry we show that Pcbp1 is detrimental for pluripotent properties, but is crucial for carbohydrate and amino acid metabolism intensification. According to this, functional approaches showed protein synthesis, glycolysis and respiration decline, while embryos deficient for Pcbp1 demonstrated growth absence after implantation.
  • 🔗 查看原文

8. GSE264035 Pcbp1 由于调节碳水化合物和氨基酸代谢,对幼稚型多能性向启动型多能性转变至关重要 [RNA-seq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:metabolism、RNA-seq
  • 📝 描述:Contributors : Evgeny Bakhmet ; Evgeny PotapenkoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusEmbryo implantation coincides with the Naïve-to-Primed pluripotency transition. From fertilization to implantation only a number of cleavages is observed without significant embryo growth. Embryo-uterine connection provides necessary nutrients for further development while metabolism intensification is occurred. We have found that in vitro Naïve-to-Primed pluripotency transition of ESCs with Pcbp1 knockout is worsened – reduction of proliferation and cell death is observed. By using ChIP-seq, RNA-seq and Mass-spectrometry we show that Pcbp1 is detrimental for pluripotent properties, but is crucial for carbohydrate and amino acid metabolism intensification. According to this, functional approaches showed protein synthesis, glycolysis and respiration decline, while embryos deficient for Pcbp1 demonstrated growth absence after implantation.
  • 🔗 查看原文

9. GSE333510 单核细胞中的基线干扰素信号传导和注射部位抗体介导的先天激活影响 mRNA 疫苗的反应原性 [NanoString nCounter 数据集]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:vaccine、antibody
  • 📝 描述:Contributors : Natacha Madelon ; Gustavo A Ruiz Buendía ; Arnaud M DidierlaurentSeries Type : Expression profiling by arrayOrganism : Mus musculusThe local and systemic symptoms that follow vaccination -collectively referred to as reactogenicity- are common, yet the mechanisms underlying individual variability remain poorly understood. Through longitudinal immune profiling of vaccinated individuals and mechanistic studies in mice, we identified key immunological determinants of reactogenicity induced by mRNA vaccines. Systemic adverse events were associated with stronger interferon and pro-inflammatory responses following the second dose of COVID-19 vaccine, which were also correlated with the magnitude of the antigen-specific adaptive responses. This heightened inflammation occurred within 24 hours of vaccination and originated primarily from the injection site and was characterized by enhanced recruitment and activation of myeloid cells, particularly monocytes. Two mechanisms contributed to this response: (1) early interferon production by muscle T cells generated after the first dose and (2) FcγR-dependent chemokine induction by antigen-specific antibodies. Consistently, serum antibody levels prior to vaccination correlated positively with reactogenicity. In addition to this local amplification mechanism, variability in reactogenicity was influenced by the baseline immune state, as individuals with a pre-existing interferon-stimulated gene signature in monocytes, detectable at both transcriptomic and epigenetic levels, were more prone to systemic symptoms. Our findings reveal molecular and cellular mechanisms driving vaccine reactogenicity, providing a framework for the design of less reactogenic vaccines.
  • 🔗 查看原文

10. GSE333235 单核细胞中的基线干扰素信号传导和注射部位抗体介导的先天激活影响 mRNA 疫苗的反应原性 [human_RNAseq]

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:vaccine、antibody
  • 📝 描述:Contributors : Natacha Madelon ; Gustavo A Ruiz Buendía ; Arnaud M DidierlaurentSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensThe local and systemic symptoms that follow vaccination -collectively referred to as reactogenicity- are common, yet the mechanisms underlying individual variability remain poorly understood. Through longitudinal immune profiling of vaccinated individuals and mechanistic studies in mice, we identified key immunological determinants of reactogenicity induced by mRNA vaccines. Systemic adverse events were associated with stronger interferon and pro-inflammatory responses following the second dose of COVID-19 vaccine, which were also correlated with the magnitude of the antigen-specific adaptive responses. This heightened inflammation occurred within 24 hours of vaccination and originated primarily from the injection site and was characterized by enhanced recruitment and activation of myeloid cells, particularly monocytes. Two mechanisms contributed to this response: (1) early interferon production by muscle T cells generated after the first dose and (2) FcγR-dependent chemokine induction by antigen-specific antibodies. Consistently, serum antibody levels prior to vaccination correlated positively with reactogenicity. In addition to this local amplification mechanism, variability in reactogenicity was influenced by the baseline immune state, as individuals with a pre-existing interferon-stimulated gene signature in monocytes, detectable at both transcriptomic and epigenetic levels, were more prone to systemic symptoms. Our findings reveal molecular and cellular mechanisms driving vaccine reactogenicity, providing a framework for the design of less reactogenic vaccines.
  • 🔗 查看原文

💡 该来源还有 19 条内容,详见 文末

🧪 博客更新 (2条)

详细内容(全部2条)

1. 研究人员揭示了一种侵袭性脑瘤如何逃避治疗

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:tumor
  • 📝 描述:Integrated DNA and single-cell RNA sequencing reveals how recurrent IDH-mutant gliomas evolve into more aggressive, treatment-resistant tumors through genetic and cellular state changes… The post Researchers uncover how an aggressive brain tumor evades treatment appeared first on RNA-Seq Blog.
  • 🔗 查看原文

2. 科学家终于攻克了一种“不可成药”的胰腺癌靶点,使患者的生存期几乎翻了一番。

  • ✍️ 作者:未知作者
  • 🏷️ 关键词:cancer
  • 📝 描述:For decades, pancreatic cancer has been one of the most lethal cancers, with few effective treatment options. A new drug, daraxonrasib, targets the KRAS mutation that fuels most pancreatic tumors—something many scientists once thought couldn’t be done. In a major clinical trial, the treatment nearly doubled survival for patients with advanced disease and reduced the risk of death by 60%.
  • 🔗 查看原文

📊 关键词统计

关键词出现次数
tumor6
cancer6
metabolism3
vaccine3
antibody3
gut2
regex:gut(-?microbiome)?2
sequencing2
ATAC-seq2
10x2
immune1
T cell1
pathway1
regex:intestin(eal)
scRNA1
ChIP-seq1
RNA-seq1
nervous1
RNAseq1
regex:lymph(oatic)?

📎 更多内容

🧬 数据前沿 其他内容 (19条)

📅 报告生成时间:2026-06-05 22:38
🤖 由 GitHub Actions 自动生成